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10.1093/rheumatology/keu136

http://scihub22266oqcxt.onion/10.1093/rheumatology/keu136
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C4135583!4135583!24729396
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suck abstract from ncbi


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pmid24729396      Rheumatology+(Oxford) 2014 ; 53 (9): 1693-703
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  • Regulatory B cells are numerically but not functionally deficient in anti-neutrophil cytoplasm antibody-associated vasculitis #MMPMID24729396
  • Todd SK; Pepper RJ; Draibe J; Tanna A; Pusey CD; Mauri C; Salama AD
  • Rheumatology (Oxford) 2014[Sep]; 53 (9): 1693-703 PMID24729396show ga
  • Objectives. B cells are central to the pathology of ANCA-associated vasculitis (AAV), a disease characterized by autoantibodies and effectively treated by rituximab. In addition to promoting inflammation, a subset of B cells act to suppress harmful autoimmune responses (Breg). The balance of effector and regulatory B cell subsets in AAV is not known. This study was conducted to assess the relative frequency of these subsets during different states of disease activity.Methods. B memory (Bmem), naive (Bnaive) and regulatory (Breg) subsets were defined by their relative expression of CD24 and CD38. Function was assessed by cytokine production and suppressive action on CD4+ Th1 activation evaluated in a co-culture system.Results. Compared with healthy controls, the frequency of Breg (CD24hiCD38hi) was significantly reduced during disease remission in both proteinase 3 (PR3)- and MPO-ANCA patients and during acute disease in PR3-ANCA patients, while the frequency of memory cells (CD24hiCD38lo) was reduced during active disease and restored during remission. Breg cell frequency showed a positive correlation, while Bmem had an inverse correlation with IL-10 production in vitro. B and T cell co-cultures revealed that memory and naive B cell subsets augmented Th1 activation in vitro, which was prevented by Breg, and this pattern did not differ between remission AAV patients and controls.Conclusion. In remission there is a numerical, but not functional, deficiency in Breg and preservation of Bmem associated with reduced IL-10 production and increased Th1 activation in vitro. This imbalance may contribute to the high rate of relapse observed in AAV, especially in PR3-ANCA patients.
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