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Nicotinic receptors of rat lymphocytes during adjuvant polyarthritis
W Maslinski1, H Laskowska-Bozek, J Ryzewski
1Clinical Immunology, Beth Israel Hospital, Harvard Medical School, Boston, MA 02215.
Resting rat lymphocytes and thymocytes express specific [3H]nicotine binding sites with Kd values 7.5 and 10 nM, respectively. Resting T lymphocytes express 5-7 times as many binding sites (1,500/cell) as do unfractionated thymocytes (250/cell), suggesting that only a subset of thymocytes express nicotinic binding sites. Neither macrophages nor B cells bear nicotinic receptors. [3H]nicotine binding to lymphocytes is competitively inhibited in the presence of the cholinergic agonist carbamylcholine with IC50 = 100 microM. The number of receptors expressed on draining lymph node lymphocytes is upregulated during the course of adjuvant induced polyarthritis: maximum of [3H]nicotine binding is observed at day 21 of the disease with a subsequent decline reaching basal level at day 36. These results show the presence of [3H]nicotine binding sites on T lymphocytes and suggest their involvement in the later immune phase of adjuvant induced polyarthritis.
Resting rat lymphocytes and thymocytes express specific [3H]nicotine binding sites with Kd values 7.5 and 10 nM, respectively. Resting T lymphocytes express 5-7 times as many binding sites (1,500/cell) as do unfractionated thymocytes (250/cell), suggesting that only a subset of thymocytes express nicotinic binding sites. Neither macrophages nor B cells bear nicotinic receptors. [3H]nicotine binding to lymphocytes is competitively inhibited in the presence of the cholinergic agonist carbamylcholine with IC50 = 100 microM. The number of receptors expressed on draining lymph node lymphocytes is upregulated during the course of adjuvant induced polyarthritis: maximum of [3H]nicotine binding is observed at day 21 of the disease with a subsequent decline reaching basal level at day 36. These results show the presence of [3H]nicotine binding sites on T lymphocytes and suggest their involvement in the later immune phase of adjuvant induced polyarthritis.