Artículos de revistas
Retinal dysfunction in patients with chronic Chagas’disease is associated to anti-Trypanosoma cruzi antibodies that crossreact with rhodopsin
Fecha
2006-12Registro en:
Matsumoto, Silvia C.; Labovsky, Vivian; Roncoroni, Marcela; Guida, Maria Catalina; Gimenez, Luisa; et al.; Retinal dysfunction in patients with chronic Chagas’disease is associated to anti-Trypanosoma cruzi antibodies that crossreact with rhodopsin; Federation of American Societies for Experimental Biology; FASEB Journal; 20; 3; 12-2006; 550-552
0892-6638
1530-6860
CONICET Digital
CONICET
Autor
Matsumoto, Silvia C.
Labovsky, Vivian
Roncoroni, Marcela
Guida, Maria Catalina
Gimenez, Luisa
Mitelman, Jorge
Gori, Horacio
Jurgelevicius, Renata
Grillo, Alejandro
Manfredi, Pablo
Levìn, Mariano J.
Paveto, Cristina
Resumen
To investigate retinal involvement in chronic Chagas' disease, we performed electroretinography and retinal fluorescein angiography studies in chagasic patients. Our results demonstrated a dissociated electrophysiological response characterized by both an abnormal reduction of the electroretinographic b-wave amplitude and a delayed latency, under the dark-adaptated condition. These alterations are compatible with a selective dysfunction of the rods. Antibodies raised against Trypanosoma cruzi that also interact with beta1-adrenergic receptor blocked light stimulation of cGMP-phosphodiesterase in bovine rod membranes. The specificity from the antibody-rhodopsin interaction was confirmed by Western blot analysis and antigenic competition experiments. Our results suggest an immunomediated rhodopsin blockade. T. cruzi infection probably induces an autoimmune response against rhodopsin in the chronic phase of Chagas' disease through a molecular mimicry mechanism similar to that described previously on cardiac human beta1-adrenergic and M2-cholinergic receptors, all related to the same subfamily of G-protein-coupled receptors.