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251 Cards in this Set

  • Front
  • Back
Name four classes of pathogens
1. extracellular 2. Intracellular 3. viruses 4. parasitic worms.
3 perio pathogens
1. P. gingivalis 2. A. a. 3. B forsythus
P. gingivalis
G-, anaerobe, non motile, rods
A. a.
G-, anaerobe, non-motile, cocco
B forsythus
G-, anaerobe, fusiform
3 Cariogenic pathogens
1. Strep mutans 2. S. sobrinus 3. Lactobacilus
Strep mutans S. sobrinus
G+, cocci chains, enamel caries
Lactobacilus
G+, rod chains, dentinal caries
Host response to extracellular pathogens (bacteria, parasites)
Innate (antimicrobial, complement, phags) Adaptive (B cells = ab's)
Host response to intracellular pathogens (bacteria, parasites,mycobacteria, spirochetes)
Innate (NK) Adaptive (T-cell, Th1 macrophage activation)
Host response to viruses
IFN-alpha/beter stimulates NK cells, T-cells (Th2 ab response), fever = viral destabilization
IFN-alpha/beter key roles
1. turns on viral interfering genes 2. Increase MHC C1 = inc susceptibility to T-cell 3. activates NK's
Innnate response to virus, list cytokines released by macrophages
macrophages release TNF-alpha, IL-1,6 = inflam. IL-12 = NK stimulation. IL-8 chemotactic
Adaptive humoral response to virus key roles (4)
Neutralization, comp fixation, opsonization, ADCC (antibody-dependent cell mediated cytotoxicity
Adaptive cell-mediated response to virus
most important after virus infects cell. T-Cells: CD8+(CTL), CD4+ (Th2 --> Bcell, Th1 --> macrophage)
Host response to multicellular parasites (extracellular worms)
Th2 ab response, Ig-Fc eosinophilic degranulation(humoral) + mast cells = inflam + inc mucous secretion in GI promoting expulsion
Host respnse to fungi
Th1 macrophage activation, Th2 opsonization/neutralization, resistant to complement
Stages of perio lesioins
Initial - early - established - advanced
Initial perio
>2-4 days, few neutro, macro or lympho
early perio
>4-14 days, inc neutros, *microabscess, T-cell
established perio
>14 days, intense neutro, B-cell differentiation, macrophages
advanced perio
> 14 days, bone dest, plasmacytes, epithelial ulceration
Virulence factors
Encapsulation, ag variation, intracellular survival, suppress immune system, Biofilm
Encapsulation
polysach coat = resist phagocytosis, usually pyogenic
ag variation
impaired recognition
intracellular survival
evades humoral response
suppress immune system
impairs immune fuction and response
Biofilm
bacterial cells form "sheltered" communities --> phagocytosis is frustrated --> host tissue damage
Virulence factors P gingivalis
encapsulation, ag variation, toxins: tissue destruction, inhibit cell fxn, impair opsonins, amplify inflam response, invades host to evade complement and antibody
Virulence factors A a
encapsulation, toxins: tissue destruction (collagenase), Ig protease, endo/leuko-toxins, suppression of T cell cytokines (IL-2,4,5)
Virulence factors Strep mutans
Degrades, sheds IgA
Systemic effects of perio
pathogens in crevice --> degrade host --> bacterial invasion --> inflam response --> bacteria into circ --> lymph nodes --> systemic
Aquired pellicle def.
host salivary proteins which coat surface teeth = binding site for cariogenic bacteria via glucans (glucosyltransferases)
cariogenic bacteria accumulation and metabolism
sucrose-dependent, sucrose --> lactic acid
colonization on enamel by S mutans list 4
1. initial (directily to pellicle) 2. interbacterial (adehere to early colonizer) 3. glucan mediated 4. sucrose dependant
_______ inhibits biofilm formation.
Lactoferrin
2 type of immunization
1. Passive (natural = mom, or artificial = ab injection.) 2. Active (natural = exposed to pathogen, or artificial = injection of vaccine)
Passive imm. Disadvantages (3)
short term, dosen't activate immune system, repeated use = dec response or hypersensitivity
Passive imm. Advantage
immediate protection
Active imm advantage
long term protection
Active imm disadvantages (1 natural, 3 artificial)
subject to infection (natural) or side effects, not life long, difficult to develop effective immunity (artificial)
Live vaccine
live pathogen attenuated to be avirulent = longer lasting, more complete immunity
Inactivated vaccine 3 types
inactivated whole pathogen (polio), toxoid = toxin proteins ( DPT) or components (flu)
List two methods used to improve response to immunization
1. Adjuvant 2. Conjugation
Adjuvant
given w/ immunogen --> potent immune response
Conjugation
immunogen (covalent linkage) to protein carrier = hapten carrier effect
hapten carrier effect
compound by itself can not stimulate and immune response unless cunjugates
hapten carrier effect
B cell recognizes hapten = internalizes it --> T cell help = humoral cell mediated ab production.
