[HTML][HTML] OX40-deficient mice are defective in Th cell proliferation but are competent in generating B cell and CTL responses after virus infection

M Kopf, C Ruedl, N Schmitz, A Gallimore, K Lefrang… - Immunity, 1999 - cell.com
M Kopf, C Ruedl, N Schmitz, A Gallimore, K Lefrang, B Ecabert, B Odermatt, MF Bachmann
Immunity, 1999cell.com
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 …
Abstract
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-γ-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.
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