Human chagasic IgG interacting with lymphocyte neurotransmitter receptors triggers intracellular signal transduction.

It is demonstrated that human IgG in Chagas' disease and the corresponding F(ab)'2 fragment attach to lymphoid cells by specific interaction with beta-adrenergic and muscarinic cholinergic receptors. This interaction resulted in the transduction of signals that increased intracellular levels of cAMP in enriched T helper cell preparations and cGMP in enriched T suppressor cell preparations. The stimulation of Ts cell muscarinic cholinergic receptors by Chagas IgG or the corresponding F(ab)'2 fraction triggers the release of the immunomodulatory substance PGE2. These results are unified in a theory of immunoregulation and could contribute to the chronic course of Chagas' disease.