| First Author | Gongora R | Year | 2000 |
| Journal | J Immunol | Volume | 165 |
| Issue | 5 | Pages | 2362-6 |
| PubMed ID | 10946258 | Mgi Jnum | J:64062 |
| Mgi Id | MGI:1888648 | Doi | 10.4049/jimmunol.165.5.2362 |
| Citation | Gongora R, et al. (2000) Stat-1 is not essential for inhibition of B lymphopoiesis by type I IFNs. J Immunol 165(5):2362-6 |
| abstractText | Type I IFNs, IFN-alpha, -beta, and -omega, are cytokine family members with multiple immune response roles, including the promotion of cell growth and differentiation. Conversely, the type I IFNs are potent inhibitors of IL-7-dependent growth of early B lineage progenitors, effectively aborting further B lineage differentiation at the pro-B cell stage. Type I IFNs alpha and beta function via receptor-mediated activation of a Jak/Stat signaling pathway in which Stat-1 is functionally important, because many IFN-induced responses are abrogated in Stat-1-deficient mice. To the contrary, we show here that the inhibition of IL-7-dependent B lymphopoiesis by IFN-alphabeta is unaffected in Stat-1-deficient mice. The present data indicate that the type I IFNs can activate an alternative signaling pathway in which neither Stat-1 nor phosphatidylinositol 3'-kinase are essential components. |
