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Huang, Huang

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Huang, Huang
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    Characterization of Human CD39+ Th17 Cells with Suppressor Activity and Modulation in Inflammatory Bowel Disease
    (Public Library of Science, 2014) Longhi, Maria Serena; Moss, Alan; Bai, A; Wu, Yan; Huang, Huang; Cheifetz, Adam; Quintana, Francisco; Robson, Simon
    Induced regulatory T-cells (iT-reg) and T helper type 17 (Th17) in the mouse share common CD4 progenitor cells and exhibit overlapping phenotypic and functional features. Here, we show that human Th17 cells endowed with suppressor activity (supTh17) can be derived following exposure of iT-reg populations to Th17 polarizing conditions. In contrast to “pathogenic” Th17, supTh17 display immune suppressive function and express high levels of CD39, an ectonucleotidase that catalyzes the conversion of pro-inflammatory extracellular nucleotides ultimately generating nucleosides. Accordingly, supTh17 exhibit nucleoside triphosphate diphosphohydrolase activity, as demonstrated by the efficient generation of extracellular AMP, adenosine and other purine derivatives. In addition supTh17 cells are resistant to the effects of adenosine as result of the low expression of the A2A receptor and accelerated adenosine catalysis by adenosine deaminase (ADA). These supTh17 can be detected in the blood and in the lamina propria of healthy subjects. However, these supTh17 cells are diminished in patients with Crohn’s disease. In summary, we describe a human Th17 subpopulation with suppressor activity, which expresses high levels of CD39 and consequently produces extracellular adenosine. As these uniquely suppressive CD39+ Th17 cells are decreased in patients with inflammatory bowel disease, our findings might have implications for the development of novel anti-inflammatory therapeutic approaches in these and potentially other immune disorders.
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    The Role of CD39 in Modulating Effector Immune Responses in Inflammatory Bowel Disease
    (2015-06-08) Huang, Huang
    Inflammatory bowel disease is associated with excessive inflammation of the bowel and intestinal tissues in genetically susceptible individuals. IBD can manifest in two major forms, ulcerative colitis and Crohn’s disease. T helper type 17 cells (Th17) are effector lymphocytes that have been linked to intestinal inflammation in both mice and humans. Effector Th17 cells and regulatory T cells (Treg) – a subset pivotal to immune-tolerance maintenance – derive from the same CD4 progenitors. Our investigation demonstrates that Th17 cells with suppressor activity (supTh17) can be generated upon induced regulatory T cell (iTreg) exposure to Th17 polarizing conditions. With immune suppressive function that differentiates it from Th17, suppressor Th17 (supTh17) expresses high levels of CD39, a membrane-bound protein that catalyzes conversion of pro-inflammatory extracellular nucleotides into nucleosides, such as adenosine. Interestingly, though supTh17 is detected in the peripheral circulation and lamina propria of healthy subjects, it is diminished in patients with Crohn’s disease. This finding has important clinical implications for the development of innovative therapeutic techniques for targeting inflammation in autoimmune diseases, such as IBD.