Cutting edge: STAT1 and T-bet play distinct roles in determining outcome of visceral leishmaniasis caused by Leishmania donovani

Lucia E. Rosas, Heidi M. Snider, Joseph Barbi, Anjali A. Satoskar, Geanncarlo Lugo-Villarino, Tracy Keiser, Tracy Papenfuss, Joan E. Durbin, Danuta Radzioch, Laurie H. Glimcher, Abhay R. Satoskar

Research output: Contribution to journalArticlepeer-review

Abstract

T-bet and STAT1 regulate IFN-γ 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 STA1+/+ 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.

Original languageEnglish (US)
Pages (from-to)22-25
Number of pages4
JournalJournal of Immunology
Volume177
Issue number1
DOIs
StatePublished - Jul 1 2006

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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