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

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Impaired CD8 T cell memory and CD4 T cell primary responses in IL-7R{alpha} mutant mice.

Loss of interleukin (IL)-7 or the IL-7 receptor alpha (IL-7Ralpha, CD127) results in severe immunodeficiencies in mice and humans. To more precisely identify signals governing IL-7 function in vivo, we have disrupted the IL-7Ralpha Y449XXM motif in mice by knock-in mutagenesis (IL-7Ralpha(449F)). Thymic precursors were reduced in number in IL-7Ralpha(449F) mice, but in marked contrast to IL-7Ralpha(-/-) knockout mice, thymocytes and peripheral T cells developed normally. Strikingly, Listeria infection revealed that CD4 and CD8 T cells had different requirements for IL-7Ralpha signals. CD4 T cells failed to mount a primary response, but despite normal CD8 primary responses, maintenance of CD8 memory was impaired in IL-7Ralpha(449F) mice. Furthermore, we show that Bcl-2 is IL-7Ralpha Y449 independent and insufficient for IL-7- mediated maintenance of CD8 memory.[1]

References

  1. Impaired CD8 T cell memory and CD4 T cell primary responses in IL-7R{alpha} mutant mice. Osborne, L.C., Dhanji, S., Snow, J.W., Priatel, J.J., Ma, M.C., Miners, M.J., Teh, H.S., Goldsmith, M.A., Abraham, N. J. Exp. Med. (2007) [Pubmed]
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