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187 Cards in this Set
- Front
- Back
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What are the three mechanisms of tumorigenesis?
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1. Introduction of new genetic material by viruses
2. Alteration of genes by radiation or chemicals - generates a new protein - induces genes not normally expressed 3. Chromosomal translocations - may become permanent when an oncogene is translocated with a promoter or enhancer => permanent activation of oncogene |
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How do tumors differ from normal cells?
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The lack of regulation of the cell cycle leads to tumor cells -- i.e. abnormal growth of cells or tissues.
See activation of oncogenes and or inactivation of tumor suppressor genes |
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List 5 agents of tumorigenesis and give specific examples of each.
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1. Viruses
- Papillomavirus - EBV - Adenovirus 2. Chemicals "ABCD" A - aflatoxin B - benzene C - chloroform D - dichlorobenzene 3. Physical agents - ionizing radiation 4. Genetic disposition - absence of repair mechanisms 5. Immunodeficiency - diminished normal immune surveillance |
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Tumor associated antigens vs. tumor specific antigens
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* Tumor associated antigens = Ag expressed following oncogenic transformation
e.g. virus induced neoantigens are shared by all tumors induced by same virus (same specificity) * Tumor specific antigens = chemically induced neoantigens are of different specificity |
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TRUE or FALSE
Tumor formation may result in the re-expression of "oncofetal antigens". |
TRUE
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What are the two main oncofetal antigens?
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* CEA (carcinoembryogenic ag)
* AFP (alpha-fetoprotein) |
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Increased levels vs. cancers present
* CEA * AFP * ß-HCG * PSA |
* CEA levels >= 2.5 and < 10.0 ng/mL are indicative of colo-rectal cancer
* AFP levels > 20ng/mL are indicative of hepatoma, non-seminal testicular, and ovarian * ß-HCG levels elevated in WOMEN are indicative of gestational trophoblastic neoplasia * PSA levels elevated in MEN with prostate cancer OR benign prostatic hypertrophy |
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What are differentiation antigens?
What is the role of these antigens in immunodiagnosis? |
Certain antigens are expressed at specific stages of cellular development and differentiation.
These antigens help ascertain in which stage of development and differentiation a certain cells has arrested in -> leading to developing the appropriate therapy for it |
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Which is more effective in host response to tumors, CMI or humoral?
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CMI
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Which cells of the CMI are found to be important in immunosurveillance of tumors?
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NK cells, CTL cells (tumor specific), and macrophages
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TRUE or FALSE
Tumor specific antibodies may mediate antibody dependent cellular cytotoxicity |
TRUE
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Which cytokines induce cellular anti-tumor activity?
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IL-2
IL-12 IFN-αβγ TNF-αβ |
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Some antibodies may protect rather than kill tumor cells. What are they called and how do they protect tumors?
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Enhancing or blocking antibodies
May function as forming complexes with soluble tumor antigen |
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List 5 different immunotherapies available for attacking tumors.
Which are active and which are passive? |
ACTIVE:
1. Cytokines 2. LAK (lymphokine activated killer cells) -- NK cells 3. TIL (tumor infiltrating lymphocytes) -- CD8+ & NK cells 4. MAK (macrophage activated killer cells) ----- PASSIVE: 5. Antibody |
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Give details as to the hypersensitivity responses mentioned below:
Type I, II, III, IV |
I: IgE mediated activation of mast cells
II: Ab mediated binding of cell or tissue bound antigens III: Ab mediated immune complexes IV: T cell mediated DTH |
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Type I hypersensitivity brings about what two disorders?
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* Anaphylaxis
* Allergies |
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If a type I hypersensitivity is not mediated by IgE, what is it called?
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Anaphylactoid
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Anaphylactoid responses mimic ___________ but do not involve ___________
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Anaphylaxis, IgE
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TRUE or FALSE
Bee stings can mimic anaphylaxis as melitin can degranulate mast cells |
TRUE
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Production of IgE by B cells is under the control of which cells?
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Th2
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IgE binds to Ag and can produce both local and systemic reactions.
Name them. |
Local: wheal and flare reaction
Systemic: serious and possibly fatal |
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The wheal and flare reaction can be demonstrated by this method.
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Prausnitz-Kustner reaction
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In which units is IgE measured?
What is the normal range? |
3-150 ng/ml, usually < 100
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What is the normal range for IgG?
