| First Author | Lee CK | Year | 1999 |
| Journal | J Exp Med | Volume | 190 |
| Issue | 10 | Pages | 1451-64 |
| PubMed ID | 10562320 | Mgi Jnum | J:58494 |
| Mgi Id | MGI:1347724 | Doi | 10.1084/jem.190.10.1451 |
| Citation | Lee CK, et al. (1999) Differential regulation of constitutive major histocompatibility complex class I expression in T and B lymphocytes. J Exp Med 190(10):1451-64 |
| abstractText | Major histocompatibility complex (MHC) class I antigens are constitutively expressed yet highly induced by interferon (IFN) during inflammation. We found that not only IFN-induced but also normal basal expression of MHC I required IFN receptors and signal transducer and activator of transcription (STAT)1, providing genetic evidence for continuous IFN signaling. Surprisingly, an IFN-independent requirement for STAT1 was also found, specifically in T lymphocytes, where MHC class I expression was not fully accounted for by IFN signaling. This IFN-independent pathway maintained tyrosine phosphorylation of STAT1 in T but not B lymphocytes even in the absence of IFN receptors. Interestingly, interleukin (IL)-7 selectively activated STAT1 and induced MHC class I in mature T but not B cells. These loss of function studies demonstrate an essential role of endogenous IFN and activated STAT1 for constitutive MHC class I expression in normal mice and define IL-7-dependent but IFN-independent regulation of STAT1 restricted to T lymphocytes. |
