The role of CD19+CD24highCD38high and CD19+CD24highCD27+ regulatory B cells in patients with type 1 autoimmune pancreatitis

Background: Patients with type 1 autoimmune pancreatitis.(AIP) have several immunologic and histologic abnormalities. It is known that depletion of B cells by rituximab is effective for treatment of IgG4-related disease (IgG4-RD) such as type 1 AIP, suggesting that B cells may be a key player in IgG4-RD. However, the role of regulatory B cells (Bregs) in type 1 AIP is unclear, and the objective of this paper is to clarify the role of Bregs in the pathophysiology of type 1 AIP by analyzing circulating Bregs. Method: We recruited 21 patients with type I AIP as determined by the International Consensus Diagnostic Criteria for AIP (ICDC). No patients received corticosteroid treatments. For comparison, we recruited 14 patients with chronic pancreatitis (CP), 20 patients with pancreatic cancer, and 25 healthy subjects as controls. We analyzed Bregs as CD19(+)CD24(high)CD38(high) and CD19(+)CD24(high)CD27(+) from peripheral blood by flow cytometry. Results: In peripheral blood, CD19(+)CD24(high)CD38(high) Bregs were significantly increased in type 1 AIP patients compared with CP, pancreatic cancer, and healthy controls. Although not significant different, CD19(+)CD24(high)CD27(+) Bregs of type 1 AIP were decreased compared to those of other groups. IL-10(+) B cells were not significantly different from type 1 AIP patients and healthy controls. In untreated type I AIP patients, the number of CD19(+)CD24(high)CD38(high) Bregs and IgG4 were not correlated. Conclusions: Our data suggested that CD19(+)CD24(high)CO38(high) Bregs seemed to increase reactively to suppress the disease activity, and are consistent with the hypothesis that CD19(+)CD24(high)CD27(+) Bregs might be involved in the development of type 1 AIP, although it still remains unclear whether the decrease of CD19(+)CD24(high)CD27(+) cells is cause or effect of AIR Copyright (C) 2014, IAP and EPC. Published by Elsevier India, a division of Reed Elsevier India Pvt. Ltd. All rights reserved.