Immediate and Delayed Hypersensitivities

Question 1

contrast immediate and delayed-type hypersensitivities

Answer 1

can be right now or within 1-2 days; delayed involves T cells so takes longer

Question 2

describe Type I hypersensitivities, including predominant cell types, inflammatory mediators, and immunoglobulins involved

Answer 2

1. these are immediate hypersensitivities, but they require a sensitized B cell (previous exposure!)
2. steps:
   a. sensitization of B cell to antigen
   b. B cells produce IgE (favored when Il-4 present in greater numbers than IFN-gamma)
   c. IgE binds mast cell or basophil via Fc receptor
   d. IgE binds antigen, and crosslinking occurs
   e. mast cells and basophils release inflammatory mediators such as histamine and inflammatory cytokines that can directly trigger sensory neurons (opportunity for intervention!)
3. examples include: erythema, edema, itching and pain, shock, wheezing and trouble breathing, eczema, and anaphylaxis!

Question 3

what are 3 treatments for anaphylaxis (WILL be on MT2!!)

Answer 3

1. epinephrine (vasoactive effects)
2. anti-histamines (can be IV)
3. cortocosteroids

Question 4

describe Type II hypersensitivities, including predominant cell types, inflammatory mediators, and immunoglobulins involved

Answer 4

1. immediate hypersensitivities that are antibody dependent, so require prior sensitization or nonspecific antibody binding
2. occur when antigen-antibody complex forms ON a host cell
3. antibodies can be made against:
   a. intrinsic antigens: pre-existing host cell antigens: inappropriate or accidental
   b. extrinsic antigens: novel antigens, created when the host cell antigen is altered and now seems foreign (ex. drug bound to a cell; tick borne diseases do this, seen in IMHA; basically pick any cell type and this can happen to it)
4. antibodies are usually IgG or IgM secreted by self-reactive B cells
5. 4 mechanisms of toxicity against host cells:
   a. activation of complement: recruits neutrophils, which degranulate and kill cells
   b. opsonization: antibody and/or complement enhance phagocytosis by macrophages and neutrophils
   c. complement cascade leads to formation of membrane attack complex, resulting in cell lysis
   d. antibody-dependent cell mediated cytotoxicity

Question 5

describe Type III hypersensitivities, including predominant cell types, inflammatory mediators, and immunoglobulins involved

Answer 5

1. immediate hypersensitivities, also IgG/IgM mediated, and require prior sensitization or nonspecific antibody binding
2. involve antigen-antibody complexes, but the antigens are SOLUBLE, so the antibody hitches a ride and follows the antigen to wherever it lands
3. example is vasculitis, where the antigen-antibody complexes adhere to vessel walls and activate complement, leading to vessel dilation, increased vascular permeability, and cytokine release

Question 6

describe Type IV hypersensitivities, including predominant cell types, inflammatory mediators, and immunoglobulins involved

Answer 6

1. delayed hypersensitivities!
2. require prior sensitization and involve T lymphocytes (take time to recruit = delayed)
3. steps:
   a. T lymphocytes binds antigen on APC
   b. the sensitized lymphocyte releases cytokines that recruit and activate macrophages
   c. the activated macrophages form a granuloma
4. examples include TB testing in people and cattle and contact hypersensitivity from chemicals (flea collar dermatitis), metals, or poison ivy