| First Author | Bonilla FA | Year | 1997 |
| Journal | Int Immunol | Volume | 9 |
| Issue | 12 | Pages | 1875-83 |
| PubMed ID | 9466315 | Mgi Jnum | J:45026 |
| Mgi Id | MGI:1101640 | Doi | 10.1093/intimm/9.12.1875 |
| Citation | Bonilla FA, et al. (1997) Targeted gene disruption of murine CD7. Int Immunol 9(12):1875-83 |
| abstractText | CD7 is a 40 kDa type I transmembrane glycoprotein member of the Ig superfamily. CD7 is a marker of mature human T cells and NK cells, and is expressed early in their development. Cross-linking CD7 positively modulates T cell and NK cell activity as measured by calcium fluxes, expression of adhesion molecules, cytokine secretion and proliferation. CD7 associates directly with phosphoinositol 3'-kinase, and CD7 ligation induces production of D-3 phosphoinositides and tyrosine phosphorylation. Severe combined immunodeficiency has been associated with a lack of lymphocyte surface CD7. The CD7 ligand is unknown. The murine CD7 homolog is encoded by a single gene on chromosome 11. In order to characterize the role of CD7 in lymphocyte development and function we have eliminated the CD7 gene by targeted disruption. CD7-deficient mice display normal histology of thymus and spleen, normal lymphocyte populations in primary and secondary lymphoid tissues, and normal serum Ig levels. Specific antibody responses after immunization with T-dependent and T-independent antigens are equivalent in wild-type and CD7 knockout mice. CD7-deficient lymphocytes respond normally to T cell mitogenic and allogeneic stimuli, and display normal NK cell cytotoxicity. |
