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Lymphocytes play key roles in the chronic inflammation critical for T2D pathogenesis. We have shown T2D patients have
an elevated ratio of pro- to anti-inflammatory T cells, and B cells that produce a pro-inflammatory cytokine profile. Thus
lymphocytes promote T2D-associated inflammation. Although the pro-inflammatory CD4
T cell balance has been specifically
implicated in T2D pathogenesis by numerous studies, mechanisms that underlie elevated CD4+ T cell inflammation are poorly
understood. B cells have recently become appreciated as regulators of CD4+ T cell subset differentiation and function, but the
possibility that the T2D-associated changes we identified in B cell function regulate T cell inflammation in T2D is untested.
Our new data demonstrate that B cells control the T2D-associated increase in CD4+ Th17-mediated inflammation in both T2D
patients and in obese/insulin resistant mice. Surprisingly, the disease-associated ability of B cells to regulate T cell function was
contact-dependent, despite the demonstration that multiple cytokines hyper-secreted by B cells from T2D patients activate T
cells. In contrast, elevated activation of CD4+ Th1 axis cytokines was B cell-independent. We conclude that both T cell-intrinsic
and T cell-extrinsic changes regulate T cell-mediated inflammation in T2D. These data indicate that B cell depletion may partially
curb T2D-associated T cell inflammation thus disease pathogenesis, but that combinatorial treatments may be required for
favorable clinical outcomes. Thus our work suggests that the currently modest efficacy of anti-inflammatory drugs in T2D may
be predictable, and that drug combinations will be required to leverage our understanding of T2D as an inflammatory disease
into new treatments.
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