The reverse stop-signal model for CTLA4 function.
Activation of the T-cell co-receptor cytotoxic T-lymphocyte antigen 4 (CTLA4) has a pivotal role in adjusting the threshold for T-cell activation and in preventing autoimmunity and massive tissue infiltration by T cells. Although many mechanistic models have been postulated, no single model has yet accounted for its overall function. In this Opinion article, I outline the strengths and weaknesses of the current models, and present a new 'reverse stop-signal model' to account for CTLA4 function.
Rudd
Christopher E
CE
Cell Signalling Section, Division of Immunology, Department of Pathology, Tennis Court Road, CB1 4QP Cambridge, UK. cer51@cam.ac.uk
D000818:Animals; D015703:Antigens, CD / Q000235:genetics / Q000502:physiology*; D000943:Antigens, Differentiation / Q000235:genetics / Q000502:physiology*; D015551:Autoimmunity / Q000235:genetics / Q000276:immunology*; D060908:CTLA-4 Antigen; D002465:Cell Movement; D008213:Lymphocyte Activation; D051379:Mice; D018345:Mice, Knockout; D015398:Signal Transduction; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*; D016211:Transforming Growth Factor alpha / Q000378:metabolism
D015703:Antigens, CD; D000943:Antigens, Differentiation; D060908:CTLA-4 Antigen; C556707:Ctla4 protein, mouse; D016211:Transforming Growth Factor alpha