Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 113, Issue 46, Pages E7231-E7239Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1603738113
Keywords
chronic infection; T-cell exhaustion; PTPN22; LCMV; CREM
Categories
Funding
- National Institute of Allergy and Infectious Diseases (NIAID) [5R21AI119353]
- NIAID [1R01AI123210-01]
Ask authors/readers for more resources
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 IFN beta-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 IFN beta/ CREM/ IL-2 axis in regulating T-lymphocyte function during chronic viral infection.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available