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GADS is required for TCR-mediated calcium influx and cytokine release, but not cellular adhesion, in human T cells.

Abstract：

:GRB2 related adaptor protein downstream of Shc (GADS) is a member of the GRB2 family of adaptors and is critical for TCR-induced signaling. The current model is that GADS recruits SLP-76 to the LAT complex, which facilitates the phosphorylation of SLP-76, the activation of PLC-γ1, T cell adhesion and cytokine production. However, this model is largely based on studies of disruption of the GADS/SLP-76 interaction and murine T cell differentiation in GADS deficient mice. The role of GADS in mediating TCR-induced signals in human CD4+ T cells has not been thoroughly investigated. In this study, we have suppressed the expression of GADS in human CD4+ HuT78 T cells. GADS deficient HuT78 T cells displayed similar levels of TCR-induced SLP-76 and PLC-γ1 phosphorylation but exhibited substantial decrease in TCR-induced IL-2 and IFN-γ release. The defect in cytokine production occurred because of impaired calcium mobilization due to reduced recruitment of SLP-76 and PLC-γ1 to the LAT complex. Surprisingly, both GADS deficient HuT78 and GADS deficient primary murine CD8+ T cells had similar TCR-induced adhesion when compared to control T cells. Overall, our results show that GADS is required for calcium influx and cytokine production, but not cellular adhesion, in human CD4+ T cells, suggesting that the current model for T cell regulation by GADS is incomplete.

journal_name

Cell Signal

journal_title

Cellular signalling

authors

Bilal MY,Zhang EY,Dinkel B,Hardy D,Yankee TM,Houtman JC

doi

10.1016/j.cellsig.2015.01.012

subject

Has Abstract

pub_date

2015-04-01 00:00:00

pages

841-50

issue

4

eissn

0898-6568

issn

1873-3913

pii

S0898-6568(15)00023-6

journal_volume

27

pub_type

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