CHIEN-KUO LEEGimeno, RRGimenoLevy, D ED ELevy2019-07-182019-07-181999-11-150022-1007https://www.scopus.com/inward/record.uri?eid=2-s2.0-0033571762&doi=10.1084%2fjem.190.10.1451&partnerID=40&md5=ef2054e3390cfa9340bbad69440c790ahttps://scholars.lib.ntu.edu.tw/handle/123456789/414247Major 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.enGene regulation | Interferon | Interleukin-7 | STAT1 | Tyrosine phosphorylationjournal article10.1084/jem.190.10.1451105623202-s2.0-0033571762https://api.elsevier.com/content/abstract/scopus_id/0033571762