Routes of vaccine administration (2)
1. Parenteral 2. Mucosal
Parenteral vaccine pros and cons
IM, ID, IV - pros = systemic immunity, avoids tolerance and ag degradation, cons = lack mucosal immunity
Mucosal vaccine pros and cons
oral/nasal - pros = systemic + mucosal immunity, cons = ag degredation and tolerance *needs adjuvant
Antibodies used for immunization and serologic testing (2)
1. Polyclonal 2. Monoclonal
Polyclonal sources - 2
animal (antivenin), human serum pool (intravenous gamma globulin = IVGG) *derived from many different B cell clones
Monoclonal
single B cell clone fused to tumor cell line then engineered "humanized" eg. anti-HER2 mAb
Polyclonal ab's
multiple isotypes and affinities
Monoclonal ab's
single isotype, selective binding properties
Dental vaccines (3 possibilities)
1. Hyperimmunization S mutans --> crossreactive ab's to heart and IgG 2. Subunit vaccine (fibrillar proteins (AgI/II) or glucosyltransferase conjuguated to cholera (adjuvant) 3. Passive S mutan ab mouthwash
List three immunodiagnostic tests
1. Agglutination 2. Immunochem 3. Immunofluorescence
Agglutination test
Coombs test = ag:ab crosslink. Eg. Hemolytic, rheumatoid, pregnancy.
Universal donor type
O+ Rh-
Univeral acceptor type
AB+ Rh+
Immunochemistry test
ab-enzyme = substrate --> chromophore. 3 types
3 types of immunochemistry tests
1. ELISA 2. Immunoblotting 3. Immunohistochemistry
ELISA
enzyme linked immunosorbant assay. Determines presence and/or concentration of ag's or ab's eg. Detect proteins in GCF
Immunoblotting
Western blot test = SDS-polyacrylamide gel + electrophoresis (PAGE) to separate proteins (break disulfide bonds) prior to ab detection. Eg. Oral prion testing
Immunohistochemistry
like ELISA but used to detect tissue ag's like immunofluorescence
Immunofluorescence
ab-fluorophone + laser = light. Used for detecting cell surface ag's in tissue. Eg. Dx plasminogen deficiency -->gingival hyperplasia
Serology
detection and measurement of antibodies to a given antigen
Serotyping
identifies ab's to particular ag
Seroconversion
first detection of ag specific ab's in = 4 x increase in titer between acute and convalescent. Primary infection IgM>>IgG, Anamnestic IgG>>IgM
Titer
inverse of greatest dilution = detectible activity
Type I hypersensitivity is
immediate or atopic allergy (anaphylaxis)
What is type I hypersensitivity mediated by?
IgE
What is the pathology triggered by in type I hypersensitivity
IgE-FcR of mast and basophils -> degranulation
What are the three phases of Type I hypersens.?
sensitization, activation, and effector
What occurs during sensitization in type I?
first exposure (protein ag only) --> production of IgE (IL-4 --> TH2 response), mechanism = genetic, downregulation of TNF
What occurs during activation of type I?
sencond exposure, ag:IgE-FcR cross linking --> mast cell/basophil degranulation (also caused by non-specific = lectins, chemicals, cold heat, pressure)
What stages occur during the effector phase?
Early stage and late stage
Early stage occurs when?
less than 4-6 hours after exposure
What mediates this early stage during effector phase?
Products of mast cells and basophils
What preformed granules are stored in the mast cells?
histamines/serotonin, chemotactic factors, heparin
What granules are made by the mast cells upon activiation?
leukotrienes, thromboxanes/prostoglandins, PAF (platelet activating factor)
Late stage of the effector phase occurs when?
greater than 4-8 hours post-exposure
What is the late stage of effector phase mediated by?
recruited neutrophils and eosinophils; cytokines (esp. IL-4) also promotes TH2-type response
Eosinophils degranulation damages what?
parasites, may also cause tissue damage
Neutrophils activation causes?
release of lysosomal contents, inflamatory mediators and chemotactic factors
What is the route of exposure with anaphylactic shock?
