• Medientyp: E-Artikel
  • Titel: B cells as master regulators of a pro-inflammatory T cell balance in obesity and glucose intolerance (176.17)
  • Beteiligte: Belkina, Anna; Snyder-Cappione, Jennifer; Jagannathan-Bogdan, Madhumita; Carr, Jordan; DeFuria, Jason; Markham, Douglas; Allen, Jessica; Bouchard, Jacqueline; Nersesova, Yanina; Watkins, Amanda; McDonnell, Marie; Apovian, Caroline; Denis, Gerald; Nikolajczyk, Barbara
  • Erschienen: The American Association of Immunologists, 2012
  • Erschienen in: The Journal of Immunology, 188 (2012) 1_Supplement, Seite 176.17-176.17
  • Sprache: Englisch
  • DOI: 10.4049/jimmunol.188.supp.176.17
  • ISSN: 0022-1767; 1550-6606
  • Schlagwörter: Immunology ; Immunology and Allergy
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  • Anmerkungen:
  • Beschreibung: Abstract Lymphocytes play key roles in the chronic inflammation critical for T2D pathogenesis. T2D patients have an elevated ratio of pro- to anti-inflammatory T cells, and B cells that fail to produce anti-inflammatory IL-10. New data show that B cells from the diet-induced obesity (DIO) mouse model of T2D secrete a pro-inflammatory balance of cytokines, including relatively low IL-10 production, which mirrors our findings in T2D patients. DIO B cells do not secrete auto-antibodies, as evidenced by anti-nuclear antigen staining. Complementary metabolic studies show that B cell-null μMT mice resist the development of glucose intolerance (but not obesity) in response to DIO. Taken together, these data support the conclusion that a pro-inflammatory B cell cytokine balance, rather than antibodies, promotes T2D. To further define roles for B cells in T2D, we immunophenotyped DIO μMT splenocytes. Regulatory T cells (Tregs) expand in DIO μMT, while Tregs fail to expand in WT mice. These data are consistent with new human studies showing B cells from T2D (but not healthy) subjects support pro-inflammatory T cells, and indicate clinical relevance of published studies showing decreased Th1 function in DIO μMT vs. WT mice. We conclude B cells are critical regulators of inflammation in T2D due to 1. Secretion of a pro-inflammatory cytokine balance; and 2. An ability to promote pro-inflammatory T cell function. Thus B cell depletion may represent a valuable tool in the T2D clinic.
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