| First Author | Shores EW | Year | 1998 |
| Journal | J Exp Med | Volume | 187 |
| Issue | 7 | Pages | 1093-101 |
| PubMed ID | 9529325 | Mgi Jnum | J:46914 |
| Mgi Id | MGI:1202229 | Doi | 10.1084/jem.187.7.1093 |
| Citation | Shores EW, et al. (1998) T cell development in mice lacking all T cell receptor zeta family members (Zeta, eta, and FcepsilonRIgamma). J Exp Med 187(7):1093-101 |
| abstractText | The zeta family includes zeta, eta, and FcepsilonRIgamma (Fcgamma). Dimers of the zeta family proteins function as signal transducing subunits of the T cell antigen receptor (TCR), the pre-TCR, and a subset of Fc receptors. In mice lacking zeta/eta chains, T cell development is impaired, yet low numbers of CD4+ and CD8+ T cells develop. This finding suggests either that pre-TCR and TCR complexes lacking a zeta family dimer can promote T cell maturation, or that in the absence of zeta/eta, Fcgamma serves as a subunit in TCR complexes. To elucidate the role of zeta family dimers in T cell development, we generated mice lacking expression of all of these proteins and compared their phenotype to mice lacking only zeta/eta or Fcgamma. The data reveal that surface complexes that are expressed in the absence of zeta family dimers are capable of transducing signals required for alpha/beta-T cell development. Strikingly, T cells generated in both zeta/eta-/- and zeta/eta-/--Fcgamma-/- mice exhibit a memory phenotype and elaborate interferon gamma. Finally, examination of different T cell populations reveals that zeta/eta and Fcgamma have distinct expression patterns that correlate with their thymus dependency. A possible function for the differential expression of zeta family proteins may be to impart distinctive signaling properties to TCR complexes expressed on specific T cell populations. |
