Microbiology and Immunology 3300B Study Guide - Final Guide: Blood Vessel, Degranulation, Fc Receptor
29 Mar 2013
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Department
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Immune Lecture 23 Study Notes
1. What is an allergy?
-an immune response to something foreign that is not associated with a pathogen
-the response itself is pathogenic
-had to have developed an immune response to it already, so an allergic reaction is a
memory response
-the allergen is the antigen that induces the reaction
2. What is hypersensitivity?
-hypersensitivity kind of means allergy
-term used clinically for allergy
-also a description of the immune mechanism
-not exclusive to the term allergy as defined above
-immune system is causing problems when it shouldn’t be
3. What is type 1 hypersensitivity?
-immediate hypersensitivity (very fast)
-IgE mediated not a lot in circulation, mainly bound to mast cells (FceR1)
-TH2 (IL4/5 cytokines) directed towards parasites that get in through the
mucosal or epithelial barriers, class switch to IgE
-some basophils (although rare) are found in tissues where parasites invade you
and are covered in IgE
-ex/ asthma
4. What are some mast cell products?
-histamine: good at increasing permeability in vasculature (leaky blood vessels,
vasodialation, airway constriction)
-enzymes in these granules are able to degrade the extracellular matrix
5. What is the immediate response of type 1?
-response is due to mast cell and basophil degranulation
-mast cells are activated and granules are released (happens within seconds)
GI tract: increased fluid secretion/peristalsis = diarrhea/vomiting
Eyes, nasal passages and airways: decreased diameter, increased mucus secretion
= congestion/blockage of airways (wheezing, coughing etc), swelling and mucus
secretion in nasal passages
Blood vessels: increased blood flow/permeability = increased fluid in tissues =
increased flow of lymph to lymph nodes, hypotension = anaphylactic shock
6. What is welting?
-allergy test; response within 5 minutes to an allergen if you were previously
exposed
7. What is allergic rhinitis?
-runny nose
8. What is allergic conjunctivitis?
-watery eyes
9. What is allergic urticaria?
-welting
10. Discuss the route of allergen entry and the mast cell activation.
(i) intravenous high dose allergen general release of histamine which acts
on blood vessels to increase permeability leading to anaphylaxic sock
(ii) Subcutaneous: low dose local release of histamine causes flaring
-air born allergies can also cause eczcema
(iii) Inhalation: low dose allergic rhinitis (upper airway) caused by
increased mucus production and nasal irritation; asthma due to
contraction of bronchial smooth muscle and increased mucus secretion
(lower airway)
(iv) Ingestion contraction of intestinal smooth muscle induces vomiting;
outflow of fluid into the gut causes diarrhea; antigen diffusing into the
blood vessels is disseminated causing urticaria, anaphylaxis or eczema
Slide 15
11. What are treatments for acute responses?
-for anaphylaxis: epinephrine
-for asthma: bronchodilators
-these are direct blockers to mast cell products
12. How do we block mast cell products?
-IgE binding to a mast cell: bind to an IgE Fc region and prevent IgE binding to Fc
receptors on mast cells
-anti-IgE antibodies such as omalizumab
13. How do we inhibit mediators?
-want to inhibit effects of mediators on specific receptors or inhibit synthesis of
specific mediators
-use antihistamines, beta blockers, lipoxygenase inhiitors
14. Antiinflammatory?
-corticosteroirs
15. Th2 response?
-induction of Tregs
-desensitization therapy by injections of specific antigens
16. What are some other ways to treat acute responses?
-desensitization protocols: short term – clinical requirements so that certain drugs
can be used, repeated administration with increasing dose
-permanent: restore tolerance, will induce a Treg response (shutting off immune
system)
17. Discuss the intermediate and late phase responses.
-intermediate is caused from IgE responses and starts within seconds/minutes of
exposure
-histamines/prostaglandins and other mediators released by mast cells = huge
increase in permeability = visible edema/reddening of the skin (welts)
-late phase response is dependent on allergen dose
-these reactions over hours afterwards; much increased area of edema; this is
caused by continuous synthesis and release of inflammatory mediators by mast cells
-delayed responses include TH2 responses which are heavily dominated by
eosinophils
-they express Fcgamma, Fcalpha and CR3
-they contain very toxic chemicals in their granules
18. What are the eosinophil products?
-they contain enzymes that will degrade the extracellular matrix, start producing
cytokines (proinflammatory responses) and cytokines to amplify the support of TH2
19. Discuss asthma and the TH2 response.
-asthma occurs in the lower airways
-can have an allergic asthma (acute attack) mast cells let granules go and will
recruit TH2 cells
-inflammatory mediators cause increase mucus secretion and smooth muscle
contraction leading to airway obstruction
-can have airway constriction
Document Summary
An immune response to something foreign that is not associated with a pathogen. Had to have developed an immune response to it already, so an allergic reaction is a memory response. Not exclusive to the term allergy as defined above. Ige mediated not a lot in circulation, mainly bound to mast cells (fcer1) Th2 (il4/5 cytokines) directed towards parasites that get in through the mucosal or epithelial barriers, class switch to ige. Some basophils (although rare) are found in tissues where parasites invade you and are covered in ige. Histamine: good at increasing permeability in vasculature (leaky blood vessels, vasodialation, airway constriction) Response is due to mast cell and basophil degranulation. Mast cells are activated and granules are released (happens within seconds) Eyes, nasal passages and airways: decreased diameter, increased mucus secretion. = congestion/blockage of airways (wheezing, coughing etc), swelling and mucus secretion in nasal passages.
