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PTPN22 encodes a tyrosine phosphatase that inhibits Src-family kinases responsible for Ag receptor signaling in lymphocytes and is strongly linked with susceptibility to a number of autoimmune diseases. As strength of TCR signal is critical to the thymic selection of regulatory T cells (Tregs), we examined the effect of murine PTPN22 deficiency on Treg development and function. In the thymus, numbers of pre-Tregs and Tregs increased inversely with the level of PTPN22. This increase in Tregs persisted in the periphery and could play a key part in the reduced severity observed in the PTPN22-deficient mice of experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis. This could explain the lack of association of certain autoimmune conditions with PTPN22 risk alleles.

Original publication

DOI

10.4049/jimmunol.1200150

Type

Journal article

Journal

Journal of immunology (Baltimore, Md. : 1950)

Publication Date

06/2012

Volume

188

Pages

5267 - 5275

Addresses

Department of Immunology and Microbial Sciences, The Scripps Research Institute, La Jolla, CA 92037, USA.

Keywords

Thymus Gland, Animals, Mice, Inbred C57BL, Mice, Knockout, Mice, Multiple Sclerosis, Encephalomyelitis, Autoimmune, Experimental, Up-Regulation, Female, T-Lymphocytes, Regulatory, Protein Tyrosine Phosphatase, Non-Receptor Type 22