Cazaux C A, Sterin-Borda L, Gorelik G, Cremaschi G A
Centro de Estudios Farmacológicos y Botánicos (CEFYBO-CONICET), Buenos Aires, Argentina.
FEBS Lett. 1995 May 8;364(2):120-4. doi: 10.1016/0014-5793(95)00366-h.
The expression of beta-adrenergic receptors on murine lymphocytes stimulated with concanavalin A was studied. A decrease in beta-adrenoceptor number on T lymphocytes and a diminished response to specific agonist stimulation at the peak of proliferation was found. The blockade of cell proliferation by tyrosine kinases or protein kinase C inhibitors reversed the decrease in beta-adrenoceptor number. PMA plus ionophore or interleukin-2 but not PMA alone were able to induce beta-adrenoceptor down-regulation accompanying cellular proliferation. These results showed that the intracellular signals triggered during lymphocyte activation are involved in beta-adrenoceptor down-regulation and it would represent the loss of a mechanism that exerts negative neuroimmune control of cellular proliferation.
研究了伴刀豆球蛋白A刺激的小鼠淋巴细胞上β-肾上腺素能受体的表达。发现T淋巴细胞上β-肾上腺素能受体数量减少，且在增殖高峰期对特异性激动剂刺激的反应减弱。酪氨酸激酶或蛋白激酶C抑制剂对细胞增殖的阻断逆转了β-肾上腺素能受体数量的减少。佛波酯加离子载体或白细胞介素-2（而非单独的佛波酯）能够在细胞增殖的同时诱导β-肾上腺素能受体下调。这些结果表明，淋巴细胞活化过程中触发的细胞内信号参与了β-肾上腺素能受体下调，这可能代表了一种对细胞增殖发挥负性神经免疫控制作用的机制的丧失。