IV (drugs, serum, venom), sytemic = most dangerous
Type 1 hypersnsitivity is characterized by
edema, erythema and smooth muscle contraction
What is the route of exposure with wheal and flare (atopic dermatitis)
Subcutaneous (Insect bites, allergy testing)
What is the route of exposure with allergic rhinitis?
Inhaled (pollen, dust mite feces)
What is the route of exposure with Bronchial asthma?
Inhaled (pollen, dust mite feces)
What is the route of exposure with food allergies?
Oral (shellfish, milk, eggs, fish, wheat)
Response to anaphylactic shock?
edema, vasodilation, tracheal occlusion, circulatory collapse,
Response to wheal and flare?
local vasoldilation, local edema
Response to allergic rhinitis (hay fever)?
edema and irritation or nasal mucosa
Response to bronchial asthma?
bronchial constriction, increased mucosa, airway inflammation
Response to food allergy?
vomiting, diarrhea, itching, and hives
How do you treat early phase of type I hyper.?
anti-histamines
How do you treat late phase of type I hyper?
corticosteroids (anti-inflammatory and immunosuppressive agents repress recruited cells)
type II hypersensitivity is?
cytolytic/cytotoxic response
What is type II hypersensitivity mediated by?
IgG/IgM
What is the pathology triggered by in type II hypersensitivity?
antibody binding to cell surface molecules leads to target cell (1. complement -mediated 2. ADCC or 3. altered receptor signaling)
Most dangerous route of exposure for type I hypersensitivity?
via stream
Types of altered signaling in type II hypersensitiviy?
antagonist (inhibiting its function); agonist (mimcks the receptor's normal ligand)
Key example of type II hyper.?
blood transfusion rxns, induced rxns (hapten), autoimmune syndromes
2 Autoimmune examples of type II hyper.
Myesthenia gravis and Grave's disease
Autoimmune disease that is antagonist?
Myesthenia gravis
Autoimmune disease that is agonist?
Grave's disease (hyperthyroidism)
Autoantibodies to acetocholine receptor impairs neuromuscular trans.?
Myesthenia gravis
Autoantibodies to thyroid hormone receptor cause stimulate cells, hyper thyroidism
Grave's disease
Type III hypersensitivity is
an immune complex disease
What is type III hyper. Mediated by?
IgG and IgM
What is the pathology of Type III triggered by?
tissue deposition of immune complexes
What are the three phases of Type III hyper.?
1. immune complex formation (IgG), immune complex deposition, complex mediated inflamm.
Immune complex formation involves?
small/medium size immune complex
Immune complex deposition involves?
deposit locally(e.g. subcutaneous) or systemically (e.g. intravenously)
Complex mediated inflammtion involves?
initiation of complement cascade (C3a, C5a), recruitment/activation of PMNs lead to inflam. And tissue damage
Example of Systemic immune complex diseases?
serum sickness; IV of animal serum, subsequent IV, anti-serum complex form, pathology
Example of localized immune complex disease?
Arthus rxn; subcutaneous injection or antigen into pt. sensitized to antigen leads to formation of immun complexes that deposit into tissue, leading to localized tissue necrosis
What is infection-induced immune complex disease?
antibodies produced in response to an infectious microorg. Cross-react against normal tissue
Example of infection induced immune complex disease?
rheumatic fever- antibodies against group A strep
What are occupational diseases?
Intrpulmonary arthus-type rxn, due to inhalation of lg. amts. Of antigenic material over time
Examples of occupational disease?
farmer's lung a.k.a. allergic alveolitis, pneumonitis
Type IV hypersensitivity is?
delayed type hypersensitivitiy
Type IV hypersensitivity is mediated by?
T cells
What is the pathology of Type IV hyper. Triggered by?
activation of sensitized TH1 cells
What are the two phases of Type IV hyper.?
Sensitization and Elicitation
Sensitization involves
primary exposure to protein or hapten-conjugates primes responding naive T cells, causing differentiation into TH1 type
Elicitation involves
subsequent exposure activated TH1 cell; resulting in cytokine/chemokine production leads to macrophage activation, inflamm. And tissue damage
Damage of Type IV hyper. Is characterized by
erythema, skin induration, cell infiltrates
Treatment of Type IV hyper.?
usually resolves once antigen is removed (≤1 week)vtopical coritcosteroids for more severe
Type IV hyper. Syndromes are?
