The role of B7 costimulation in T-cell immunity
CD4(+) T cells are considered to be the major controlling element of the adaptive immune response. They recognize foreign peptides by interaction of the T cell receptor (TCR) with peptide complexed to major histocompatibility complex (MHC) class II molecules on the surface of antigen presenting cells (APC). Once activated CD4(+) T cells orchestrate the various phases of the immune response. They are responsible for the production of numerous cytokines, which activate specific immune effector cell populations including B cells, eosinophils, mast cells and macrophages. Not surprisingly, the activation of CD4(+) T cells needs to be tightly regulated and is subject to finely tuned control mechanisms. The requirement for a second or 'costimulatory' signal, in addition to the antigenic signal, provides a key element for the exquisite control of T cell activation. One of the major signalling pathways responsible for delivery of this costimulatory signal is induced by interaction of CD28 on T cells with B7 molecules found only on APC. The present review outlines our current understanding of the physiological role of B7 costimulatory signals in regulating CD4(+) T cell responses.
Keywords: b7-1 ; b7-2 ; cd28 ; costimulation ; effector cell ; humoral immunity ; memory cell ; th1/th2 cell ; accessory molecule cd28 ; ctla-4 counter-receptor ; cd28-deficient mice ; lymphocytes-t ; messenger-rna ; posttranscriptional regulation ; antigen presentation ; cytokine production ; activation pathway ; langerhans cells
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Record created on 2010-01-07, modified on 2016-08-08