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MyD88 is essential to sustain mTOR activation necessary to promote T helper 17 cell proliferation by linking IL-1 and 11-23 signaling.

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Title: MyD88 is essential to sustain mTOR activation necessary to promote T helper 17 cell proliferation by linking IL-1 and 11-23 signaling.
Authors: JiHoon Chang1, Burkett, Patrick R.2,3, Borges, Christopher M.4, Kuchroo, Vijay K.2, Turka, Iaurence A.5 lturka@partners.org, Chang, Cheong-Hee1 heechang@umich.edu
Source: Proceedings of the National Academy of Sciences of the United States of America. 2/5/2013, Vol. 110 Issue 6, p2270-2275. 6p.
Subjects: Myeloid differentiation factor 88, T cell differentiation, T helper cells, Autoimmune diseases, Allergic encephalomyelitis, Rapamycin, Cell proliferation, Immune system
Abstract: Myeloid differentiation primary response protein 88 (MyD88) is classically known as an adaptor, linking TLR and IL-iR to downstream signaling pathways in the innate immune system. In addition to its role in innate immune cells, MyD88 has been shown to play an important role in I cells. How MyD88 regulates helper T-cell differentiation remains largely unknown, however. Here, we demonstrate that MyD88 is an important regulator of IL-17-producing CD4+ T helper cells (Th17) cell proliferation. MyD88-deficient CD4+ T cells showed a defect in Thi7 cell differentiation, but not in Thi cell or Th2 cell differentiation. The impaired IL-17 production from MyD88-deficient CD4+ T cells is not a result of defective RAR-related orphan receptor γt (RORyt) expression. In- stead, MyD88 is essential for sustaining the mammalian target of rapamycin (mIOR) activation necessary to promote Thu cell pro- liferation by linking IL-1 and IL-23 signaling. MyD88-deficient CD4+ T cells showed impaired mIOR activation and, consequently. reduced Th17 cell proliferation. Importantly, the absence of MyD88 in I cells ameliorated disease in the experimental autoimmune encephalomyelitis model. Taken together, our results demonstrate that MyD88 has a dual function in Thu cells by delivering IL-1 signaling during the early differentiation stage and integrating IL- 23 signaling to the mTOR complex to expand committed Thu cells. [ABSTRACT FROM AUTHOR]
Copyright of Proceedings of the National Academy of Sciences of the United States of America is the property of National Academy of Sciences and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: MyD88 is essential to sustain mTOR activation necessary to promote T helper 17 cell proliferation by linking IL-1 and 11-23 signaling.
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  Data: <searchLink fieldCode="DE" term="%22Myeloid+differentiation+factor+88%22">Myeloid differentiation factor 88</searchLink><br /><searchLink fieldCode="DE" term="%22T+cell+differentiation%22">T cell differentiation</searchLink><br /><searchLink fieldCode="DE" term="%22T+helper+cells%22">T helper cells</searchLink><br /><searchLink fieldCode="DE" term="%22Autoimmune+diseases%22">Autoimmune diseases</searchLink><br /><searchLink fieldCode="DE" term="%22Allergic+encephalomyelitis%22">Allergic encephalomyelitis</searchLink><br /><searchLink fieldCode="DE" term="%22Rapamycin%22">Rapamycin</searchLink><br /><searchLink fieldCode="DE" term="%22Cell+proliferation%22">Cell proliferation</searchLink><br /><searchLink fieldCode="DE" term="%22Immune+system%22">Immune system</searchLink>
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  Label: Abstract
  Group: Ab
  Data: Myeloid differentiation primary response protein 88 (MyD88) is classically known as an adaptor, linking TLR and IL-iR to downstream signaling pathways in the innate immune system. In addition to its role in innate immune cells, MyD88 has been shown to play an important role in I cells. How MyD88 regulates helper T-cell differentiation remains largely unknown, however. Here, we demonstrate that MyD88 is an important regulator of IL-17-producing CD4+ T helper cells (Th17) cell proliferation. MyD88-deficient CD4+ T cells showed a defect in Thi7 cell differentiation, but not in Thi cell or Th2 cell differentiation. The impaired IL-17 production from MyD88-deficient CD4+ T cells is not a result of defective RAR-related orphan receptor γt (RORyt) expression. In- stead, MyD88 is essential for sustaining the mammalian target of rapamycin (mIOR) activation necessary to promote Thu cell pro- liferation by linking IL-1 and IL-23 signaling. MyD88-deficient CD4+ T cells showed impaired mIOR activation and, consequently. reduced Th17 cell proliferation. Importantly, the absence of MyD88 in I cells ameliorated disease in the experimental autoimmune encephalomyelitis model. Taken together, our results demonstrate that MyD88 has a dual function in Thu cells by delivering IL-1 signaling during the early differentiation stage and integrating IL- 23 signaling to the mTOR complex to expand committed Thu cells. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
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  Data: <i>Copyright of Proceedings of the National Academy of Sciences of the United States of America is the property of National Academy of Sciences and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1073/pnas.1206048110
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        Text: English
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        Type: general
      – SubjectFull: T cell differentiation
        Type: general
      – SubjectFull: T helper cells
        Type: general
      – SubjectFull: Autoimmune diseases
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      – SubjectFull: Allergic encephalomyelitis
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      – SubjectFull: Rapamycin
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      – SubjectFull: Cell proliferation
        Type: general
      – SubjectFull: Immune system
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      – TitleFull: MyD88 is essential to sustain mTOR activation necessary to promote T helper 17 cell proliferation by linking IL-1 and 11-23 signaling.
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              Text: 2/5/2013
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