Type II Hypersensitivity: Caused by IgG response to chemically reactive small molecules that become covalently bound to the outside surface of cells. Chemical reaction modifies the structure of the human cell surface components that are perceived as foreign antigens. IgG antibodies produced cause the modified human cells to become subject to complement activation. Example: Penicillin (small reactive molecule), Transfusion reactions such as erythroblastosis fetalis.
Type III Hypersensitivity: Small soluble immune complexes of antigen and specific IgG form deposits in the walls of small blood vessels or the alveoli of the lungs. At those sites, immune complex activate complement and inflammatory response. Example: Antibodies or proteins derived from non-human animal species such as porcine/bovine insulin.
Type IV Hypersensitivity/Delayed-type Hypersensitivity: Mediated by antigen-specific effector T cells, and mostly it is CD4 TH1 cells. Become apparent 1-3 days after exposure to antigen. Examples: Nickel allergy leading to red, itchy, and blistering skin rash. Peptides containing nickel residues are presented by MHC Class II. Some can involve CD8+ T cells too such as poison ivy. Against Mycobacterium tuberculosis.
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