Jones-mote, contact, TB test, and Granulomatous
Rxn time, clinical appearance of jone-mote (cutaneous basophil hypers.
24 hours, skin swelling
Histological appearance and antigen of Jones-mote
basophils. Lymphocytes and mononuclear cells; intradermal
Rxn time, clinical appearance of contact (epidermal)
48 hours; eczema (dermatitis)
Histological appearance and antigen of contact
mononuclear cells, edema, and raised epidermis; haptens: (poison ivy) Metals
Rxn time and clinical appearance of TB test
48 hours; local induration and swelling +/- fever
Histological appearance and antigen of TB test
mononuclear cells, lymphocytes, and macrophages; Tuberculin mycobacterial leishmanial
Rxn time and clinical appearance of Granulomatous
4 weeks; skin induration
Histological appearance and antigen of granulomatous
granulomous, giant cells, macs, fibrosis +/- necrosis; persistant Ag or Ab:Ag complexin macrophages
Type IV dental reactions are elicited by what substances
metals, composite resins
Sx of type IV dental reactions include swollen lips, rashes of the head and neck and_____________ in the oral cavity.
lesions
Auto-reactive B cells usually do not pose a problem as long as auto reactive __ _____ are removed by the ________
t cells, thymus
Auto reactive B cells are as dangerous as auto-reactive T cells. T/F
False, auto-reactive B cells won't have T-cell help for activation
T cells may cross react to B cell presented ag, or with a novel ______.
epitope
Can mitogens activate T and B cells?
Yes, both
modes of activation of auto reactive b cells are:
(A)T cell reacts with novel or modified self antigen and stimulates b cell activity (B) mitogens may trigger T or B cells against self antigens
Acute rheumatic fever
Type II Hypersensitivity/ anti- strep ab. vs. cardiac muscle --> Myocarditis &valve scarring
Autoimmune hemolytic anemia
Type II Hypersensitivity/ Rh antigen --> RBC destruction
Goodpasture’s syndrome
Type II Hypersensitivity/ab vs. basement membrane type IV collagen --> lung hemorrhage, renal failure, vasculitis
Hemolytic anemia, Goodpasture's and RF are all type II reactions causing cell _______.
destruction (Type II)
Grave's disease, Myasthenia gravis, insulin-resistant diabetes and hypoglycemia are Type II hypersensitivity reactions involving ______ ______
surface receptors
Grave’s disease
Type II Hypersensitivity/ ab. Stimulate thyroid --> hyperthyroidism
Hashimoto's thyroiditis
Type IV / Thyroglobulin --> Destruction of Thyroid
Hypoglycemia
Type II Hypersensitivity/ ab. Have insulin-like effect (agonist) --> hypoglycemia
Insulin dependent diabetes mellitus
Type IV Hypersensitivity / pancreatic B cell ag --> Beta cells of pancreas destroyed
insulin-resistant (receptor) diabetes
Type II Hypersensitivity/ ab blocks effect of insulin by binding receptor (antagonist) --> hyperglycemia
Mixed essential cryoglobulinemia
Type III Hypersensitivity IgG --> vasculitis
Multiple sclerosis
Type IV Hypersensitivity / myelin basic protein -->brain invasion by CD4+ T cells, paralysis
Myasthenia gravis
Type II / Ab binds acetylcholine receptors --> impaired neuromuscular transmission
Subacute bacterial endocarditis
Type III Hypersensitivity / bacterial ag --> glomerulonephritis
Systemic lupus erythematosus (SLE)
Type III Hypersensitivity /Arthritis glomerulonephritis, vasculitis
SBE, mixed essential cryoglobulinemia and SLE are all type ___ reactions
III
Insulin-dependent diabetes, Rheumatoid arthritis, EAE, MS and Hashimoto's thyroditis are all reactions of what type?
IV
Rheumatoid arthritis
Type IV Hypersensitivity / joint inflammation and destruction
In _________ ________, auto antibodies disrupt the desmosomes of epithelial cells (struatum spinosum) causing sloughing of tissue, bullae and ulceration
Pemphigus vulgaris
Pemphigus vulgaris is usually treated with:
Corticosteroids and immunosuppressive
In benign mucous membrane pemphigoid, auto-antibodies are produced against the ______ _______ of the oral mucosa and ______.
basement membrane, eyes (gingiva peels off)
benign mucous membrane pemphigoid is usually treated with:
Corticosteroids and immunosuppressive
Auto antibodies mediate destruction of secretory acini of salivary glands in ________ syndrome
Sjogren's
Clinical symptoms of Sjogren's are ________ (dry mouth), ________ (dry eyes) cobblestone/fissured tongue and _____ filiform papillae.
