| First Author | Kopf M | Year | 1999 |
| Journal | Immunity | Volume | 11 |
| Issue | 6 | Pages | 699-708 |
| PubMed ID | 10626892 | Mgi Jnum | J:59204 |
| Mgi Id | MGI:1351153 | Doi | 10.1016/s1074-7613(00)80144-2 |
| Citation | Kopf M, et al. (1999) OX40-deficient mice are defective in Th cell proliferation but are competent in generating B cell and CTL Responses after virus infection. Immunity 11(6):699-708 |
| abstractText | OX40, a member of the TNF receptor superfamily, is expressed on activated T cells and implicated in stimulation of T cells and T-dependent humoral responses. We generated OX40-/- mice and found that the formation of extrafollicular plasma cells, germinal centers, and antibody responses was independent of OX40. After infection with LCMV and influenza virus, OX40-/- mice retain primary and memory cytotoxic T cell responses with normal expansion and decline of specific CTL. In contrast, CD4+ T cell proliferation and the number of IFN-gamma-producing CD4+ T cells were reduced in OX40-/- mice. Moreover, the number of CD4+ T cells infiltrating the lungs of influenza virus-infected OX40-/- mice was reduced. These results define a unique role of OX40 in the generation of optimal CD4+ T cell responses in vivo. |