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5.4 - 16.1 mg/ml, usually ~10 mg/ml
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Very high levels of IgE are seen in which atopic disease?
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Eczema
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Allergens and IgE levels can be determined by which tests?
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* Skin prick test = semi-quantitative and specific
* RAST = quantitative and specific |
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How is a skin prick test administered?
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1. Place small drop of allergen solution on the patient's skin
2. Insert into intra-epidermis using hypodermic needle 3. Wheal and flare response = positive (+) result |
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What two chemicals act as positive and negative controls?
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+ = histamine
- = saline |
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Which blocker should be discontinued prior to testing?
Which diseases preclude the test from being carried out? |
H1 blockers
Eczema and other similar conditions |
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Name the advantages and disadvantages of the skin prick test.
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Advantages:
- cheap - results available immediately - sensitive to Ag - results visible to patient Disadvantages: - must know the procedure for these tests |
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How is a RAST test administered?
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1. Insoluble Ag incubated in test serum to react with Ag-specific Ab
2. Then incubated in radiolabeled anti-human IgE => binds radiolabel in a specific and quantifiable way |
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Does RAST require knowledge of skin testing technique?
Does it require availability of allergen extracts? |
No to both
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Does RAST pose a risk of systemic reaction?
Can it be used with current skin conditions such as eczema, dermatitis, psoriasis? |
No
Yes |
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Compared to the skin prick test, what are the advantages and disadvantages of RAST?
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advantages: can be used on patients using antihistamines and antidepressants
disadvantages: expensive and time consuming |
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What is the significance of results with allergy testing?
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1. results may not correlate with a clinical condition
2. one needs to have an idea what the allergen is prior to testing 3. positive result DOES NOT correlate with improvement in condition |
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Transmission of atopicity is ____________ and ____________
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multigenic and autosomal
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Which antigens elicit strong IgE responses?
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penicillin
certain pollens |
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What determines a protein to be an allergen?
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It's shape and surface features
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TRUE or FALSE
Repeated exposure is necessary for an allergy to develop. |
TRUE
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List some of the common allergens.
* Airborne * Food |
AIRBORNE
- grass, tree pollen - mold spores - animal dander - house-dust mite FOOD - fish/shellfish - eggs - peanuts - milk - gluten |
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This type of mast cells occurs in the skin, intestinal submucosa, breast, and axillary lymph nodes
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MC-TC
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This type of mast cells occur in the lung and intestinal mucosa.
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MC-T
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Mast cells contain these type of proteinases
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* tryptase
* chymase |
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This humoral cell type is associated with an inflammatory response to helminth parasites.
Name the two major proteins it contains. |
Eosinophils
Major basic protein (MBP) Major cationic protein (MCP) |
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Regulation of eosinophils appear to be controlled by ________ and ________
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IL-5
Eotaxin |
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IgE attaches to eosinophills through this receptor.
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Fc-RII (CD23)
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The cross-linking of this molecule on the surface of mast cells and basophils results in mediators and cytokines.
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Fc-RI
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Basophils and mast cells release two types of mediators. Name them.
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* preformed mediators (incl. biogenic amines)
* newly synthesized mediators |
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Name a preformed mediator (biogenic amine).
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Histamine
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Histamine binds to which target cell receptors?
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H1, H2, H3, H4
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What are the effects of histamine?
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1. smooth muscle contraction resulting in increased peristalsis of gut & bronchospasms in lung
2. vasodilation: large vessels constricted & small ones dilated -> "blushing effect" |
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List some of the newly formed mast cell mediators.
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* PGD2 = vasodilation, smooth muscle contraction
* LTC4/LTD4/LTE4 = vasodilation, smooth muscle contraction * PAF = vasoconstriction, increased permeability |
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These mediators have similar effects to histamine but over a much longer period of time
AND are responsible for much of the late phase response to anaphylaxis LIPOXYGENASE PATHWAY |
Leukotrienes
LTC4, LTD4, LTE4 |
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This group of mediators causes contraction of cardiac and smooth muscle
AND it can activate many leukocytes inclduing platelets and mast cells |
PAF
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This group of mediators causes contractions of smooth muscle
AND acts as a vasoldilator and bronchoconstrictor AND will stimulate pain and stimulate the hypothamalus to induce fever CYCLOOXYGENASE PATHWAY |
Prostaglandin D2
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What is the treatment for anaphylactic shock?
