Trypanosoma cruzi antigens down-regulate T lymphocyte proliferation by muscarinic cholinergic receptor-dependent release of PGE2
Acta physiol. pharmacol. ther. latinoam
;
48(3): 115-23, 1998. tab, graf
Article
in English
| LILACS
| ID: lil-216879
RESUMO
Here we demonstrate that T. cruzi antigen molecule SAPA (shed acute phase antigen) with neuraminidase-trans sialidase activity triggers down-regulation of T lymphocyte proliferation by interacting with T lymphocyte muscarinic acetylcholine receptors (mAChR). SAPA attachment to mAChR from Lyt 2.2+ T cells resulted in synthesis of cyclic GMP (cGMP) and secretion of PGE2, an immunoregulator effector substance. These T suppressor cell signals were blunted by atropine and by indomethacin. Cell sorter analysis showed that the interaction of SAPA with purified T cells, affected the ratio of L3T4+/Lyt 2.2+ T cells increasing the percentage of Lyt 2.2+ T cells, effect that was inhibited by the mAChR antagonist, atropine. The interaction between SAPA and mAChR from Lyt 2.2+ T cells may result, therefore, in the down-regulation of the host immune response as consequence of T suppressor/cytotoxic cells activation and PGE2 release as they were observed. These results support the theory of an immunosuppressive state that contribute to the chronic course of Chagas'disease.
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Index:
LILACS (Americas)
Main subject:
Atropine
/
Trypanosoma cruzi
/
T-Lymphocytes
/
Dinoprostone
/
Down-Regulation
/
Indomethacin
/
Receptors, Muscarinic
/
Cyclooxygenase Inhibitors
/
Muscarinic Antagonists
/
Antigens, Protozoan
Limits:
Animals
Language:
English
Journal:
Acta physiol. pharmacol. ther. latinoam
Journal subject:
Pharmacology
/
Physiology
/
Therapeutics
Year:
1998
Type:
Article
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