Self-renewal of B-1 lymphocytes is dependent on CD19
Self-renewal of B-1 lymphocytes is dependent on CD19
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DOI：
10.1002/eji.1830260137
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发表时间：
1996-01-01
影响因子：
5.4
通讯作者：
Fearon, DT
中科院分区：
文献类型：
--
作者：
Krop, I;deFougerolles, AR;Fearon, DT
B淋巴细胞的B-1亚群通过成熟细胞的自我更新来维持，并且该过程可能涉及通过膜免疫球蛋白（mIg）的信号传导。我们确定了CD 19（一种通过mig共同刺激B细胞的膜蛋白）是否在这一过程中发挥作用。出生前用大鼠抗小鼠CD 19单克隆抗体1D 3处理小鼠，可下调CD 19表达，出生时B-1a细胞数量减少6倍：B-2细胞相对不受影响。用1D 3长期处理成年小鼠导致腹膜B-1a细胞每天损失约2%，而不会减少脾B-2细胞的恢复。B-1a细胞的损失与其复制抑制有关，而不是与加速周转有关。因此，CD 19参与B-1a细胞的发育和自我更新，可能是通过其通过mIgM放大信号的能力。
The B-1 subset of B lymphocytes is maintained by self-renewal of mature cells, and this process may involve signaling through membrane immunoglobulin (mIg). We determined whether CD19, a membrane protein that co-stimulates B cells by mig, has a role in this process. Pre-natal treatment of mice with 1D3, a rat anti-mouse CD19 monoclonal antibody, down-regulated CD19 expression and reduced by sixfold the number of B-1a cells at birth: B-2 cells were relatively unaffected. Prolonged treatment of adult mice with 1D3 caused the loss of approximately 2% per day of peritoneal B-1a cells, without diminishing the recovery of splenic B-2 cells. The loss of B-1a cells was associated with inhibition of their replication rather than with accelerated turnover. Therefore, CD19 is involved in the development and self-renewal of B-1a cells, perhaps through its ability to amplify signaling through mIgM.