| First Author | Maine CJ | Year | 2016 |
| Journal | Proc Natl Acad Sci U S A | Volume | 113 |
| Issue | 46 | Pages | E7231-E7239 |
| PubMed ID | 27799548 | Mgi Jnum | J:238853 |
| Mgi Id | MGI:5824441 | Doi | 10.1073/pnas.1603738113 |
| Citation | Maine CJ, et al. (2016) PTPN22 contributes to exhaustion of T lymphocytes during chronic viral infection. Proc Natl Acad Sci U S A 113(46):E7231-E7239 |
| abstractText | The protein encoded by the autoimmune-associated protein tyrosine phosphatase nonreceptor type 22 gene, PTPN22, has wide-ranging effects in immune cells including suppression of T-cell receptor signaling and promoting efficient production of type I interferons (IFN-I) by myeloid cells. Here we show that mice deficient in PTPN22 resist chronic viral infection with lymphocytic choriomeningitis virus clone 13 (LCMV cl13). The numbers and function of viral-specific CD4 T lymphocytes is greatly enhanced, whereas expression of the IFNbeta-induced IL-2 repressor, cAMP-responsive element modulator (CREM) is reduced. Reduction of CREM expression in wild-type CD4 T lymphocytes prevents the loss of IL-2 production by CD4 T lymphocytes during infection with LCMV cl13. These findings implicate the IFNbeta/CREM/IL-2 axis in regulating T-lymphocyte function during chronic viral infection. |
