Este relatório recebeu apoio do Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) e Coordenação Aperfeiçoamento de Pessoal de Nível Superior (CAPES). Y.M. Gomes é bolsista de pesquisa do CNPq (nº 306427 / 2006-0). Durante o período do estudo, a VMB Lorena recebeu um CNPq Ph.D. bolsa de estudos, AS Melo e SCM Braz receberam uma bolsa (06407432421) e CNPq (nº 133106 / 2009-8) M.Sc. Bolsa de estudos, respectivamente.Along with several other aspects of Chagas disease, the mechanisms responsible for the different clinical outcomes observed in chronic infected individuals have not yet been clarified. It is believed that the host immune response to the parasite plays an important role in the development of the pathology. Therefore, the aim of this study was to evaluate the relationship between IL-10 and IFN-γ gene expression profile, after in vitro stimulation of peripheral blood mononuclear cells (PBMC) with Trypanosoma cruzi recombinant antigens CRA (cytoplasmatic repetitive antigen) and FRA (flagellar repetitive antigen), and the clinical forms of chronic Chagas disease. Twenty patients with the cardiac form of the disease (CARD), of whom 10 had the mild cardiac form (CARD 1) and 10 the severe cardiac form (CARD 2), and 20 patients with the indeterminate form (IND), were selected at the Chagas Disease Unit of the Oswaldo Cruz University Hospital, University of Pernambuco, Recife, Pernambuco, Brazil. The PBMCs of these individuals were cultured in the presence of CRA or FRA for 3 days and IL-10 and IFN-γ gene expression was evaluated by detection of its messenger RNA using Real Time Quantitative PCR. Although no significant difference was observed between the groups of individuals studied, we found that most patients with IND displayed high levels of IFN-γ gene expression, while the majority of patients with CARD 1 presented high levels of IL-10. The results of this study thus highlight the important role that inflammatory cytokines play in patients with the IND group controlling for parasite replication, and that anti-inflammatory cytokines play in determining susceptibility to progression to symptomatic clinical forms of the disease.2050-01-01