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The transcription factor IRF4 is essential for TCR affinity-mediated metabolic programming and clonal expansion of T cells.

Man, Kevin; Miasari, Maria; Shi, Wei; Xin, Annie; Henstridge, Darren C; Preston, Simon; Pellegrini, Marc; Belz, Gabrielle T; Smyth, Gordon K; Febbraio, Mark A; Nutt, Stephen L; Kallies, Axel.
Nat Immunol; 14(11): 1155-65, 2013 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-24056747
During immune responses, T cells are subject to clonal competition, which leads to the predominant expansion of high-affinity clones; however, there is little understanding of how this process is controlled. We found here that the transcription factor IRF4 was induced in a manner dependent on affinity for the T cell antigen receptor (TCR) and acted as a dose-dependent regulator of the metabolic function of activated T cells. IRF4 regulated the expression of key molecules required for the aerobic glycolysis of effector T cells and was essential for the clonal expansion and maintenance of effector function of antigen-specific CD8(+) T cells. Thus, IRF4 is an indispensable molecular 'rheostat' that 'translates' TCR affinity into the appropriate transcriptional programs that link metabolic function with the clonal selection and effector differentiation of T cells.
Selo DaSilva