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T-bet is rapidly induced by interferon-γ in lymphoid and myeloid cells
Differentiation of naive CD4(+) T cells into IFN-γ-producing T helper 1 (T(H)1) cells is pivotal for protective immune responses against intracellular pathogens. T-bet, a recently discovered member of the T-box transcription factor family, has been reported to play a critical role in this process, p...
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The National Academy of Sciences
2001
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| Acesso em linha: | https://ncbi.nlm.nih.gov/pmc/articles/PMC64996/ https://ncbi.nlm.nih.gov/pubmed/11752460 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1073/pnas.261570598 |
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pubmed-649962002-01-28 T-bet is rapidly induced by interferon-γ in lymphoid and myeloid cells Lighvani, Andre A. Frucht, David M. Jankovic, Dragana Yamane, Hidehiro Aliberti, Julio Hissong, Bruce D. Nguyen, Bai V. Gadina, Massimo Sher, Alan Paul, William E. O'Shea, John J. Proc Natl Acad Sci U S A Biological Sciences Differentiation of naive CD4(+) T cells into IFN-γ-producing T helper 1 (T(H)1) cells is pivotal for protective immune responses against intracellular pathogens. T-bet, a recently discovered member of the T-box transcription factor family, has been reported to play a critical role in this process, promoting IFN-γ production. Although terminal T(H)1 differentiation occurs over days, we now show that challenge of mice with a prototypical T(H)1-inducing stimulus, Toxoplasma gondii soluble extract, rapidly induced IFN-γ and T-bet; T-bet induction was substantially lower in IFN-γ-deficient mice. Naive T cells expressed little T-bet, but this transcription factor was induced markedly by the combination of IFN-γ and cognate antigen. Human myeloid antigen-presenting cells showed T-bet induction after IFN-γ stimulation alone, and this induction was antagonized by IL-4 and granulocyte/macrophage colony-stimulating factor. Although T-bet was induced rapidly and directly by IFN-γ, it was not induced by IFN-α, lipopolysaccharide, or IL-1, indicating that this action of IFN-γ was specific. Moreover, T-bet induction was dependent on Stat1 but not Stat4. These data argue for a model in which IFN-γ gene regulation involves an autocrine loop, whereby the cytokine regulates a transcription factor that promotes its own production. These findings substantially alter the current view of T-bet in IFN-γ regulation and promotion of cell-mediated immune responses. The National Academy of Sciences 2001-12-18 /pmc/articles/PMC64996/ /pubmed/11752460 http://dx.doi.org/10.1073/pnas.261570598 Text en Copyright © 2001, The National Academy of Sciences |
| institution |
US National Library of Medicine |
| collection |
PubMed Central |
| language |
en |
| format |
Article |
| topic |
Biological Sciences |
| spellingShingle |
Biological Sciences Lighvani, Andre A. Frucht, David M. Jankovic, Dragana Yamane, Hidehiro Aliberti, Julio Hissong, Bruce D. Nguyen, Bai V. Gadina, Massimo Sher, Alan Paul, William E. O'Shea, John J. T-bet is rapidly induced by interferon-γ in lymphoid and myeloid cells |
| description |
Differentiation of naive CD4(+) T cells into IFN-γ-producing T helper 1 (T(H)1) cells is pivotal for protective immune responses against intracellular pathogens. T-bet, a recently discovered member of the T-box transcription factor family, has been reported to play a critical role in this process, promoting IFN-γ production. Although terminal T(H)1 differentiation occurs over days, we now show that challenge of mice with a prototypical T(H)1-inducing stimulus, Toxoplasma gondii soluble extract, rapidly induced IFN-γ and T-bet; T-bet induction was substantially lower in IFN-γ-deficient mice. Naive T cells expressed little T-bet, but this transcription factor was induced markedly by the combination of IFN-γ and cognate antigen. Human myeloid antigen-presenting cells showed T-bet induction after IFN-γ stimulation alone, and this induction was antagonized by IL-4 and granulocyte/macrophage colony-stimulating factor. Although T-bet was induced rapidly and directly by IFN-γ, it was not induced by IFN-α, lipopolysaccharide, or IL-1, indicating that this action of IFN-γ was specific. Moreover, T-bet induction was dependent on Stat1 but not Stat4. These data argue for a model in which IFN-γ gene regulation involves an autocrine loop, whereby the cytokine regulates a transcription factor that promotes its own production. These findings substantially alter the current view of T-bet in IFN-γ regulation and promotion of cell-mediated immune responses. |
| author |
Lighvani, Andre A. Frucht, David M. Jankovic, Dragana Yamane, Hidehiro Aliberti, Julio Hissong, Bruce D. Nguyen, Bai V. Gadina, Massimo Sher, Alan Paul, William E. O'Shea, John J. |
| author_facet |
Lighvani, Andre A. Frucht, David M. Jankovic, Dragana Yamane, Hidehiro Aliberti, Julio Hissong, Bruce D. Nguyen, Bai V. Gadina, Massimo Sher, Alan Paul, William E. O'Shea, John J. |
| author_sort |
Lighvani, Andre A. |
| title |
T-bet is rapidly induced by interferon-γ in lymphoid and
myeloid cells |
| title_short |
T-bet is rapidly induced by interferon-γ in lymphoid and
myeloid cells |
| title_full |
T-bet is rapidly induced by interferon-γ in lymphoid and
myeloid cells |
| title_fullStr |
T-bet is rapidly induced by interferon-γ in lymphoid and
myeloid cells |
| title_full_unstemmed |
T-bet is rapidly induced by interferon-γ in lymphoid and
myeloid cells |
| title_sort |
t-bet is rapidly induced by interferon-γ in lymphoid and
myeloid cells |
| publisher |
The National Academy of Sciences |
| publisher_facet |
The National Academy of Sciences |
| publishDate |
2001 |
| url |
https://ncbi.nlm.nih.gov/pmc/articles/PMC64996/ https://ncbi.nlm.nih.gov/pubmed/11752460 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1073/pnas.261570598 |
| _version_ |
1758997653830500352 |