Krop I, de Fougerolles A R, Hardy R R, Allison M, Schlissel M S, Fearon D T
Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, USA.
Eur J Immunol. 1996 Jan;26(1):238-42. doi: 10.1002/eji.1830260137.
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.
B淋巴细胞的B-1亚群通过成熟细胞的自我更新得以维持，这一过程可能涉及通过膜免疫球蛋白（mIg）进行信号传导。我们确定了CD19（一种通过mIg共刺激B细胞的膜蛋白）在此过程中是否发挥作用。用大鼠抗小鼠CD19单克隆抗体1D3对小鼠进行产前治疗，可下调CD19表达，并使出生时B-1a细胞数量减少6倍；B-2细胞相对未受影响。用1D3对成年小鼠进行长期治疗，导致腹膜B-1a细胞每天约损失2%，而脾脏B-2细胞的恢复未受影响。B-1a细胞的损失与其复制受到抑制有关，而非周转加速。因此，CD19可能通过其放大mIgM信号传导的能力，参与B-1a细胞的发育和自我更新。
