Intracellular signal transduction mediated by ligation of MHC class I molecules.
A great deal of knowledge has accumulated regarding signal transduction after ligation of MHC class I (MHC-I) molecules. In recent years focus has been given to delineation of the intracellular signal pathways activated after MHC-I ligation. Activation of tyrosine kinases leading to a rise in the intracellular free calcium concentration ([Ca2+]i) is the major initial event occurring after MHC-I ligation of T cells. Curiously, the MHC-I-induced signaling is not dependent upon the cytoplasmic tail of the MHC-I molecule, suggesting that the MHC-I molecule induces intracellular signaling through association with other membrane-embedded molecules. More distal signaling events after MHC-I ligation includes activation of the Jak/Stat pathway leading to Stat-3 activation, and activation of the PI3-kinase leading to JNK activation and apoptosis. This review will sum up what is currently known about signaling induced by ligation of MHC-I.
Skov
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Department of Medical Anatomy, the Panum Institute, University of Copenhagen, Denmark. S.Skov@mai.ku.dk
D000818:Animals; D002448:Cell Adhesion; D002462:Cell Membrane; D005544:Forecasting; D015395:Histocompatibility Antigens Class I / Q000502:physiology*; D006801:Humans; D007424:Intracellular Fluid; D015398:Signal Transduction
D015395:Histocompatibility Antigens Class I