| First Author | Inouye S | Year | 2004 |
| Journal | J Biol Chem | Volume | 279 |
| Issue | 37 | Pages | 38701-9 |
| PubMed ID | 15226319 | Mgi Jnum | J:92853 |
| Mgi Id | MGI:3054612 | Doi | 10.1074/jbc.M405986200 |
| Citation | Inouye S, et al. (2004) Impaired IgG production in mice deficient for heat shock transcription factor 1. J Biol Chem 279(37):38701-9 |
| abstractText | Heat shock factor 1 (HSF1) is a major transactivator of heat shock proteins in response to heat shock, and it is also involved in oogenesis, spermatogenesis, and placental development. However, we do not know the molecular mechanisms controlling developmental processes. In this study, we found that HSF1-null mice exhibited a significant decrease in the T cell-dependent B cell response. When mice were immunized intraperitoneally with sheep red blood cells, the sheep red blood cell-specific IgG production, especially IgG2a production, in HSF1-null mice was about 50% lower than that in wild-type mice at 6 days after the immunization, whereas IgM production was normal. The number of bromodeoxyuridine-incorporated spleen cells in immunized HSF1-null mice was one-third that in immunized wild-type mice, indicating reduced proliferation of the spleen cells. We analyzed levels of cytokines and chemokines in spleen cells and in peritoneal macrophages stimulated with lipopolysaccharide and interferon-gamma and found that expression levels of interleukin-6 and CCL5 were significantly lower in HSF1-null cells than those in wild-type cells. Furthermore, we demonstrated that the IL-6 gene is a direct target gene of HSF1. These results revealed a novel molecular link between HSF1 and a gene related to immune response and inflammation. |