What helps to alleviate the late phase response? |
Epinephrine
Corticosteroids |
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This drug acts as a mast cell stabilizer for asthma and other respiratory conditions.
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Sodium cromoglycate
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Name four ways that type II hypersensitivity causes damage.
Give examples of each. |
1. activate complement leading to cell damage == immune thrombocytopenic purpura (ITP), intravascular autoimmune hemolytic anemia
2. activate ADCC for cytotoxic cell attack == autoimmune thyroiditis 3. antibodies induce phagocytosis of target cells. This occurs when M cells destroy red cells in the spleen and liver == extravascular autoimmune hemolytic anemia 4. Bind to receptors to either: activate the function of a cell or organ == hyperthyroidism OR switch off the function of a cell or organ == hypothyroidism |
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Name the different immunological conditions that bring about type III hypersensitivity.
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1. large amount of Ag and Ab accumulate creating a lattice
2. Ab-Ag complexes do not activate the classical complement cascade == complement deficiency 3. Ab-Ag complexes evade activation of the classical complement pathway |
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TRUE or FALSE
Immune complexes circulate throughout the body and are deposited in various sites, most notably: kidneys, joints, skin |
TRUE
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Immune complexes activate and recruit what?
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activate complement (through IgM, IgG3,1,2) and directly or indirectly recruit a number of inflammatory cells (neutrophils, M)
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How does the immune system protect against immune complexes?
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* The complement cascade and M cells act to remove IC.
* Erythrocytes carry away IC using CR1 to the liver and spleen * M cells attach to the IC using FcR and carry out phagocytosis |
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What are the basic clinical and immunological characteristics of Lupus?
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It affects the vasculature, kidneys, skin, joints, CNS, serous tissue
It's incidence approaches 1:2500 in the general population Higher in females between menarche and menopause *** Numerous ANAs will be found in Lupus |
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What is the difference between Serum sickness and Arthus reaction?
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Arthus reaction (LOCAL):
local tissue bound type III reaction that occurs after IM injection of antigens = pain and necrosis Serum sickness (SYSTEMIC): problem occurs when equine antiserum for bacterial toxins is administered. after subsequent administration, arthritis, myalgia, malaise, fever occur = IC may activate complement, release anaphylatoxins and cause mast cell degranulation |
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Differentiate between glomerulonephritis due to Goodpasture's syndrome and that due to the Lupus
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GOODPASTURE'S SYNDROME
Ab cross-reacts with the glomerular basement membrane and the alveolar basement membrane (type II) linear deposition of IgG along the glomerular basement membrane LUPUS clumps of immune complex deposited on the glomerular basement membrane that have a "lumpy-bumpy" appearance |
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What is the mechanism operating in type IV hypersensitivity?
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Immune response mediated by CD4+ T cells -- archetypal Th1 response
In some situations CD8+ T cells are also recruited. As expected from Th1 cells, the "effector cells" are largely M. |
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DTH is a major immune response against tissues or organs that the body detects as dangerous. Name them.
What are some of the common conditions in which type IV takes place? |
DTH acts against solid organ transplants (heart, liver, kidney) and solid tumors.
Acute: - poison ivy - hair dye - nickel - cement - cosmetics - latex |
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The substances that induce contact hypersensitivity are usually ____________
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haptens
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What is the function of type I hypersensitivity?
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As an anaphylactic reaction, it rids the body of parasites and tapeworms
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An individual who has an allergy is _____________
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Atopic
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TRUE or FALSE
Diseases can occur in isolation but they can also present with a mixture of hypersensitivity responses. |
TRUE
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Name a anaphylactoid responses.
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Bee stings can mimic anaphylaxis!
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IgE binds to which receptor on mast cells and basophils?
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FcER
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What is worrying about type I hypersensitivity?
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It can sometimes have a late phase reaction that occurs about 2 hours later and peaks at about 24 hours.
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TRUE or FALSE
The presence of staph aureus in the skin can exacerbate eczema in 50% of the cases |
TRUE
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TRUE or FALSE
Children of atopic parents show greater likelihood of also being atopic |
TRUE
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These cytokines induce the production of IgE
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IL-4, IL-13
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Name two important allergens that cause a reaction in people.
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Penicillin
Pollen antigen |
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What are the four fungi cell types?
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1. Yeasts (single celled)
2. Molds (filamentous) 3. Dimorphic (filamentous -> yeast) 4. mushroom, puffballs (filamentous cells organized into visible fruiting bodies) |
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Describe the general cell structure of the fungi.
