Abstract
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.
Publication types
-
Comparative Study
-
Research Support, N.I.H., Extramural
-
Research Support, Non-U.S. Gov't
-
Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
-
Animals
-
DNA-Binding Proteins / deficiency
-
DNA-Binding Proteins / genetics
-
Genetic Predisposition to Disease
-
Immunity, Innate / genetics
-
Inflammation / genetics
-
Inflammation / immunology
-
Inflammation / parasitology
-
Leishmania donovani / immunology*
-
Leishmaniasis, Visceral / genetics
-
Leishmaniasis, Visceral / immunology*
-
Leishmaniasis, Visceral / parasitology*
-
Leishmaniasis, Visceral / pathology
-
Liver Diseases, Parasitic / genetics
-
Liver Diseases, Parasitic / immunology
-
Liver Diseases, Parasitic / parasitology
-
Liver Diseases, Parasitic / pathology
-
Mice
-
Mice, Inbred BALB C
-
Mice, Knockout
-
STAT1 Transcription Factor / deficiency
-
STAT1 Transcription Factor / genetics
-
STAT1 Transcription Factor / physiology*
-
T-Box Domain Proteins
-
T-Lymphocyte Subsets / immunology
-
T-Lymphocyte Subsets / transplantation
-
Th1 Cells / immunology
-
Th1 Cells / metabolism
-
Transcription Factors / deficiency
-
Transcription Factors / genetics
-
Transcription Factors / physiology*
Substances
-
DNA-Binding Proteins
-
Rag2 protein, mouse
-
STAT1 Transcription Factor
-
Stat1 protein, mouse
-
T-Box Domain Proteins
-
T-box transcription factor TBX21
-
Transcription Factors