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POSH Regulates CD4+ T Cell Differentiation and Survival

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Journal J Immunol
Date 2016 Apr 17
PMID 27084103
Citations 5
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Abstract

The scaffold molecule POSH is crucial for the regulation of proliferation and effector function in CD8(+) T cells. However, its role in CD4(+) T cells is not known. In this study, we found that disruption of the POSH scaffold complex established a transcriptional profile that strongly skewed differentiation toward Th2, led to decreased survival, and had no effect on cell cycle entry. This is in stark contrast to CD8(+) T cells in which POSH regulates cell cycle and does not affect survival. Disruption of POSH in CD4(+) T cells resulted in the loss of Tak1-dependent activation of JNK1/2 and Tak1-mediated survival. However, in CD8(+) T cells, POSH regulates only JNK1. Remarkably, each type of T cell had a unique composition of the POSH scaffold complex and distinct posttranslational modifications of POSH. These data indicate that the mechanism that regulates POSH function in CD4(+) T cells is different from CD8(+) T cells. All together, these data strongly suggest that POSH is essential for the integration of cell-type-specific signals that regulate the differentiation, survival, and function of T cells.

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References
1.
Mooney L, Whitmarsh A . Docking interactions in the c-Jun N-terminal kinase pathway. J Biol Chem. 2003; 279(12):11843-52. DOI: 10.1074/jbc.M311841200. View

2.
Bursen A, Moritz S, Gaussmann A, Moritz S, Dingermann T, Marschalek R . Interaction of AF4 wild-type and AF4.MLL fusion protein with SIAH proteins: indication for t(4;11) pathobiology?. Oncogene. 2004; 23(37):6237-49. DOI: 10.1038/sj.onc.1207837. View

3.
Avruch J, Tornqvist H, Gunsalus J, Price D, Kyriakis J, Yurkow E . The role of tyrosine-and serine-threonine-protein phosphorylation in insulin action. Adv Second Messenger Phosphoprotein Res. 1990; 24:295-300. View

4.
Mayer B, Eck M . SH3 domains. Minding your p's and q's. Curr Biol. 1995; 5(4):364-7. DOI: 10.1016/s0960-9822(95)00073-x. View

5.
Zhang W, Sloan-Lancaster J, Kitchen J, Trible R, Samelson L . LAT: the ZAP-70 tyrosine kinase substrate that links T cell receptor to cellular activation. Cell. 1998; 92(1):83-92. DOI: 10.1016/s0092-8674(00)80901-0. View