* general * membrane * cell wall |
GENERAL
eukaryotic cells with all of the organelles intact MEMBRANE made up of "ERGOSTEROL", a major sterol membrane CELL WALL complex carbohydrate composed of "chitin with glucan" and mannose-proteins |
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Which parts of the fungi cell are targets of anti-fungal drugs?
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ergosterol membrane
cell wall glucan |
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Define the following terms:
Saprobes/saprophytes Symbionts Commensals Parasites |
* Saprobes/saprophytes
fungus living on dead organic material == breakdown wide range of organic materials including CELLULOSE * Symbionts benefit each other (lichens = combination of fungus with algae) * Commensals 2 organisms living together where one benefits; other not harmed * Parasites 2 organisms living together; one not benefiting and in cases harmed |
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Name the two routes that most fungi infect us by?
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1. airborne spores
2. traumatic implantation |
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Define the following:
* yeast, hyphae, pseudohyphae |
yeast: single celled fungi
hyphae: septate or aseptate filament of a fungus pseudohyphae: chains of cells formed by budding that, when elongated, resemble true hyphae; they differ from true hyphae by being constricted at the septa, forming branches that begin with a septation, and having terminal cells smaller than the other cells. |
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Define.
* dimorphic fungi |
Alternate between hyphal and yeast forms depending on environmental conditions
yeast @ 37C on enriched media hyphae @ 30C or lower on most media == "if it's cold, it's mold" |
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Define.
* septate and aseptate |
filamentous fungi have one of these two types of hyphae
ASEPTATE - lack regular cross walls - width is irregular - RAPID GROWTH - serious opportunists -> fatal overnight - phylum: zygomycota SEPTATE - has cross walls - UNIFORM WIDTH - most of the filamentous fungi fall under this heading |
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Define.
* dematiaceous and hyaline |
There are 2 basic colors for hyphase
dematiaceous = dark hyaline = colorless |
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Which type of hyphae is known for its rapid growth?
Which one is known for its uniform width? |
aseptate = rapid growth
septate = uniform width |
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In order to see the basic colors of hyphae, what must one do to the microscope?
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Lower it light output
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Name the four major dimorphic pathogenic genera found in the US general population
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"Blasted Cocci Spread Histo"
Blastomyces Coccidioides Sporothrix Histoplasma |
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Describe Candida albicans.
* yeast? * does it have hyphae and/or pseudohyphae? * part of normal flora? * opportunistic? * major cause of nosocomial bloodstream infections? * drug resistance a problem? |
* yeast
* both hyphae and pseudohyphae * normal flora * opportunistic * causes nosocomial infections * drug resistance seen in several Candida species |
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Define.
blastoconidia and conidia |
Both are spores
* blastoconidia = blastospores = buds (asexual spores) * conidia = spore bearing stalks - microconidia (small) or macroconidia (large) |
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Which of the following is used for ID of fungal cultures?
blastoconidia or conidia |
conidia
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Name the four ways that fungi cause disease.
Give examples for each. |
1. infections
- mycoses - adherence and invasion of tissue 2. allergy - airborne spores 3. mycotoxicosis - alfatoxin in stored peanuts 4. poisonings - poisonous mushroom ingestion - fermentation of carbs -> alcoholism |
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How do we acquire fungal infections?
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* Immune system plays important role in whether we get sick or not from our exposures
* Cell-mediated immunity is most important |
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How do we diagnose fungal infections?
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1. Direct detection with special fungal stains
2. Fungal cultures and antifungal susceptibilities 3. Serology: pt. Ab to fungus for system 4. Genetic probes 5. Skin testing: exposure or anergy? |
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Name the fungal stains used for detection and the color of the fungi as a result.
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Gomori silver stain - black
Periodic Acid Schiff - pink Calcofluor - white Immunofluorescents - ? |
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What is the classical treatment for Goodpasture's syndrome?
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Removal of the antibody through plasmapheresis can be of great value
plasmapheresis == rotating the blood quickly allowing the plasma to rise to the top and removing it automatically e.g. see cows and milk |
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Name a disease associated with type III hypersensitivity and the build-up of immune complexe lattice.
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Henoch-Schonlein Purpura
- IgA forms IC - demonstrated in respiratory infection where IC builds up in skin, gut, kidney - leads to PURPURA |
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This fungal culture is a gold standard used through labs
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Sabouraud's
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TRUE or FALSE
Enriched media with antibiotics and cycloheximide is used as a fungal culture |
TRUE
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For disease to occur the autoantibody titer is usually ___________ and it must be the ___________ type.
