Immunology Notes

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Department
Microbiology and Immunology
Course
Microbiology and Immunology 3300B
Professor
Rodney Dekoter
Semester
Fall

Description
Immunology NotesNov 2212 Atopy Susceptibility to allergic disease multiple allergies Type I andor Th2 associated Examples are eczema babies with this are more likely to get other allergies allergies hay fever asthma There is genetic susceptibility having parents that have allergies increases your chances of getting allergies Rates are increasing Allergy does not equal atopy Genetic factors There have been many attempts to isolate the genes responsible There are many associated polymorphisms and few causes There are many susceptibility genes for asthma These include genes responsible for triggering an immune response or directing CD4 Th cell differentiation genes that regulate Th2 cell differentiation and genes expressed in epithelial cells Environmental factors Hygiene hypothesisgrowing up in a clean environment Atopy is linked to a decrease in children with more siblings a decrease in attended daycare and a decrease in farm children Atopy has also increased in the western world developed countries and increases with higher income It increases as countries improve hygiene water decontamination pasteurization Rates of asthma and allergies go up High genetic susceptibility to atopy and a hygienic environment makes the person more likely to develop atopic allergic disease Low genetic susceptibility and a less hygienic environment makes the person less likely to develop atopic allergic disease nonatopic Hygiene hypothesis mechanisms Initially thought to be a lack of Th1 stimulation due to lack of exposure to pathogens that promotes Th2 response Helminthic infections or parasites Th2 are protective in atopy provide protection against allergies Experimental supportAnimal models of disease small clinical trials stimulating the immune system with parasites or antigens resulted in improvement in allergy anecdotal evidence Hygiene hypothesis mechanisms Immune disregulation through development Some risk factors are linked to early life Immune development in association with commensals Susceptible people are less able to regulate their immune system properly Mechanisms of Th2 induction Enzymatic antigenspapain fruit Der P1 dust mites Routeskin and mucosa Doselow dose Route and dose tend to drive towards a Th2 response Types of hypersensitivity Type IMediated by IgE directed against soluble antigens and induces mast cell activation Examples are allergic asthma atopic eczema systemic anaphylaxis some drug allergies Type IIMediated by IgG Directed against either cell or matrix associated antigen which induces complement FcR cells phagocytes NK cells or cellsurface receptor which induces antibody Examples are some drug allergies or chronic urticaria Type IIIMediated by IgG directed against soluble antigen and induces complement phagocytes Examples are serum sickness arthus reaction Type IVMediated by Th1 cells directed against soluble antigen and induces macrophages activation Examples are allergic contact dermatitis tuberculin reaction Mediated by Th2 cells directed against soluble antigen and induces IgE production eosinophil activation mastocytosis Examples are chronic asthma chronic allergic rhinitis Mediated by CTL cytotoxic T cells directed against cellassociated antigen and induces cytotoxicity damage is caused directly by CTLs Examples are graft rejection allergic contact dermatitis to poison ivy Type I hypersensitivity Immediate hypersensitivity IgE mediated with help from Th2 CD4 Th2 cells provide help to B cells for antibody production especially switching to IgE IgE secreted by plasma cells B cells binds to Fc receptor on FcRI on tissue resident mast cells IgE also binds to circulating basophils Both mast cells and basophils have granules and inside the granules are toxic and proinflammatory granules Antigen binding to IgE on these cells leads to amplification of IgE production An allergic response is secondary You cant be allergic to something youve never encountered before
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