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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Maintenance of human T cell anergy: blocking of IL-2 gene transcription by activated Rap1.

In the absence of costimulation, T cells activated through their antigen receptor become unresponsive (anergic) and do not transcribe the gene encoding interleukin-2 (IL-2) when restimulated with antigen. Anergic alloantigen-specific human T cells contained phosphorylated Cbl that coimmunoprecipitated with Fyn. The adapter protein CrkL was associated with both phosphorylated Cbl and the guanidine nucleotide-releasing factor C3G, which catalyzes guanosine triphosphate (GTP) exchange on Rap1. Active Rap1 (GTP-bound form) was present in anergic cells. Forced expression of low amounts of Rap1-GTP in Jurkat T cells recapitulated the anergic defect and blocked T cell antigen receptor (TCR)- and CD28- mediated IL-2 gene transcription. Therefore, Rap1 functions as a negative regulator of TCR- mediated IL-2 gene transcription and may be responsible for the specific defect in IL-2 production in T cell anergy.[1]

References

  1. Maintenance of human T cell anergy: blocking of IL-2 gene transcription by activated Rap1. Boussiotis, V.A., Freeman, G.J., Berezovskaya, A., Barber, D.L., Nadler, L.M. Science (1997) [Pubmed]
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