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high, correct
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___________ is associated with disease or can actually be involved in pathology
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antibodies
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Name three diseases in which T cells are involved in the pathogenesis.
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1. Insulin dependent diabetes mellitus (type 1 IDDM)
2. Hashimoto's thyroiditis 3. Multiple sclerosis |
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TRUE OR FALSE
If a patient has one organ specific autoimmune disease, they have a higher than normal chance of having another autoimmune disease at another site. |
TRUE
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Which autoantibodies is usually present in autoimmune diseases?
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IgG
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Type IV hypersensitivity is mediated by ________ (CD4+/CD8+) T cells of the _______ (Th1/Th2) type
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CD4+, Th1
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What are the factors behind autoimmunity?
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1. Exposure to pathogen or stimulus
2. Genetics 3. Gender, age, hormones |
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There is evidence that the following disease are linked to previous viral or bacterial exposures:
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1. Type 1 IDDM
2. Multiple sclerosis 3. DeQuervain's thyroiditis 4. Guillain-Barre syndrome |
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Describe MS.
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- episodes of neurological defects, separated in time, attributable to demyelinating white matter lesions that are separated in space.
- alternating relapses, remissions - cell immunity directed against myelin proteins (MBP) - more common at higher latitudes but migration to lower latitudes before age 15 decreases risk = some benefit from vitamin D - presence of oligoclonal bands in CSF = found in tertiary syphilis, SSPE, and rubeola infections |
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Describe deQuervain's thyroiditis.
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Mimics symptoms of autoimmune thyroiditis due to a known viral infection
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Describe Guillain-Barre syndrome.
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- acute inflammatory demyelinating polyneuropathy
- ascending paralysis + associated with CMV, EBV, and C. Jejuni |
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Why do infections initiate autoimmunity?
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1. Molecular mimicry = cross reacts with self Ag leading to an autoimmune disease
2. Disruption of cell or tissue barrier = if organism can break down immunoprivileged site, then autoimmune response can occur against the sequestered self-ag |
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What is an example of disruption of cell or tissue barrier?
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Mumps or orchitis leading to male sterility
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Name two 'reactive arthritides' diseases.
What are the commonly associated with? What are negatively associated with? |
Ankylosing spondylitis, Reiter's syndrome
Associated with HLA-B27 Negatively associated for RF (seronegative arthritides) |
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Describe ankylosing spondylitis.
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Chronic inflammatory disease affecting the vertebrae and sacroiliac joints
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What are the triad of symptoms associated with Reiter's syndrome?
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"Can't see, can't pee, can't climb a tree"
- Arthritis - Non-gonococcal urethritis - Conjunctivitis |
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Which bacterial infections is associated with AR and which with RS?
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AR = Klebsiella spp.
RS = Chlamydia Trachomatis |
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What is the association between Type 1 IDDM and HLA?
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HLA-DR3, HLA-DR4
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These two disease are linked to gender instead of genetics for their autoimmunity manifestations.
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- Lupus
- Pemphigus vulgaris |
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This autoimmune disease is always associated with pregnancy.
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Herpes Gestationis
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Define primary and secondary immunodeficiencies.
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Primary: idiopathic; as not being secondary to an infection, malignancy, or drugs
Secondary: acquired during life and are subsequents to other disease, condition, or therapy |
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What is the DiGeorge Syndrome?
What are some of the physical manifestations? |
Congenital thymic hypoplasia due to incomplete development of 3/4 pharyngeal pouches
- abnormal facies, hypoparathyroidism, CHD |
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What is the Wiskott-Aldrich syndrome?
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- x-linked disease
- WASp (protein) functions as a bridge between signaling and movement of actin filament in the cytoskeleton - limited to hematopoietic lineages |
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What is WAS characterized by?
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- Thrombocytopenia
- Eczema - Immunodeficiency (increased bacterial or viral infections) |
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What is CVI (common variable immunodeficiency)?
When does it occur in life? What are the complications of this condition? |
low total IgG, IgA levels
3rd, 4th decade of life infections and lymphoma (bacterial infections) |
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What is the most common primary immunodeficiency disease?
