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Interleukin 35 Regulatory B Cells

期刊

JOURNAL OF MOLECULAR BIOLOGY
卷 433, 期 1, 页码 -

出版社

ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jmb.2020.07.019

关键词

regulatory B cell (Breg); Breg immunotherapy; interleukin 35; interleukin 10; interleukin-35-producing Breg (i35-Breg)

资金

  1. National Eye Institute
  2. National Institutes of Health, Bethesda, Maryland

向作者/读者索取更多资源

B lymphocytes play a central role in host immunity by orchestrating humoral immune responses and producing neutralizing antibodies. Recent recognition shows that B cells also help maintain peripheral tolerance and suppress autoimmune diseases, with rare populations of regulatory B cells producing anti-inflammatory cytokines. The newly discovered i35-Bregs can suppress autoimmune diseases by inducing infectious tolerance in conventional B cells.
B lymphocytes play a central role in host immunity. They orchestrate humoral immune responses that modulate activities of other immune cells and produce neutralizing antibodies that confer lasting immunity to infectious diseases including smallpox, measles and poliomyelitis. In addition to these traditional functions is the recent recognition that B cells also play critical role in maintaining peripheral tolerance and suppressing the development or severity of autoimmune diseases. Their immune suppressive function is attributed to relatively rare populations of regulatory B cells (Bregs) that produce anti-inflammatory cytokines including interleukin 10 (IL-10), IL-35 and transforming growth factor-beta. The IL-35-producing B cell (i35-Breg) is the newest Breg subset described. i35-Bregs suppress central nervous system autoimmune diseases by inducing infectious tolerance whereby conventional B cells acquire regulatory functions that suppress pathogenic Th17 responses. In this review, we discuss immunobiology of i35-Breg cell, i35-Breg therapies for autoimmune diseases and potential therapeutic strategies for depleting i35-Bregs that suppress immune responses against pathogens and tumor cells. Published by Elsevier Ltd.

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