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Retinal dysfunction in patients with chronic Chagas' disease is associated to anti‐ Trypanosoma cruzi antibodies that cross‐react with rhodopsin
Author(s) -
Matsumoto Silvia C.,
Labovsky Vivian,
Roncoroni Marcela,
Guida María C.,
Giménez Luisa,
Mitelman Jorge,
Gori Horacio,
Jurgelevicius Renata,
Grillo Alejandro,
Manfredi Pablo,
Levin Mariano J.,
Paveto Cristina
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.05-4654fje
Subject(s) - rhodopsin , chagas disease , retinal , biology , trypanosoma cruzi , antibody , electroretinography , receptor , immunology , virology , biochemistry , parasite hosting , world wide web , computer science
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 ?1‐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 ?1‐adrenergic and M2‐cholinergic receptors, all related to the same subfamily of G‐protein‐coupled receptors.