These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: T-bet inhibits the in vivo differentiation of parasite-specific CD4+ Th17 cells in a T cell-intrinsic manner.
    Author: Guo S, Cobb D, Smeltz RB.
    Journal: J Immunol; 2009 May 15; 182(10):6179-86. PubMed ID: 19414771.
    Abstract:
    CD4(+) Th17 cells have emerged as a new T cell subset in the Th1/Th2 paradigm, and efforts have shifted toward understanding the factors that regulate their development in vivo. To analyze the role of the transcription factor T-bet in regulation of Th17 cells, we used a murine model of Trypanosoma cruzi infection, a protozoan parasite that causes Chagas disease in humans. Infection of Tbx21(-/-) mice led to normal, unimpaired development of Ag-specific CD4(+) T cells producing IFN-gamma. However, a robust Th17 response developed concomitant with Th1 responses. Despite significant IFN-gamma production, the physiological effects of Th17 responses prevailed as there was a sharp increase in Gr-1(+)Ly6G(+) neutrophils. Adoptive transfer of T cells from infected Tbx21(-/-) mice into Rag-2(-/-) mice (Tbx21(+/+)) revealed that CD4(+) T cells maintained their IL-17-producing phenotype, including those cells capable of producing both IFN-gamma and IL-17. Furthermore, and in contrast to the effects of IL-2 on Th17 development, IL-2 had no effect on IL-17 production by primed T cells. Importantly, adoptive transfer of T cells from naive Tbx21(-/-) mice into infected Rag-2(-/-) mice recapitulated the differentiation of T. cruzi-specific Th17 cells observed in infected Tbx21(-/-) mice. Conversely, transfer of wild-type T cells into infected Tbx21(-/-) mice did not reveal an increase in Th17 development. These results demonstrate that T-bet regulates the differentiation of T. cruzi-specific Th17 cells in vivo in a T cell-intrinsic manner. These data provide important insight into the role of T-bet in regulation of parasite-specific Th17 responses.
    [Abstract] [Full Text] [Related] [New Search]