CD39 and B cells
The expression of CD39 is ubiquitous in B cells; however, CD73
expression is uncommon. In certain mouse strains, approximately 30–50%
of B-1 cells (B220+CD23−) and IL-10
producing B (B10) cells
(B220+CD5+CD1dhigh)
are CD73high, whereas few conventional B-2 cells
(B220+CD23+AA4.1−)
express CD73. In keeping with expression of both CD73 and CD39,
CD73+ B cells produce ADO in the presence of ATP
substrate, whereas B-2 cells do not [49]. Figueiro
et al. defined CD39high B cells as the major
contributor to the regulatory network operated by human B lymphocytes[50]. CD39high B cells
co-cultured with autologous effector T cells suppressed T-cell
activation/proliferation and increased the secreted levels of IL-6 and
IL-10. The proliferation and functions of these
CD39high B cells are regulated by A1R-
and A2AR-mediated autocrine signaling. Saze et al. found
that the production of AMP and ADO by
CD39+CD73+ B cell subsets is related
to the control of CD4 and CD8 effector immunity[51]. The absence of CD39 did not change the
number of B cells in peripheral blood and spleen. However,
CD39-/- mice showed impaired B cell memory response to
T-dependent, suggesting that CD39 may contribute to the antibody
affinity maturation and the post-germinal centers B cell differentiation[52].
B cells express P2XR and P2YR [53] which allows
ATP to regulate B cell activation, adhesion, migration, and IgE
secretion [54]. ATP-driven P2X7R activation is
crucial for secretion of IgM, indicating that this receptor plays a key
role in the humoral response [55]. It can be
speculated that CD39 may affect the ATP-mediated B cell regulation.