CD22 is a functional ligand for SH2 domain-containing protein-tyrosine phosphatase-1 in primary T cells

Sathish, Jean Gerard, Walters, Jenna, Luo, Jin Cai, Johnson, Kenneth G., LeRoy, Frances Gertrude, Brennan, Paul ORCID: https://orcid.org/0000-0001-8792-0499, Kim, Kwang P., Gygi, Steven P., Neel, Benjamin G. and Matthews, Reginald James 2004. CD22 is a functional ligand for SH2 domain-containing protein-tyrosine phosphatase-1 in primary T cells. Journal of Biological Chemistry 279 (46) , pp. 47783-47791. 10.1074/jbc.M402354200

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Abstract

The intracellular Src homology 2 (SH2) domain-containing protein-tyrosine phosphatase (SHP-1) has been characterized as a negative regulator of T cell function, contributing to the definition of T cell receptor signaling thresholds in developing and peripheral mouse T lymphocytes. The activation of SHP-1 is achieved through the engagement of its tandem SH2 domains by tyrosine-phosphorylated proteins; however, the identity of the activating ligand(s) for SHP-1, within mouse primary T cells, is presently unresolved. The identification of SHP-1 ligand(s) in primary T cells would provide crucial insight into the molecular mechanisms by which SHP-1 contributes to in vivo thresholds for T cell activation. Here we present a combination of biochemical and yeast genetic analyses indicating CD22 to be a T cell ligand for the SHP-1 SH2 domains. Based on these observations we have confirmed that CD22 is indeed expressed on mouse primary T cells and capable of associating with SHP-1. Significantly, CD22-deficient T cells demonstrate enhanced proliferation in response to anti-CD3 or allogeneic stimulation. Furthermore, the co-engagement of CD3 and CD22 results in a raising of TCR signaling thresholds hence demonstrating a previously unsuspected functional role for CD22 in primary T cells.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Medicine
Subjects:	R Medicine > R Medicine (General)
ISSN:	1083-351X
Last Modified:	17 Oct 2022 08:30
URI:	https://orca.cardiff.ac.uk/id/eprint/302

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