1
Return

PTPN22 regulates T cell synapse formation through PSTPIP1-dependent actin remodeling

delete2026-06-09
delete0
PRE
AI
M
Megan D. Joseph
C
Cecilia Zaza
O
Olivia P. L. Dalby
E
Efstratios Kirtsios
M
Michael L. Dustin
A
Andrew P. Cope
S
Sabrina Simoncelli *
DOI:10.1126/scisignal.ady6063delete
deleteOriginal
deleteOriginal request for help
deleteShare
deleteSave
Abstract

Abstract

En 中文
The protein tyrosine phosphatase PTPN22 suppresses T cell stimulation by acting on tyrosine-phosphorylated signaling molecules associated with the T cell receptor (TCR). Through super-resolution imaging analysis, Joseph et al. showed that PTPN22 also modulates T cell stimulation at the plasma membrane through its interaction with the cytoskeletal adaptor protein PSTPIP1. In PTPN22-deficient Jurkat cells, PSTPIP1 accumulated at TCRs, leading to excessive actin cytoskeletal remodeling, TCR clustering, and downstream signaling, which enhanced responses to low-affinity antigen. These findings highlight a pathway that may underlie aberrant T cell responses in autoimmunity. —John F. Foley

Journal

Science Signaling cover
Science Signaling
IF:
6.6
Papers:
3.0K
Citations:
1.4W

Organization

K
king's college london
Scholars:
4.7K
Papers: 2.3K
Citations: 0
U
university college london
Scholars:
7.3K
Papers: 4.0K
Citations: 1
U
university of oxford
Scholars:
9.6W
Papers: 8.5W
Citations: 137
Cited Papers

Cited Papers

Citing Papers

Citing Papers