Anti-Fc epsilon R1 antibody injections activate basophils and mast cells and delay Type 1 diabetes onset in NOD mice

作者：Huebner Marc P; Larson David; Torrero Marina N; Mueller Ellen; Shi Yinghui; Killoran Kristin E; Mitre Edward

来源：Clinical Immunology, 2011, 141(2): 205-217.

DOI：10.1016/j.clim.2011.08.004

• Fc epsilon R1
• Type 1 diabetes
• Nonobese diabetic (NOD)
• IL-4
• Histamine
• IgE

Mounting evidence suggests that helminth infections protect against autoimmune diseases. As helminths cause chronic IgE-mediated activation of basophils and mast cells we hypothesized that continuous activation of these cells could prevent diabetes onset in nonobese diabetic (NOD) mice in the absence of infection. Anti-Fc epsilon R1 activated basophils and mast cells and resulted in the release of IL-4 and histamine into the bloodstream. Anti-Fc epsilon R1-treated NOD mice showed a type 2 shift in insulin-specific antibody production and exhibited significant delays in diabetes onset. IL-4 responses played a partial role as the protective effect of anti-Fc epsilon R1 therapy was diminished in IL-4-deficient NOD mice. In contrast, histamine signaling was not required as anti-Fc epsilon R1-mediated protection was not reduced in mice treated with histamine receptor blockers. These results demonstrate that anti-Fc epsilon R1 therapy delays diabetes onset in NOD mice and suggest that chronic basophil and mast cell activation may represent a new avenue of therapy for Th1-associated autoimmune diseases. Published by Elsevier Inc.

• 出版日期2011-11
• 单位河北医科大学