The heavy metal lead exhibits B cell-stimulatory factor activity by enhancing B cell Ia expression and differentiation.

Abstract

Lead (Pb) has been shown to enhance B cell differentiation and to induce T cell proliferation in vitro. Our work demonstrates a direct enhancing effect of Pb on IgM production by T cell depleted-, LPS-activated B cells. Pb also caused a significant, dose-dependent increase in the B cell surface density of both products from the I-region of the murine MHC, I-A and I-E, that was comparable to and within the same time frame as other conventional B cell activators. Pb did not alter B cell surface density of MHC class-I molecules, but it did modulate the levels of other relevant activation Ag such as sIgD and Fc epsilon R. The modulation of the B cell phenotype caused by Pb was not due to release of IL-4 from residual T cells or endotoxin contamination of any culture reagents. Hg also increased cell surface MHC class II molecule density; however, neither Ni, Zn, nor Cd modulated Ia, indicating that immunomodulatory metals have different mechanisms of action. These results suggest that the mechanism of Pb immunopotentiation might be due to increased B-Th cell collaboration and that Pb can act as a B cell stimulatory factor. In addition to the obvious environmental implications of these results, determining Pbs mechanism of action on B cells may yield important information relevant to B cell activation in general.