Type 1: Causes – Hypersensitivity

by Peter Delves, PhD

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    Right, now having given you a little overview of those four different types, let’s now look in a bit more detail at each one. So Type I hypersensitivity - IgE-mediated mast cell degranulation. You’ve already seen this picture. So these Type I hypersensitivity reactions, IgE-mediated mast cell degranulation. That’s what we usually think of as allergic types of responses, allergy. And this type of response often referred to as atopy, an inappropriate production of IgE antibodies is caused by a multitude of different factors. Genetics is important, but other factors also are important. Regarding the genes, there is not a single dominant allergy gene; it’s rather that several genes contribute to the development of the allergic process. Amongst them, the gene encoding the FcεR1, the gene encoding the cytokine interleukin-4 which is very important in causing B-cells to class switch to IgE production, CD14, HLA-DR, there are a number of different genes. So it’s really the combination of genes that’s important, not any one single specific gene. And of course the environment is also very important, it’s not a purely genetic situation we have here. And early microbial exposure, and early allergen exposure perhaps in the uterus seem to play an important role. Immune responsiveness overall is abnormal, with a decreased production of gamma interferon, and perhaps overall a more Th2 type of environment with those Th2 cells that secrete cytokines such as interleukin-4 and interleukin-5 and interleukin-6. They’re the more dominant population. And remember, all of these responses are normal responses. So a Type I hypersensitivity reaction is based upon something that is a normal protective immune response. For example against a parasitic worm infection. If you have a parasitic worm infection in your gut for example, you’d be very grateful to having this sort of response because it...

    About the Lecture

    The lecture Type 1: Causes – Hypersensitivity by Peter Delves, PhD is from the course Hypersensitivity and Autoimmune Disease. It contains the following chapters:

    • A Closer Look on Type I Hypersensitivity
    • Anaphylaxis
    • Mast Cell Mediators
    • Synthesis of Leukotrienes and Prostaglandins

    Included Quiz Questions

    1. Leukotriene B₄
    2. Leukotriene C₄
    3. Prostaglandin D₂
    4. Leukotriene D₄
    5. Prostaglandin E₂
    1. Immediate response- IgE mediated Late phase reaction- CD4+ Helper T cell, monocyte, and eosinophil mediated
    2. Immediate response- IgG mediated Late phase reaction- CD4+ Helper T cell, monocyte, and eosinophil mediated
    3. Immediate response- CD4+ Helper T cell, monocyte, and eosinophil mediated Late phase reaction- IgE mediated
    4. Immediate response- Eosinophil mediated Late phase reaction- CD4+ Helper T cell, monocyte, and IgE mediated
    5. Immediate response- IgE and CD4+ Helper T cell mediated Late phase reaction- Monocyte and eosinophil mediated
    1. Neutrophil chemotaxis
    2. Eosinophil chemotaxis
    3. Smooth muscle constraction
    4. Anticoagulant effect
    5. Increased vascular permeability
    1. Prostaglandins
    2. Leukotrienes
    3. Heparin
    4. Histamine
    5. Arachidonic Acid

    Author of lecture Type 1: Causes – Hypersensitivity

     Peter Delves, PhD

    Peter Delves, PhD

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