| First Author | Peterson AC | Year | 2003 |
| Journal | Eur J Immunol | Volume | 33 |
| Issue | 10 | Pages | 2687-95 |
| PubMed ID | 14515252 | Mgi Jnum | J:284510 |
| Mgi Id | MGI:6390297 | Doi | 10.1002/eji.200324294 |
| Citation | Peterson AC, et al. (2003) T cell development and function in CrkL-deficient mice. Eur J Immunol 33(10):2687-95 |
| abstractText | 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. |
