Interleukin-10 mediated autoregulation of murine B-1 B-cells and its role in Borrelia hermsii infection.
Interleukin-10 mediated autoregulation of murine B-1 B-cells and its role in Borrelia hermsii infection.
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DOI：
10.1371/journal.pone.0011445
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发表时间：
2010-07-06
期刊：
影响因子：
3.7
通讯作者：
Bondada S
中科院分区：
文献类型：
--
作者：
Sindhava V;Woodman ME;Stevenson B;Bondada S
B细胞通常是免疫反应的积极调节者，主要通过产生抗体来实现。然而，最近的研究表明，B细胞的不同亚群主要通过分泌IL-10来发挥调节功能。在这里，我们发现腹膜B-1(B-1P)细胞在几种Toll样受体(TLR)配体的刺激下产生高水平的IL-10。高水平的IL-10抑制B-1P细胞对所有TLR配体的增殖和分化反应，在体外和体内都是以自分泌的方式研究的。IL-10主要作用于G1/S间期，抑制B-1P细胞二次分裂及后续分裂。IL-10通过阻断经典的NF-κB途径抑制TLR诱导的B-1P细胞活化。CD40或BAFF联合刺激可阻断TLR刺激时IL-10对B-1P细胞的抑制作用。最后，从IL-10−/−小鼠的腹膜腔过继转移的B-1P细胞对赫氏疏螺旋体的清除效果好于野生型B-1P细胞。本研究描述了由B-1P细胞来源的IL-10介导的B-1P细胞的一种新的自我调节特性，该特性可能影响B-1P细胞在感染和自身免疫中的功能。
B cells are typically characterized as positive regulators of the immune response, primarily by producing antibodies. However, recent studies indicate that various subsets of B cells can perform regulatory functions mainly through IL-10 secretion. Here we discovered that peritoneal B-1 (B-1P) cells produce high levels of IL-10 upon stimulation with several Toll-like receptor (TLR) ligands. High levels of IL-10 suppressed B-1P cell proliferation and differentiation response to all TLR ligands studied in an autocrine manner in vitro and in vivo. IL-10 that accumulated in cultures inhibited B-1P cells at second and subsequent cell divisions mainly at the G1/S interphase. IL-10 inhibits TLR induced B-1P cell activation by blocking the classical NF-κB pathway. Co-stimulation with CD40 or BAFF abrogated the IL-10 inhibitory effect on B-1P cells during TLR stimulation. Finally, B-1P cells adoptively transferred from the peritoneal cavity of IL-10−/− mice showed better clearance of Borrelia hermsii than wild-type B-1P cells. This study described a novel autoregulatory property of B-1P cells mediated by B-1P cell derived IL-10, which may affect the function of B-1P cells in infection and autoimmunity.
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影响因子：
5
作者：
Blenman, Kim R. M.;Duan, Byian;Morel, Laurence
通讯作者：
Morel, Laurence
DOI：
10.1073/pnas.0813411106
发表时间：
2009-03-17
影响因子：
11.1
作者：
Cole, Leah E.;Yang, Yang;Vogel, Stefanie N.
通讯作者：
Vogel, Stefanie N.
影响因子：
3.6
作者：
Dasu, Trivikram;Sindhava, Vishal;Bondada, Subbarao
通讯作者：
Bondada, Subbarao
影响因子：
4.4
作者：
Alugupalli, KR;Gerstein, RM;Leong, JM
通讯作者：
Leong, JM
DOI：
10.4049/jimmunol.181.7.4590
发表时间：
2008-10-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Gururajan M;Simmons A;Dasu T;Spear BT;Calulot C;Robertson DA;Wiest DL;Monroe JG;Bondada S
通讯作者：
Bondada S