Immunity and Hypersensitivity
Immunity and Hypersensitivity ( 5 Questions)
Type I hypersensitivity is not involved in tuberculin skin test, as it does not involve IgE antibodies or mast cells.
Type II hypersensitivity is not involved in tuberculin skin test, as it does not involve IgG or IgM antibodies or target cells.
Type III hypersensitivity is not involved in tuberculin skin test, as it does not involve immune complexes or complement activation.
Type IV hypersensitivity is involved in tuberculin skin test, as it involves the activation of helper T cells that recognize the mycobacterial antigens injected into the skin and release cytokines that recruit macrophages and other inflammatory cells. This leads to a delayed and indurated reaction at the site of injection.
Type V hypersensitivity is also involved in tuberculin skin test, as it involves the activation of cytotoxic T cells that recognize the mycobacterial antigens presented by MHC class I molecules on infected cells and destroy them by releasing perforin and granzymes. This leads to a cell-mediated reaction at the site of infection.
Choice A reason: Type I hypersensitivity is not involved in tuberculin skin test, as it does not involve IgE antibodies or mast cells.
Choice B reason: Type II hypersensitivity is not involved in tuberculin skin test, as it does not involve IgG or IgM antibodies or target cells.
Choice C reason: Type III hypersensitivity is not involved in tuberculin skin test, as it does not involve immune complexes or complement activation.
Choice D reason: Type IV hypersensitivity is involved in tuberculin skin test, as it involves the activation of helper T cells that recognize the mycobacterial antigens injected into the skin and release cytokines that recruit macrophages and other inflammatory cells. This leads to a delayed and indurated reaction at the site of injection.
Choice E reason: Type V hypersensitivity is also involved in tuberculin skin test, as it involves the activation of cytotoxic T cells that recognize the mycobacterial antigens presented by MHC class I molecules on infected cells and destroy them by releasing perforin and granzymes. This leads to a cell-mediated reaction at the site of infection.