Abstract
Nicotine has been shown to affect B lymphocyte immune response. In this study, we have explored the presence of nicotinic receptors in B lymphocyte-derived cell lines, myeloma X63-Ag8 and hybridoma 1D6. We found that myeloma expressed on average 10,170 ± 1,100 [3H]epibatidine and 6,730 ± 370 125I-α-bungarotoxin binding sites per cell, thus reflecting the presence of both homomeric and heteromeric nicotinic receptors. More specifically, the presence of α4- and α7-containing nicotinic receptor subunits was demonstrated in both myeloma and hybridoma cells with subunit-specific antibodies. It was significantly higher in dividing than in resting cells. Long-term exposure to nicotine, at physiological concentration found in smokers, resulted in up-regulation of both α4 and α7 subunits in hybridoma cells. Additionally, nicotine stimulated hybridoma cell proliferation, whereas it decreased antibody production. In contrast, α7-specific snake toxins inhibited cell proliferation but increased antibody production. It is concluded that myeloma and hybridoma cells express α4- and α7-containing nicotinic receptors, which participate in regulating cell proliferation and function.
- Received April 15, 2003.
- Accepted July 3, 2003.
- The American Society for Pharmacology and Experimental Therapeutics
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