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T cell development and function in CrkL-deficient mice

✍ Scribed by Amy C. Peterson; Reinhard E. Marks; Patrick E. Fields; Akira Imamoto; Thomas F. Gajewski

Publisher
John Wiley and Sons
Year
2003
Tongue
English
Weight
257 KB
Volume
33
Category
Article
ISSN
0014-2980

No coin nor oath required. For personal study only.

✦ Synopsis

Abstract

The adapter protein CrkL has been implicated in multiple signal transduction pathways in hematopoietic cells. In T lymphocytes, the recruitment of CrkL‐C3G complexes has been correlated with hyporesponsiveness, implicating CrkL as a potential negative regulator. To test this hypothesis we examined T cell activation in CrkL‐deficient mice. The CrkL^–/–^ genotype was partially embryonic lethal. In viable CrkL^–/–^ mice, peripheral blood counts were normal. The thymus from CrkL^–/–^ mice had 40% fewer cells compared to littermates, but the proportion of thymocyte subsets was comparable. There was no discernable alteration in T cell function as reflected by T cell numbers, expression of memory markers, IL‐2 production, proliferation, and differentiation into Th1/Th2 phenotypes. Immunization induced comparable levels of IgG2a and IgG1 antibodies. Chimeric mice, generated by transfer of CrkL^–/–^ fetal liver cells into irradiated RAG2^–/–^ recipients, also showed normal T cell function, arguing against selection via partial embryonic lethality. Our results indicate that CrkL is not absolutely required for T cell development or function, and argue against it being an essential component of a negative regulatory pathway in TCR signaling.

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