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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Kopf, M. et al.

Kopf, Ruedl, Schmitz, Gallimore, Lefrang, Ecabert, Odermatt, Bachmann,

OX40-deficient mice are defective in Th cell proliferation but are competent in generating B cell and CTL Responses after virus infection.

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.[1]

References

OX40-deficient mice are defective in Th cell proliferation but are competent in generating B cell and CTL Responses after virus infection. Kopf, M., Ruedl, C., Schmitz, N., Gallimore, A., Lefrang, K., Ecabert, B., Odermatt, B., Bachmann, M.F. Immunity (1999) [Pubmed]

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