| First Author | Ranger AM | Year | 1998 |
| Journal | Immunity | Volume | 8 |
| Issue | 1 | Pages | 125-34 |
| PubMed ID | 9462518 | Mgi Jnum | J:78376 |
| Mgi Id | MGI:2384284 | Doi | 10.1016/s1074-7613(00)80465-3 |
| Citation | Ranger AM, et al. (1998) Delayed lymphoid repopulation with defects in IL-4-driven responses produced by inactivation of NF-ATc. Immunity 8(1):125-34 |
| abstractText | The NF-AT family of transcription factors activates early immune response genes such as cytokines. In the adult, NF-ATc is expressed exclusively in the lymphoid system and is induced upon lymphocyte activation. NF-ATc null mutant mice die in utero of cardiac failure, precluding analysis of the role of NF-ATc in lymphocyte activation. By using RAG-2-deficient blastocyst complementation, we now demonstrate that young, highly chimeric mice lacking NF-ATc have impaired repopulation of both thymus and peripheral lymphoid organs. Furthermore, NF-ATc deficiency impaired T lymphocyte activation and secretion of IL-4. B lymphocytes displayed reduced proliferation and a selective loss of IL-4-driven immunoglobulin isotypes both in vivo and in vitro. Our data demonstrate that NF-ATc is essential for the optimal generation and function of mature T and B lineage cells, with an especially profound effect on IL-4-driven responses. |
