کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3345867 | 1215751 | 2013 | 8 صفحه PDF | دانلود رایگان |

• Basophils and Th2 environment contribute to systemic lupus erythematosus pathogenesis.
• Basophil activation could occur through different stimuli during lupus.
• Basophils amplify autoantibody production by supporting autoreactive B cell maturation and plasma cell survival.
• Basophil-mediated T cell differentiation could be induced through various signals.
Systemic lupus erythematosus is a complex autoimmune disease of multifactorial origins. All compartments of the immune system appear to be affected, at least in some way, and to contribute to disease pathogenesis. Because of an escape from negative selection autoreactive T and B cells accumulate in SLE patients leading to the production of autoantibodies mainly raised against nuclear components and their subsequent deposition into target organs. We recently showed that basophils, in an IgE and IL-4 dependent manner, contribute to SLE pathogenesis by amplifying autoantibody production. Here, we summarize what we have learned about the deleterious role of basophils in lupus both in a mouse model and in SLE patients. We discuss which possible pathways could be involved in basophil activation and recruitment to secondary lymphoid organs during SLE, and how basophils may amplify autoantibody production.
Journal: Current Opinion in Immunology - Volume 25, Issue 6, December 2013, Pages 704–711