Molecular mimicry between Trypanosoma cruzi and human β-tubulin as a potential autoimmune mechanism in Chagas disease–associated megaviscera

Abstract Chagas disease, caused by Trypanosoma cruzi, affects a significant proportion of patients who develop digestive and cardiac complications, including megaviscera. This pathogenesis has been associated with autoimmune mechanisms mediated by molecular mimicry. In this study, an in silico evaluation of cross reactivity of β-tubulin 1.9 of T. cruzi and the human tubulin β-4A isoform 3 was conducted. Using bioinformatics tools, homologous regions were identified and potential immunogenic epitopes were predicted, considering their modeling and docking. The epitope GQSGAGNNWAKGHYTEGAELIDS was found to have high affinity and favorable antigenic properties, as well as binding capacity with TLR2. These findings suggest that this epitope could participate in molecular mimicry processes implicated in the development of chagasic megaviscera.Clinical trial number: not applicable.