Abstract

The molecular mechanisms governing the increased cell surface expression of major histocompatibility complex (MHC) class II molecules (Ia) on lead-treated mouse B cells was investigated. Lead has been shown to directly cause a selective, two-fold increase in the B cell's surface density of both products of the I region of the mouse MHC, I-A and I-E. In the present study, Western blot analysis showed that Pb increases the total cellular pool of I-A beta-chain by twofold. The increase in cellular I-A was not found to be due to increased messenger RNA (mRNA) for either the alpha- or the beta-chain of I-A. Biosynthetic labeling studies showed that Pb increases the translation or the stability of the Ia-associated invariant chain (Ii or gamma) and possibly the beta-chain of Ia. Collectively these results suggest that Pb increases the B cell's surface Ia by influencing translational or posttranslational regulation of Ia and/or Ia-associated chains.

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