My NCBISign In

Display Settings:

Format

Send to:

Choose Destination
    Mol Immunol. 2007 Jul;44(13):3283-90. Epub 2007 Apr 2.

    TGF-beta 1 inhibition of IFN-gamma-induced signaling and Th1 gene expression in CD4+ T cells is Smad3 independent but MAP kinase dependent.

    Park IK, Letterio JJ, Gorham JD.

    Source

    Department of Pathology, Dartmouth Medical School, One Medical Center Drive, Lebanon, NH 03756, USA.

    Abstract

    In addition to classic Smad signaling pathways, the pleiotropic immunoregulatory cytokine TGF-beta1 can activate MAP kinases, but a role for TGF-beta1-MAP kinase pathways in T cells has not been defined heretofore. We have shown previously that TGF-beta1 inhibits Th1 development by inhibiting IFN-gamma's induction of T-bet and other Th1 differentiation genes, and that TGF-beta1 inhibits receptor-proximal IFN-gamma-Jak-Stat signaling responses. We now show that these effects of TGF-beta1 are independent of the canonical TGF-beta1 signaling module Smad3, but involve a specific MAP kinase pathway. In primary T cells, TGF-beta1 activated the MEK/ERK and p38 MAP kinase pathways, but not the JNK pathway. Inhibition of the MEK/ERK pathway completely eliminated the inhibitory effects of TGF-beta1 on IFN-gamma responses in T cells, whereas inhibition of the p38 pathway had no effect. Thus, TGF-beta1's inhibition of IFN-gamma signaling in T cells is mediated through a highly specific Smad3 independent, MEK/ERK-dependent signaling pathway.

    PMID:
    17403540
    [PubMed - indexed for MEDLINE]
    PMCID: PMC2134969
    Free PMC Article

    Images from this publication.See all images (6) Free text

    Fig. 2
    Fig. 5
    Fig. 3
    Fig. 4
    Fig. 1
    Fig. 6

    Publication Types, MeSH Terms, Substances, Grant Support

    Publication Types

    MeSH Terms

    Substances

    Grant Support

    LinkOut - more resources

    Full Text Sources

    Other Literature Sources

      Supplemental Content

      Click here to read Click here to read

      Related citations

      See reviews... See all...

      Cited by 5 PubMed Central articles

      See all...

      Related information

      • Related Citations
        Calculated set of PubMed citations closely related to the selected article(s) retrieved using a word weight algorithm. Related articles are displayed in ranked order from most to least relevant, with the “linked from” citation displayed first.
      • References for this PMC Article
        Citation referenced in PubMed article. Only valid for PubMed citations that are also in PMC.
      • Substance (MeSH Keyword)
        PubChem chemical substance (submitted) records that are classified under the same Medical Subject Headings (MeSH) controlled vocabulary as the current articles.
      • Free in PMC
        Free full text articles in PMC
      • Cited in PMC
        Full-text articles in the PubMed Central Database that cite the current articles.

      Recent activity

      Clear Turn Off Turn On

      Your browsing activity is empty.

      Activity recording is turned off.

      Turn recording back on

      See more...
      You are here: NCBI > Literature > PubMed
      Write to the Help Desk