Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
38 Cards in this Set
- Front
- Back
|
Which Ab is involved in Immediate hypersensitivity rxns?
|
IgE (coats mast cells --> granule release)
|
|
|
Are hypersensitive rxns the result of a first time antigen exposure?
|
No. these all require a prior exposure (sensitized host)
|
|
|
In addition to the MHC II binding with the TCR, what co-receptors are required to activate a T cell?
|
B7 (on APC) = CD28 (on Tcell)
|
|
|
Which two cytokines direct T cells to become Th1 or Th2?
|
IL-12 --> Th1
IL-4 --> Th2 |
|
|
* Which cells produce cytokines essential for turning on IgE producing B cells ?
|
Th2
|
|
|
In the germinal center, B cells undergo: somatic hypermutation, affinity maturation and class switching. Which cell are these dependent on?
|
antigen-specific Th cells
|
|
|
What does histamine cause? Which rxn is this involved in?
|
increased vascular permeability vasodilation
bronchoconstriction secretion of mucous Immediate (secreted by mast cells, which IgE on their surface) |
|
|
What is the most important of the primary mediators in the Immediate hypersensitivity rxn?
|
Histamine
Others: proteases chemotactic factors TNF (upregulates adhesion molecules) |
|
|
* What are the second round of mediators in an Immediate hypersensitivity rxn?
|
Lipid mediators:
Leukotriene C4 & D4 (*Bronchoconstriction, spasm) |
|
|
What cells play an important role in the late phase rxn of Immediate rxns?
|
Eosinophils: secrete cytokines that call in other eosinophils and mast cells --> prolong the rxn
|
|
|
* What determines the clinical manifestation of an IgE-mediated hypersensitivity rxn?
|
dose and route of allergen administration:
IV: anaphylaxis Ingestion: food allergy Inhalation: upper and lower airway Subcutaneous: wheal and flare |
|
|
What is Localized swelling of the deeper layers of skin and subcutaneous tissue?
|
Angioedema - associated with food allergy (ingestion rxn of Immediate Hypersensitivity)
|
|
|
What is the role of Positive & negative feedback loops in the Th1 or Th2 differentiation of the Immediate rxn?
|
"locks in" the response
|
|
|
What symptoms are caused by Inhalation of allergens (Upper and Lower)?
|
Immediate:
Upper: Allergic rhinitis and conjunctivitis (hay fever) --> mucosal mast cells --> histamines! Lower: Allergic Asthma |
|
|
What are the classic symptoms of chronic asthma?
|
wheezing, coughing, SOB
|
|
|
What are the histologic changes of someone with chronic asthma?
|
Goblet-cell hyperplasia in the epithelial-cell lining
BM is thickened with collagen deposition in submucosa cellular infiltrate |
|
|
What is the most bronchospastic agent in the Immediate hypersensitivity rxn?
|
leukotrienes
|
|
|
What are the targets of Asthma tx?
|
Mast cell "stabilizers"
Bronchodilators (epinephrine) Blocking inflammation (corticosteroids) Leukotriene inhibitors (Singulair) |
|
|
What types of Ag's trigger allergic asthma?
|
favor production of IgE
small, highly soluble proteins present transmucosally at very low levels (ilicits Th2/IgE response) |
|
|
Where is the irritation in a wheal and flare rxn?
|
Subcutaneous and Local
Note: wheal = center welt; flare = surrounding redness Histamines! |
|
|
What does it mean if someone is "atopic"?
|
prone to produce IgE Abs and strong allergic responses
triad = allergic rhinitis, asthma, atopic dermatitis or hives |
|
|
What are the four mechanisms of Type II (direct target) Hypersensitivity?
|
Opsonization and Phagocytosis (Used to be known as “Complement Dependent Reactions”)
Complement & Fc Receptor-Mediated Inflammation Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC) Antibody-Mediated Cellular Dysfunction |
|
|
What is an event that would trigger a Direct/Complement-induced Lysis Type II rxn?
|
Major transfusion reaction (ABO mismatch)--> lysis of transfused rbcs
|
|
|
* What is meant by "Type A" blood?
|
There is an A antigen on it's surface --> circulating B Abs. If transfused to a non-A ,this will be seen as A antigen and attacked
|
|
|
What are the two "Opsonization and Phagocytosis" Type II rxns?
|
1. Direct lysis (via complement)
2. Opsonization and phagocytosis (also via complement) Examples: major and minor blood transfusion rxns |
|
|
What is Erythroblastosis Fetalis an example of?
What is the medication for this? |
Type II Opsonization and Phagocytosis
Rhogam (Rh+ fetus generates Rh-Abs in mother --> second pregnancy --> memory immune response against fetal rbc's by mother's Rh-Abs) |
|
|
What are Autoimmune Hemolytic Anemia, Leukopenia, Thrombocytopenia examples of?
|
Type II: Opsonization and Phagocytosis
** Hallmark: IgG or IgM attaching to the *surface* Ag of another cell Making Abs (IgG or IgM) to your own cells |
|
|
do all Type II rxns result in lysis?
|
No! Complement & Fc Receptor-Mediated Inflammation
|
|
|
How does Complement & Fc Receptor-Mediated Inflammation damage tissue?
What type is this? |
Type II:
Deposited Abs activate complement--> C5a and C3a recruits neutrophils and monocytes --> activation of leukocytes--> release of enzymes, ROS --> damage to tissues |
|
|
What type of Rxn (specific) is Goodpasture Syndrome associated with?
|
Type II: Complement and Fc Receptor-mediated Inflammation
|
|
|
What is another name for anti-glomerular basement antibody disease, that damages the kidney and lung tissue?
|
Goodpasture syndrome (Type II)
|
|
|
How are the immune complexes arranged in Goodpasture Syndrome?
|
Linear deposition of immune complexes, characteristic of classic Anti-GBM disease
|
|
|
Does Antibody-Dependent Cell-Mediated Cytotoxicity rely on the complement system?
|
no
|
|
|
What is antibody binding to a specific target cell receptor doesn’t lead to cell death, but rather to change in function without causing cell injury or inflammation?
|
Type II (direct): Antibody-mediated Cellular Dysfunction
e.g. Myathenias Gravis, Graves disease |
|
|
What is an autoimmune disease which is characterized by variable muscular weakness and fatigability of voluntary muscles, caused by the presence of antibodies to Ach receptors in motor end plates of skeletal muscle --> impaired neuromuscular transmission?
|
Myasthenia Gravis
|
|
|
What disease causes hyperthyroidism?
|
Graves Disease
Type II (Antibody-Mediated Cellular Dysfunction) |
|
|
Is complement required for all Type II rxns?
|
No.
ADCC; Fc-mediated opsonization and Fc-mediated inflammation; Ab-mediated cellular dysfunction |
|
|
General: Type II characteristics:
|
Antibody-mediated (typically IgG or IgM)
Antibodies formed against antigens on cell surfaces or in connective tissues; they are directly or indirectly cytotoxic Injury is mediated by several Ab-dependent mechanisms: |
