The B-1 subset of B lymphocytes is maintained by self-renewal of matur
e cells, and this process may involve signaling through membrane immun
oglobulin (mIg). We determined whether CD19, a membrane protein that c
o-stimulates B cells by mig, has a role in this process. Pre-natal tre
atment of mice with 1D3, a rat anti-mouse CD19 monoclonal antibody, do
wn-regulated CD19 expression and reduced by sixfold the number of B-1a
cells at birth: B-2 cells were relatively unaffected. Prolonged treat
ment of adult mice with 1D3 caused the loss of approximately 2% per da
y of peritoneal B-1a cells, without diminishing the recovery of spleni
c B-2 cells. The loss of B-1a cells was associated with inhibition of
their replication rather than with accelerated turnover. Therefore, CD
19 is involved in the development and self-renewal of B-1a cells, perh
aps through its ability to amplify signaling through mIgM.