Functional nicotinic acetylcholine receptors are expressed in B lymphocyte-derived cell lines.
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-alpha-bungarotoxin binding sites per cell, thus reflecting the presence of both homomeric and heteromeric nicotinic receptors. More specifically, the presence of alpha4- and alpha7-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 alpha4 and alpha7 subunits in hybridoma cells. Additionally, nicotine stimulated hybridoma cell proliferation, whereas it decreased antibody production. In contrast, alpha7-specific snake toxins inhibited cell proliferation but increased antibody production. It is concluded that myeloma and hybridoma cells express alpha4- and alpha7-containing nicotinic receptors, which participate in regulating cell proliferation and function.
D000818:Animals; D001402:B-Lymphocytes / Q000378:metabolism*; D002455:Cell Division / Q000502:physiology; D051379:Mice; D011978:Receptors, Nicotinic / Q000096:biosynthesis* / Q000502:physiology; D014407:Tumor Cells, Cultured
D011978:Receptors, Nicotinic