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This response involves the interaction of T cells, monocytes, and macrophages. This reaction is caused when CD4 + T h 1 cells recognize foreign antigen in a complex with the MHC class II on the surface of antigen-presenting cells. These can be macrophages that secrete IL-12, which stimulates the proliferation of further CD4 + T h 1 cells.
T cells are called T cells because they mature in the thymus. The two types of T cells that cause damage to tissues in type IV hypersensitivity are CD8+ T cells also known as killer T cells or cytotoxic T cells, as well as CD4+ T cells also known as helper T cells. CD8+ killer T cells do exactly what their name implies - they kill things.
Their key effector cytokine is IL-10. Their main effector cells are NK cells as well as CD8 T cells, IgG B cells, and IL-10 CD4 T cells. The key THαβ transcription factors are STAT1 and STAT3 as well as IRFs. IL-10 from CD4 T cells activate NK cells' ADCC to apoptose virus-infected cells and to induce host as well as viral DNA fragmentation ...
Hypersensitivity (also called hypersensitivity reaction or intolerance) is an abnormal physiological condition in which there is an undesirable and adverse immune response to an antigen. [ 1 ] [ 2 ] It is an abnormality in the immune system that causes immune diseases including allergies and autoimmunity .
In molecular biology, CD4 (cluster of differentiation 4) is a glycoprotein that serves as a co-receptor for the T-cell receptor (TCR). CD4 is found on the surface of immune cells such as helper T cells , monocytes , macrophages , and dendritic cells .
Like other drug-induced SCARs disorders, the DRESS syndrome is a type IV hypersensitivity reaction in which a drug or its metabolite stimulates cytotoxic T cells (i.e. CD8 + T cells) or T helper cells (i.e. CD4 + T cells) to initiate autoimmune reactions that attack self tissues. DRESS syndrome is a SCARs type IV, subtype IVb reaction.
In type I hypersensitivity, B cells are stimulated (by CD4 + T h 2 cells) to produce IgE antibodies specific to an antigen. The difference between a normal infectious immune response and a type 1 hypersensitivity response is that in type 1 hypersensitivity, the antibody is IgE instead of IgA, IgG, or IgM.
It was believed that CD4 + T cells were not involved directly in antitumour immunity, but rather functioned simply in the priming of CD8 + T cells, through activation of antigen-presenting cells (APCs) and increased antigen presentation on MHC class I, as well as secretion of excitatory cytokines such as IL-2 (Pardol and Toplain, 1998, Kalams ...
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