Xerostomia; xerophthalmia' atrophied
This fungus often infects the oral cavity as a result of xerostomia.
Candida albicans (thrush)
With lupus, auto antibodies are produced against what type of antigens?
antinuclear antigens (ANA)
Lupus affects what parts of the body?
skin, joints, lungs, kidneys, heart, brain, just about any other organ or system of the body (70% systemic)
Oral Lichen planus is also known as _____ ________.
Wickhams striae
Oral Lichen planus is presumed to be caused by an autoimmune reaction to ______ cells of the oral mucosa and skin.
Basal
T/F Oral Lichen planus can lead to squamous cell carcinoma
TRUE
B cell deficiencies generally lead to an increase in ___________ infections
Bacterial
T cell deficiencies generally lead to an increase in ______, _______, and ________ infections.
viral, fungal, protozoal(mostly opportunistic)
What general immune cell deficiency leads to increased infections with pyogenic bacteria and bacteria of usually low virulence,
Phagocytic cell deficiency
NK cell deficiency leads to increased _________ infections.
Viral
SCID patients are most susceptible to CMV, Pneumocystis carnii and _____ ______
Candida albicans (thrush)
SCID is a reduction in the number of which lymphocytic cells?
B and T
X linked SCID (40-50%)
T cells reduced most, variable B
Both T and B cells reduced in (30%)
ADA, defective VDJ, RAG proteins
Bare lymphocytes (no MHC 2) Ataxia Telangectasia and WASP are all forms of
SCID both T and B cells variable (20%)
DiGeorge syndrome is a T cell deficiency syndrome that is cause by:
Thymic aplasia (no thymus)
T cell deficiency diseases include __ _______, T cell mutations and chronic mucocutaneous ________
DiGeorge's, candidiasis
chronic mucocutaneous candidiasis is a defect in what?
cell-mediated immunity to fungi
X-linked gamma globulinemia results in no B cellls T or F
False --> no mature B cells --> repeated bacterial infection
Common variable immunodeficiency is a __ cell deficiency disease that has a specific decrease of these two antibody classes.
B : IgG, IgA = susceptible to pyogenic bacteria
selective immunoglobulin deficiency involve which antibodies and lead to what
IgM, IgA mostly A --> respiratory infection
XLA, common variable immunodef., and selective immunoglobulin def. are all _ ___ immunodeficiency diseases
B Cell
Lack of IgA will lead to susceptibility to __________ infections.
Respiratory(mucosal)
Lack of IgM leads to susceptibility of these types of organisms.
Encapsulated bacteria
Name three specific phagocyte immunodeficiency diseases:
LAD (leukocyte adhesion deficiency)/ CHS (Chediak-Higashi syndrome)/ CGD (Chromic granulomatous disease)
Main result of LAD (leukocyte adhesion deficiency)
impaired migration of phagocytes to site of infection (neutropenia)
Main result of CHS (Chediak-Higashi syndrome)
Impaired phagosome-lysosome fusion and poor intracellular ----giant lysosomes
Main result of CGD (Chromic granulomatous disease)
Poor of organisms due to defective NADPH oxidase that forms hydrogen peroxide and superoxide
Complement deficiencies generally lead to increased _____________ infections
Bacterial
Deficiency of early complement components (C1-C4) leads to:
infections with Encapsulated bacteria(G -)/ poor clearance of immune complexes
Deficiency of late complement components (C5-C9) leads to:
Deficient membrane attack complex (MAC) / impaired defense against G- bacteria
Complement regulatory factor deficiency causes Hereditary angiodema (uncontrolled release of vasoactive peptides) and _______ ______ causing uncontrolled host bystander cell
Paroxysmal Nocturnal Hemoglobulinemia
Certain staph infections can cause secondary immunodeficiency by producing ____________ which activate 2 - ___ % of T cells and cause massive cytokine production
Superantigens; 20
HIV infects these two types of immune cells.
macrophages and CD4+ T cells
T/F HIV is a retrovirus?
TRUE
Why does treatment of transplant recipients or cancer patients cause secondary immunodeficiency?
