Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 204, Issue 3, Pages 619-631Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20061871
Keywords
-
Categories
Funding
- NIGMS NIH HHS [R01 GM054351, GM54351] Funding Source: Medline
Ask authors/readers for more resources
Loss of interleukin (IL)-7 or the IL-7 receptor alpha (IL-7R alpha, 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-7R alpha Y449XXM motif in mice by knock-in mutagenesis (IL-7R alpha(449F)). Thymic precursors were reduced in number in IL-7R alpha(449F) mice, but in marked contrast to IL-7R alpha(-/-) knockout mice, thymocytes and peripheral T cells developed normally. Strikingly, Listeria infection revealed that CD4 and CD8 T cells had different requirements for IL-7R alpha signals. CD4 T cells failed to mount a primary response, but despite normal CD8 primary responses, maintenance of CD8 memory was impaired in IL-7R alpha(449F) mice. Furthermore, we show that Bcl-2 is IL-7R alpha Y449 independent and insufficient for IL-7-mediated maintenance of CD8 memory.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available