On human B cells the antigen receptor complex is composed of the membr
ane form of the immunoglobulin molecule and the non-covalently associa
ted Ig alpha/beta heterodimer. A small subpopulation of normal B cells
and chronic lymphocytic leukemia B cells express (analogous to T cell
s) the transmembrane molecule CD5, a counterstructure of B cell-specif
ic CD72. Numbers of CD5(+) B cells are increased in several physiologi
cal and pathological conditions. Moreover, CD5(+) B cells are being he
ld responsible for the production of autoreactive antibodies and seem
to have signaling characteristics distinct from conventional B cells.
On T cells, CD5 associates with the T cell receptor CD3 complex and li
gation of CD5 leads to the generation of co-stimulatory signals, that
act on T cell activation. We here demonstrate that CD5 is associated w
ith the B cell receptor (BCR) complex and serves as substrate for BCR-
induced tyrosine kinase activity. Hence, CD5(+) B cells have a unique
potential to modulate BCR signals.