70 research outputs found
MassIVE MSV000093068 - Identification of PIP5K1a-associated proteins in human Th17 cells by IP-MS
No full textTh17 Memory Cells Aren't Fooled By Sugar-Coating
No full textKlebsiella bacteria evade humoral immunity by altering their polysaccharide capsular antigens. In this issue of Immunity, Chen et al. (2011) propose a new vaccination strategy, demonstrating that Th17 memory cells can provide cross-protection against multiple serotypes of Klebsiella pneumoniae
Faculty Opinions recommendation of A non-conserved amino acid variant regulates differential signalling between human and mouse CD28.
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Investigating the regulatory cells that mediate recovery from CNS-targeted autoimmune disease
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CD73 is expressed by inflammatory Th17 cells in experimental autoimmune encephalomyelitis but does not limit differentiation or pathogenesis.
No full textCD73 works together with CD39 to convert extracellular ATP to immunoregulatory adenosine, thus inhibiting inflammation. TGFβ-mediated CD73 expression on 'regulatory' Th17 cells limits their ability to eradicate tumors, similar to the immunosuppressive mechanism described for CD73 on Tregs. However, CD73 is also expressed on Th17 cells thought to be inflammatory in Crohn's disease. CD73 has previously been reported to contribute to inflammation in the central nervous system (CNS). In experimental autoimmune encephalomyelitis (EAE), we found that inflammatory cytokine-producing Th17 cells showed increased CD73 expression as disease progressed. We therefore hypothesized that CD73 could be important for limiting the expansion or pathogenic function of Th17 cells in autoimmune inflammation of the CNS. Surprisingly, EAE development was not enhanced or inhibited by CD73 deficiency; there was correspondingly no difference in induction of Th17-associated cytokines IL-17, IFNγ or GM-CSF or recruitment of either inflammatory or regulatory cells to the central nervous system. We confirmed that CD73 was similarly not required for differentiation of Th17 cells in vitro. These data show that while CD73 expression is regulated during EAE, this enzyme is not absolutely required to either promote or limit Th17 cell expansion or EAE severity
T Cells Doing It for Themselves: TGF-β Regulation of Th1 and Th17 Cells
No full textThe source of TGF-β, which regulates inflammation in various disease settings, is unclear. In this issue of Immunity, Li et al. (2007) find that not only does T cell-produced TGF-β regulate Th1-cell-mediated inflammation, but it is also required for the generation of Th17 cells in vivo
Th17 Cell Differentiation: The Long and Winding Road
No full textThe characterization of the new lineage of IL-17-producing CD4+ T helper (Th17) cells has revolutionized our current understanding of T cell-mediated immunity. Over the past five years, there have been many twists and turns as the pathways that lead to Th17 cell differentiation have been elucidated. Not least of these was the discovery that TGF-β is a crucial cytokine for Th17 cell development, suggesting that Th17 and regulatory T cell subsets share reciprocal developmental pathways during the pathogenesis or control of inflammation. This review aims to bring together the observations that have formed current opinion on factors that promote and contain Th17 cell development, in both mouse and man. Unresolved controversies in this field are also discussed: For example, IL-23 is absolutely required for disease pathogenesis in many models of Th17-cell-mediated autoimmunity, yet its role in Th17 cell development is relatively unclear
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