Cutting Edge: STAT1 and T-bet Play Distinct Roles in Determining Outcome of Visceral Leishmaniasis Caused byLeishmania donovani | Zendy

Lucia E. Rosas | Zendy; Heidi Snider | Zendy; Joseph Barbi | Zendy; Anjali A. Satoskar | Zendy; Geanncarlo LugoVillarino | Zendy; Tracy L. Keiser | Zendy; Tracy L. Papenfuss | Zendy; Joan E. Durbin | Zendy; Danuta Radzioch | Zendy; Laurie H. Glimcher | Zendy; Abhay R. Satoskar | Zendy

Open Access

Cutting Edge: STAT1 and T-bet Play Distinct Roles in Determining Outcome of Visceral Leishmaniasis Caused byLeishmania donovani

Author(s) -

Lucia E. Rosas,

Heidi Snider,

Joseph Barbi,

Anjali A. Satoskar,

Geanncarlo LugoVillarino,

Tracy L. Keiser,

Tracy L. Papenfuss,

Joan E. Durbin,

Danuta Radzioch,

Laurie H. Glimcher,

Abhay R. Satoskar

Publication year - 2006

Publication title -

the journal of immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.737

H-Index - 372

eISSN - 1550-6606

pISSN - 0022-1767

DOI - 10.4049/jimmunol.177.1.22

Subject(s) - stat1 , leishmania donovani , visceral leishmaniasis , biology , immunology , adoptive cell transfer , leishmaniasis , leishmania , inflammation , immune system , t cell , parasite hosting , interferon , world wide web , computer science

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.

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