CD22 expression mediates the regulatory functions of peritoneal B-1a cells during the remission phase of contact hypersensitivity reactions.
CD22 expression mediates the regulatory functions of peritoneal B-1a cells during the remission phase of contact hypersensitivity reactions.
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DOI：
10.4049/jimmunol.0901719
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发表时间：
2010-05-01
期刊：
影响因子：
--
通讯作者：
Fujimoto M
中科院分区：
文献类型：
--
作者：
Nakashima H;Hamaguchi Y;Watanabe R;Ishiura N;Kuwano Y;Okochi H;Takahashi Y;Tamaki K;Sato S;Tedder TF;Fujimoto M
虽然接触性超敏反应（CHS）已被认为是T细胞介导的免疫反应的原型，但最近已证明调节性B细胞亚群在抑制CHS中的重要作用。CD 22是Siglecs之一，是负调节B细胞受体信号传导的B细胞特异性分子。为了阐明B细胞在CHS中的作用，研究了CD 22-/-小鼠中的CHS。与野生型小鼠相比，CD 22-/-小鼠从CHS反应中恢复延迟。野生型腹膜B-1a细胞的转移逆转了在CD 22-/-小鼠中观察到的延长的CHS反应，并且这被同时注射IL-10受体Ab所阻断。虽然CD 22-/-腹膜B-1a细胞能够产生野生型水平的IL-10，但腹腔内注射差异标记的野生型/CD 22-/- B细胞表明，CHS诱导后5天，较少数量的CD 22-/- B细胞驻留在淋巴器官中，表明活化的CD 22-/-腹膜B-1细胞的存活或保留缺陷。因此，我们目前的研究揭示了腹膜B-1a细胞在CHS中的调节作用。两种不同的调节性B细胞亚群协同抑制CHS反应。虽然脾脏CD 1 dhiCD 5 + B细胞在抑制CHS急性加重期中具有关键作用，但腹膜B-1a细胞可能作为“调节性B细胞”抑制晚期缓解期。CD 22缺乏通过损害迁移到淋巴器官的腹膜B-1a细胞的保留或存活而导致CHS缓解紊乱。
While contact hypersensitivity (CHS) has been considered a prototype of T cell-mediated immune reactions, recently a significant contribution of regulatory B cell subsets in the suppression of CHS has been demonstrated. CD22, one of the Siglecs, is a B cell-specific molecule that negatively regulates B cell receptor signaling. To clarify the roles of B cells in CHS, CHS in CD22-/- mice was investigated. CD22-/- mice showed delayed recovery from CHS reactions compared with wild type mice. Transfer of wild type peritoneal B-1a cells reversed the prolonged CHS reaction seen in CD22-/- mice, and this was blocked by the simultaneous injection with IL-10 receptor Ab. While CD22-/- peritoneal B-1a cells were capable of producing IL-10 at wild type levels, intraperitoneal injection of differentially labeled wild type/CD22-/- B cells demonstrated that a smaller number of CD22-/- B cells resided in lymphoid organs 5 days after CHS elicitation, suggesting a defect in survival or retention in activated CD22-/- peritoneal B-1 cells. Thus, our current study reveals a regulatory role for peritoneal B-1a cells in CHS. Two distinct regulatory B cell subsets cooperatively inhibit CHS responses. While splenic CD1dhiCD5+ B cells have a crucial role in suppressing the acute exacerbating phase of CHS, peritoneal B-1a cells are likely to suppress the late remission phase as “regulatory B cells”. CD22 deficiency results in disturbed CHS remission by impaired retention or survival of peritoneal B-1a cells that migrate into lymphoid organs.
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影响因子：
32.4
作者：
Mizoguchi, A;Mizoguchi, E;Bhan, AK
通讯作者：
Bhan, AK
影响因子：
4.4
作者：
Du, C;Sriram, S
通讯作者：
Sriram, S
DOI：
10.1084/jem.186.10.1749
发表时间：
1997-11-17
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Mizoguchi A;Mizoguchi E;Smith RN;Preffer FI;Bhan AK
通讯作者：
Bhan AK
影响因子：
4.4
作者：
Fujimoto, M;Kuwano, Y;Sato, S
通讯作者：
Sato, S
影响因子：
4.4
作者：
Evans, Jamie G.;Chavez-Rueda, Karina A.;Mauri, Claudia
通讯作者：
Mauri, Claudia