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Characterization of (-)-(3H)-DHA binding to intact mouse lymphocytes: effect of experimental autoimmune orchitis on
Autoimmune orchitis induced an increment in the beta-adrenoceptor populations in intact mouse lymphocytes, depending on their source. Characterization of (-)-(3H)-DHA specific binding to intact normal cells indicate that thymic cells do not have the ability of binding a beta-adrenergic ligand. In contrast, spleen and lymph node cells showed a homogeneous population of beta-adrenergic receptors. (-)-(3H)-DHA binding was a rapid, reversible and stereospecific process. Competition experiments indicated the order of potency of the agonists and led to their definition as being of the beta 2-adrenoceptor subtype. Saturation assays and Scatchard analysis indicated a single class of binding sites (being free of allosteric or cooperative interaction) in both control and immune cells. However, spleen and lymph node cells from mice hyperimmunized with testicular preparations showed a marked increase in the number of beta-adrenoceptor sites with no changes in chi d. These results emphasize the use of lymphocytes possessing a homogeneous population of beta 2-adrenoceptors as an easily available model for monitoring beta-adrenoceptors in disease.
Autoimmune orchitis induced an increment in the beta-adrenoceptor populations in intact mouse lymphocytes, depending on their source. Characterization of (-)-(3H)-DHA specific binding to intact normal cells indicate that thymic cells do not have the ability of binding a beta-adrenergic ligand. In contrast, spleen and lymph node cells showed a homogeneous population of beta-adrenergic receptors. (-)-(3H)-DHA binding was a rapid, reversible and stereospecific process. Competition experiments indicated the order of potency of the agonists and led to their definition as being of the beta 2-adrenoceptor subtype. Saturation assays and Scatchard analysis indicated a single class of binding sites (being free of allosteric or cooperative interaction) in both control and immune cells. However, spleen and lymph node cells from mice hyperimmunized with testicular preparations showed a marked increase in the number of beta-adrenoceptor sites with no changes in chi d. These results emphasize the use of lymphocytes possessing a homogeneous population of beta 2-adrenoceptors as an easily available model for monitoring beta-adrenoceptors in disease.