Weinstein Y, Melmon K L
Immunol Commun. 1976;5(5):401-16. doi: 10.3109/08820137609033857.
Mixed lymphocytes from human peripheral blood, murine spleens, lymph nodes or thymus glands have pharmacologically specific receptors for histamine, beta mimetic catecholamines and prostaglandins. When these cells are exposed to the panoply of drugs mentioned above, their intracellular cyclic AMP concentrations increase. The biologic consequences of such an increase were at first elusive. Now we know that the immune potential of some murine spleen cells may be modulated and the release of lysosomal enzymes and histamine from human leukocytes may be inhibited. This paper concentrates on the effects that manipulation of cells with amine receptors has on their immune function. Recent studies have revealed that a subpopulation of splenic suppressor T cells responds to increases in its cyclic AMP content by reversing its suppressive effects on the humoral antibody response. When these T cells are removed from the murine cell population by their differential adherence to insolubilized conjugates of histamine with albumin, the remainder of the cells are more responsive to sheep cell antigen, as tested by transferring the spleen cells together with the antigen into lethally irradiated recipient animals. The suppressor T cells that adhere to the insolubilized conjugates of histamine-albumin (called histamine-rabbit serum albumin-Sepharose, or HRS) are Ia positive, they appear to have receptors for histamine, beta adrenergic amines and prostaglandins of the E series, and when stimulated by these agents their in vivo and in vitro suppressor actions are reversed. The reversal seems quantitatively dependent on cyclic AMP accumulation. Receptors for the amines and prostaglandins are found on the T cell precursors of cell mediated immunity. They develop on some T effector cells in selected models of allogeneic target cell lysis. The receptors also appear to develop on selected B cells once these cells become committed to antibody production. The distribution of receptors on all leukocytes has not been adequately studied nor has their full potential in the immune response been studied in detail.
来自人外周血、小鼠脾脏、淋巴结或胸腺的混合淋巴细胞具有针对组胺、β-拟交感儿茶酚胺和前列腺素的药理学特异性受体。当这些细胞暴露于上述一系列药物时，其细胞内的环磷酸腺苷（cAMP）浓度会增加。这种增加的生物学后果起初并不明确。现在我们知道，一些小鼠脾脏细胞的免疫潜能可能会受到调节，并且人白细胞中溶酶体酶和组胺的释放可能会受到抑制。本文重点关注用胺受体对细胞进行操作对其免疫功能的影响。最近的研究表明，脾脏抑制性T细胞亚群会通过逆转其对体液抗体反应的抑制作用来响应其环磷酸腺苷含量的增加。当通过将这些T细胞与组胺-白蛋白不溶性偶联物进行差异黏附从鼠细胞群体中去除时，其余细胞对绵羊细胞抗原的反应性更高，这是通过将脾细胞与抗原一起转移到致死性照射的受体动物中进行测试的。黏附于组胺-白蛋白不溶性偶联物（称为组胺-兔血清白蛋白-琼脂糖，或HRS）的抑制性T细胞是Ia阳性的，它们似乎具有组胺、β-肾上腺素能胺和E系列前列腺素的受体，并且当受到这些物质刺激时，它们在体内和体外的抑制作用会被逆转。这种逆转似乎在数量上依赖于环磷酸腺苷的积累。胺和前列腺素的受体存在于细胞介导免疫的T细胞前体上。在同种异体靶细胞裂解的特定模型中，它们在一些T效应细胞上发育。一旦这些B细胞开始产生抗体，受体似乎也会在选定的B细胞上发育。尚未对所有白细胞上受体的分布进行充分研究，也未对它们在免疫反应中的全部潜能进行详细研究。
