TRYPANOSOMA-CRUZI ATTACHMENT TO LYMPHOCYTE MUSCARINIC CHOLINERGIC AND BETA-ADRENERGIC RECEPTORS MODULATES INTRACELLULAR SIGNAL TRANSDUCTION

被引:17
作者
BORDA, ES
STERINBORDA, LJ
PASCUAL, JO
GORELIK, G
FELIX, JC
VONKREUTER, BF
SANTOSBUCH, CA
机构
[1] CORNELL UNIV,MED CTR,COLL MED,DEPT PATHOL,1300 YORK AVE,NEW YORK,NY 10021
[2] CONSEJO NACL INVEST CIENT & TECN,CTR ESTUDIOS FARMACOL & BOT,BUENOS AIRES,ARGENTINA
关键词
LYMPHOCYTE-T; CAMP; CGMP; PGE2; INTRACELLULAR SIGNAL; HELPER CELL; SUPPRESSOR CYTOTOXIC CELLS;
D O I
10.1016/0166-6851(91)90151-U
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Plasma membrane vesicles of Trypanosoma cruzi (PMVs) formed saturation binding isotherms with naive murine T lymphocytes. Parasite membrane attachment to the muscarinic cholinergic receptors of Lyt 2.2+ T cells (suppressor cells) resulted in the synthesis of cGMP, attenuation of cAMP levels and in the secretion of prostaglandin E2, an immunoregulator effector substance. These T suppressor cell signals were blunted by atropine and by monospecific antibody against T. cruzi surface epitopes. The interaction of T. cruzi PMVs with the beta-adrenergic receptors of Lyt L3T4+ T cells (helper cells) resulted in the synthesis of cAMP and in the attenuation of cGMP levels. T helper cells did not secrete prostaglandin E2 when T. cruzi PMVs were added to this system. These T helper cell signals were blunted by propranolol and by monospecific antibody against T. cruzi surface epitopes. The interaction of T. cruzi with T lymphocytes may result, therefore, in the down-regulation of the immune response induced by prostaglandin E2 T suppressor cell secretion and by cAMP inhibition of proliferation of T helper cells.
引用
收藏
页码:91 / 100
页数:10
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