Chemotherapy or irradiation kills rapidly dividing cells, including lymphocytes. Cell signaling pathways are also effected.
oral conditions common in HIV patients that are listed in the lecture notes include:(3)
candidiasis, Oral hairy leukoplakia, Kaposi's sarcoma
What conditions: are associated with the following viruses? Epstein-Barr virus, Human Herpes virus
Epstein-Barr: Oral Hairy Leukoplakia / Human Herpes virus: Kaposi's Sarcoma
Name five general treatments of immunodeficiency:
Antibiotics, gamma globulins, bone marrow transplants, gene therapy, antiviral
T/F A Xenograph is between individuals of the same species.
False--- between different species.
An __________ comes from a different site of the same individual.
autograph
T/F An allograph is from a genetically related individual?
False
What is another name for an isograph?
syngenic or syngraph
What is the time frame of each of the 4 types of graph rejection?
hyperacute : minutes to hours/ Accelerated : 2-5 days/ Acute : 7-21 days/ chronic : months to years
Which two of the four types of rejection occur because of prior exposure to transplanted antigens?
Hyperacute, accelerated
T/F acute graft rejection occurs because of prior exposure to transplanted antigens?
FALSE
What immune components are responsible for hyperacute, acute, and accelerated graft rejection?
hyperacute : antibodies, acute : T cells, accelerated : T cells
T/F Rejection of transfusions is mainly cell mediated.
False :(humoral-- antibodies destroy rbcs with non matching A,B,or RH antigens)
T/F Graft verses host disease seen with bone marrow transplants occurs when immature T cells attack host tissues.
False, (mature T cells)
How can Graft verses host (GVH) disease be avoided in bone marrow transplants?
deplete donor bone marrow of mature T cells before transplant good matching
Six characteristics of GVH disease:
enlarged liver, spleen, and lymph nodes; diarrhea; anemia; and weight loss
Two methods used to decrease likelihood of graft/transplant rejection:
A: find closest match of minor and major histocompatibility antigens B: immunosuppression after grafting
Three factors influencing cancer:
genetic predisposition, lifestyle, immune status
Four listed cause of cancer:
Chemical carcinogens, irradiation, stochastic DNA events, viruses
A carcinoma is of _________ origin.
Epithelial
Leukemia is generally found in ______ or _____ _______ and lymphoma is generally found in _______ tissue
blood, bone marrow/ lymphoid
multiple myeloma displays effected _______ cells and is found where?
plasmacyte, in bone marrow
B cell acute lymphoblastic leukemia (B-ALL) is cancer of B cells and normally found where?
blood, bone marrow
Follicular and Burkitt's lymphoma are found in peripheral lymphoid organs effecting mature __ cells.
B
Chronic lymphocytic leukemia (B-CLL) is a cancer of CD5+ B cells and is found in bone marrow, and ____.
organs
Acute lymphoblastic luekemia/lymphoma (T-ALL) affect _____
thymocytes
Adult T cell leukemia occurs in the and ______
periphery
Where do lymphoid cancers often exhibit chromosomal translocations?
Ig or TCR loci
Intra-oral lymphomas may be found on the gingiva or hard palate T/F
True - they may be misdiagnosed for Kaposi's sarcoma
Acute leukemia oral manifestation
gingival swelling and bleeding
Hepatitis B virus is associated with which type of cancer?
Hepatocellular carcinoma
Epstein-Barr virus is associated with which type of cancer?
B cell lymphoma
HHV8 (+HIV) is associated with which type of cancer?
Kaposi's sarcoma
Human T cell lymphotrophic virus (HTLV-1) is associated with which type of cancer?
T cell leukemia
Human papillomaviruses 16 and 18 are associated with which type of cancer?
Cervical carcinoma
Mutations, abnormal gene activation and viral encoded genes refered to as _____ antigens are often expressed and detected by the immune system.
novel
3 key cellular responses to cancer
novel ag's, cell mediated immunity (most important), ab's
TH1 T cells activate __________
macrophages
CD8+ cytotoxic T cells detect _____ ______ on MHC
altered peptides
Which cell is cytotoxic to cells with loss of MHC and ADCC
NK cells
Lymphokine activated killer cells (LAK) are activated by____?
IL-2
Humoral immunity against tumor cells includes ________ _________, inhibition of _____ and __________.
Complement fixation; adesion; opsonization
Inhibition of adhesion is a defense against _______
metastasis
3 types of cancer Tx
Radiation, chem and immunotherapy
Cell stimulating cytokines; tumor specific ag's, T cells and ab's are all forms of?
Immunotherapy