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Lecture

Lecture 29- Hypersensitivity Reactions.docx

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Department
Physiology
Course Code
PHGY 313
Professor
Russell Jones

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Lecture 29 - Hypersensitivity Reactions - 04/03/2013  Hypersensitivity Reaction: An over-reacting immune response that causes injury. o The reaction is stimulated by an antigen that shouldn't hurt you  About 50 million Americans suffer from allergies, a type of hypersensitivity reaction  When you have an allergic reaction, you usually have compound reactions with 2 or more different allergens o For example, dust mites, ragweed, or dog hair  Other common sources of allergens are given in Fig 1 Fig 1: Common antigens inducing allergies  There are 4 main type of hypersensitivity reactions, shown in Fig 2 A general overview of the 4 types: o Immediate Hypersensitivity: A soluble antigen crosslinks with IgE antibodies on mast cells, causing a rapid degranulation of vesicles containing histamine and leukotrienes  Allergic rhinitis and asthma fall in this category o Antibody mediated: antibodies bind to target antigens on the surface of cells. They activate the complement system or bind to receptors and alter signalling o Immune Complex Disease: bacterial toxin is bound by IgG in the circulation. Normally complement is fixed to a cluster of antigen, tagging it for removal by macrophages. If the clearance is inefficient, the immune complexes can travel through the circulation and deposit on walls of blood vessels and glomeruli.  Inflammation occurs where it shouldn't, leading to nephritis or vasculitis. o Delayed Hypersensitivity: Takes a while to occur because of the activation of the adaptive immune system. The formation of new cells is involved. Figure 2:Guide to hypersensitivity reactions The Hygiene Hypothesis:  Allergies are becoming more rampant in the world.  Theory: Lack of exposure to antigens during childhood makes the immune system lazy and we react to atypical antigens when we're older. It is thought that exposure to antigens stimulates a Th1 immune response leading to non-atopy (i.e., no predisposition to an allergic reaction) o There is a reciprocal balance between Th1 and Th2, where low Th1 activation is correlated to promoting atopic Th2 responses o Children with high genetic susceptibility or who live in a sterile environment will stimulate a Th2 response and atopy (a predisposition to an allergic reaction)  Many countries have a higher incidence of asthma (NA, Brazil, UK, Australia)  Evidence against: Japan, a highly developed and sanitary country has half the asthma rates than North America  Other causes of atopy have to exist o Diet is very likely: what you eat changes the microbiota in your gut  Furthermore, diabetes and obesity distribution is similar to the distribution of allergies Type 1 Reactions  A person must be first exposed to antigen to make IgE. Once made it strongly binds to Tc receptors on mast cells, basophils, and eosinophils  It's mediated mast cells, but dictated by T cells to make the antibody in the first place. o Driven by Th2 cells. Recall that TH2 cells make IL4, a B cell recognizes it, and class switches to IgE and becomes a plasma cell  After the first encounter, you are sensitized to the antigen. In the second and subsequent times, there is massive degranulation of mast cells releasing histamine.  A deficiency in RAG proteins would result in no allergic reactions  Note: Fig 3 is not accurate in the sense that APCs don't present antigen in the airway, but in the lymph node that drains the airway. Fig 3: Type 1 reactions Mast Cells:  Residents of the airways  Large cells with granules of histamine and leukotrienes  Have Fc receptors that bind to the constant region of IgE only  Mast cells have multiple antigen specificities because different IgE antibodies are able to bind to it  Bound IgE is monomeric, but the second contact causes cross-linking of 2 IgE antibodies triggering the degranulation  The location of the degranulation is important o GI tract: leads to diarrhea, vomiting o Airway: bronchoconstriction and difficulty breathing (due to a combination of mucous production and constriction) o Systemic blood vessels: Vasodilation, increased permeability. This can lead to systemic anaphylaxis when antigens encounter mast cells in the blood  Systemic anaphylaxis: a severe type
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