Are there IgE levels high or low? Are they susceptible to allergies? What might they develop if given blood products containing IgA? |
Selective IgA deficiency
High IgE Susceptible to allergies Develop anaphylaxis if given IgA with blood products |
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What is Bruton's Disease?
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- mutation in gene coding for Bruton tyrosine kinase (BTK)
- BTK is critical to the maturation of pre-B cells to mature B cells - These pts have NO PLASMA CELLS and NO SERUM ANTIBODIES |
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What bacterial infections do Bruton's Disease pts suffer from?
To which therapy do patients respond to? |
Encapsulated bacteria
- S. pneumoniae - H. Influenzae Gamma-globulin therapy |
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What is the marker for SCID?
What is the only hope for these patients? |
Low T cell count
Bone marrow transplant or enzyme replacement |
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Lack of C1 inhibitor causes what disease?
What is the most feared complication of HAE? |
Hereditary angioedema (HAE): an acute swelling of subcutaneous or submucosal tissue
Laryngeal edema |
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C1 inhibitor inhibits the components of what pathways?
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Fibrinolytic, clotting, and kinin pathways
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A deficiency of C5, C6, C7, C8 is associated with which infection?
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Neisseria infection = gram negative (-)
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Name a primary phagocyte deficiency.
What is it deficient in? What infections take advantage of this? How can it be detected? |
CGD (chronic granulomatous disease)
It lacks the ability to carry out a oxidative burst Gram negative (-) = S. aureus, Enterobacteriaceae By NBT (nitro-blue tetrazolium) = goes from yellow to blue |
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Name two opportunistic infections.
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PCP (pneumocystis jiroveci)
M. avium complex (MAC) |
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Give the definitions for the following:
Allograft Isograft Autologous Homograft Xenograft |
Allograft: genetically distinct individuals of the same species
Isograft: genetically identical individuals (twins) of the same species Autologous: transplants within one individual Homograft: graft from same species Xenograft: graft from another species |
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Rejectin is an immunological process with both _________ and ___________
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memory, specificity
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For optimal graft outcome, compatibility at 3 HLA loci is needed. What are they?
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HLA-A, HLA-B, HLA-C
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For related donors, what technique is used to confirm a match?
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Mixed lymphocyte reaction (MLR)
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Name the typing carried out on elective transplant.
Name the typing carried out on cadaver transplants. |
HLA typing
ABO tpying |
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What is the mixed lymphocyte reaction (MLR)?
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Donor and recipient cells cultured together.
- if compatible, nothing happens otherwise cells will proliferate - measured by uptake of H3-thymidine |
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Why is mixed lymphocyte reaction important for bone marrow transfer?
What test is carried out to assure not alloreactivity occurs? |
Because we could have a graft versus host disease (GVHD) come up.
one way MLC = irradiation of both donor and recipient cells, if no proliferation, then a match |
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Name a minor histocompatibility gene influencing graft rejection.
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HY proteins on encoded on the Y chromosome can become a problem if the donor is male and recipient female
LEADS TO REJECTION |
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What are the immunological steps in graft rejection?
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1. CD4+ of Th1 type initiate DTH (type IV)
2. CD8+ and NK cells kill donor cells 3. Ab give rise to complement activation and ADCC |
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What type of hypersensitivity is witnessed by:
xenografts allografts |
xenografts = type III
allografts = type II |
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In a bone marrow transplant, GVHD can occur.
What does GVHD attack in the recipient? |
- skin (blister)
- gut (slough) - liver (hepatitis) |
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What is the difference between:
Acute GVH Chronic GVH |
Acute GVH = difficult to treat once established
Chronic GVH = attack similar sites to acute GVHD; symptoms similar to autoimmune diseases |
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TRUE OR FALSE
Skin is a major barrier against infection |
TRUE
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How does skin defend against infection?
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- fatty acids inhibit microbial growth
- bacterial commensals on the surface as part of the normal flora |
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What are three expulsion mechanisms for getting rid of pathogens?
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1. cough and sneeze reflex
2. vomiting and diarrhea 3. urinary flow |
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Eczema is exacerbated by the presence of ______________ on the skin
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S. aureus
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High body temperature inhibits the growth of ______________
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M. leprae
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Poliovirus resides in the gut without causing disease but only when it reaches the __________ does paralysis occur
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CNS
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What is the virulent version of E. coli
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O157:H7
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What is vertical transmission?
