| First Author | Rosas LE | Year | 2006 |
| Journal | J Immunol | Volume | 177 |
| Issue | 1 | Pages | 22-5 |
| PubMed ID | 16785492 | Mgi Jnum | J:134384 |
| Mgi Id | MGI:3785635 | Doi | 10.4049/jimmunol.177.1.22 |
| Citation | Rosas LE, et al. (2006) Cutting edge: STAT1 and T-bet play distinct roles in determining outcome of visceral leishmaniasis caused by Leishmania donovani. J Immunol 177(1):22-5 |
| abstractText | T-bet and STAT1 regulate IFN-gamma gene transcription in CD4+ T cells, which mediate protection against Leishmania. Here we show that T-bet and STAT1 are required for the induction of an efficient Th1 response during Leishmania donovani infection, but they play distinct roles in determining disease outcome. Both STAT1(-/-) and T-bet(-/-) mice failed to mount a Th1 response, but STAT1(-/-) mice were highly resistant to L. donovani and developed less immunopathology, whereas T-bet(-/-) mice were highly susceptible and eventually developed liver inflammation. Adoptive cell transfer studies showed that RAG2(-/-) recipients receiving STAT1(+/+) or STAT1(-/-) T cells developed comparable liver pathology, but those receiving STAT1(-/-) T cells were significantly more susceptible to infection. These unexpected findings reveal distinct roles for T-bet and STAT1 in mediating host immunity and liver pathology during visceral leishmaniasis. |
