IMM2022 Lecture Notes - Lecture 1: Degranulation, Diabetes Mellitus Type 1, Interleukin 4

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HYPERSENSITIVITES
Results in tissue damage or pathology that is associated with unwanted immune responses
and causes autoimmune diseases and allergy
Type I hypersensitivity
Immediate hypersensitivity
TH2, IgE, mast cells (derived mediators -> vasoactive amines;
loosens epithelial cells to allow fluid into tissues), eosinophils
(cytokine mediated inflammation)
Allergic responses
Type II hypersensitivity
Antibody mediated diseases
Self-reactive antibodies
IgM, IgG
Antibodies -> destruction, activation or inhibition
Complement and Fc receptor mediated recruitment and activation
of leukocytes, opsonisation and phagocytosis of cells
Eg. Graves disease (excessive secretion of thyroid hormones)
Type III hypersensitivity
Immune complex-mediated diseases
Immune complexes of circulating antigens and IgM or IgG
antibodies deposited in vascular basement membrane
Key characteristic: The presence of antibodies bound to antigen in
the circulation
Complement and Fc receptor
Occurs when antigen-antibody complexes that are not adequately
cleared by innate immune accumulates (excess antigens)
Eg. SLE (autoantibodies generated to nuclear components combine
to form a complex)
Type IV hypersensitivity
T cell-mediated diseases
CD4 (cytokine mediated inflammation, can cause tissue injury) and
CD8 (T cell-mediated cytolysis, can cause cell death and tissue
injury)
Macrophage activation and direct target cell lysis
Tend to be localised to single area, localised inflammation,
stimulate T cells non-specifically.
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