What is horizontal transmission? |
vertical transmission is from mother to offspring
horizontal transmission is human to human via: - respiratory - oral/fecal - sexual - direct contact (not common) |
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Name the cell surface CD that the following viruses attach to:
HIV Rhinovirus Measles |
HIV - CD4
Rhinovirus - CD54 (ICAM-1) Measles - CD46 |
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Define Obligate intracellular pathogens.
What are some viruses or parasites that belong to this group? |
Must invade and replicate only inside cells
VIRUSES, RICKETTSIAS, CHLAMYDIAE are examples |
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Contrast bacteremia and septicemia.
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Bacteremia: presence of viable bacteria circulating in bloodstream
Septicemia: systemic disease associated w/ presence and persistence of pathogenic microorganism or their toxins in the bloodstream |
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S. aureus releases this toxin and it is associated with this condition.
Is the toxin a superantigen? |
SEB, food poisoning
Yes, it is a superantigen |
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Superantigens are mostly produced by gram __________ bacteria.
They stimulate ___________ to become activated and produce _________ and _________ Superantigens have local effects as in ______ but have systemic effects as in ____________ |
positive
IFN-gamma, TNF-alpha local = SEB systemic = toxic shock syndrome |
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What are intrinsic virulence factors?
Name one produced by E. coli O157:H7. What does it cause? |
They are encoded on genes carried on the chromosome of a bacteriophage
Shiga-like toxin, HUS (hemolytic uremic syndrome) in children |
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Activation of MAC is effective against gram ___________ bacteria
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negative and less so against gram (+)
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Neutrophils secrete which cytokine?
What is it useful for? |
IL-12, producing Th1 response (and type IV hs)
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Opsonization by complement will utilize which complement receptors?
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CR3, CR4
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This cytokine recruits neutrophils to sites of inection.
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IL-8
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These cytokines can cause inflammation and initiate acute phase response
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IL1, IL-6, TNF
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During septicemia ___________ numbers soar and are causes for the production of pus during pyogenic infection
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neutrophils
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_____________ binds to the C protein of penumococci and activates the classical complement pathway.
Is this a useful marker in suspected bacterial infections |
C reactive protein (CRP)
Yes, definitely! |
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Superantigens stimulate host T cells only if they have the correct TCR type, what is it?
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TCR Vβ
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Name two superantigens causing a response
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SEB = s. aureus, food poisoning
TSST-1 = toxic shock syndrome |
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Associate the theory with the immunity:
Innate, acquired stranger theory, danger theory |
Innate = stranger
Acquired = danger |
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Innate immune system is activated by these macromolecules on microbes
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PRRs
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TLR4 binds to what?
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Gram (-) LPS
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TLR2 binds to what?
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Gram (+) cell walls
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_________ from damaged cells can activate the immune system
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Uric acid
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Which Igs can activate complement and which can acts as opsonins?
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Opsonins = IgG 1,3,4 and IgA
Activate complement = IgG 3,1,2, IgM |
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Humans produce twice as much ________ (Ig) as all other Ab combined.
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IgA
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This type of hypersensitivity reaction is geared towards protozoa, tuberculosis.
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Type IV (DTH)
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This type of hypersensitivity reaction is geared towards intestinal parasites.
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Type I
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M. leprae has to extreme forms, name them and which T cell helper is associated with each?
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Lepromatous leprosy (LL) = IgG, poor cellular response, Th2
Tuberculoid leprosy (TT) = macrophage, strong cellular response, Th1 |
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Effective resistance to many fungi is a _________ (Th1/Th2) response
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Th1
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What is a Th2 response associated with (w/ respect to fungi)?
Can it cause pathology? It can result in the production of ____________. |
Susceptibility to fungal infection
Yes IgE |
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If an immunodeficient individual is unable to produce the required Th1 response to fungal infection, what occurs?
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Some will produce a Th2 response allowing the infection to spread and induce IgE to the fungus
ABPA (allergic bronchopulmonary aspergillosis) occurs! |
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Which MHC classes do each of the IFNs upregulate?
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IFN-αβ = MHC I
IFN-γ = MHC II |
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IgA can enhance virus infectivity in some situations.
Which viruses take advantage of this opportunity? |
- Dengue
- RSV |
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EBV (HHV-4) infecs B cells via this CD marker.
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CD21 / CR2
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How does EBV work?
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1. Attacking T cells become activates -> begin looking like monocytes
2. CD8+ cells kill B cells 3. Continue killing of B cells results in their proliferation and ultimately B cell lymphoma |
