Expressão de receptores Fcg em leucócitos de portadores das formas clínicas indeterminada e cardíaca da doença de Chagas

Abstract

Introduction: Fc receptors for IgG (FcgR) are molecules that interfacehumoral and cellular immunity and contribute to activate and or modulateimmune response. In humans, three classes can be distinguished: RI (CD64), RII (CD32); and RIII (CD16). FcgRI, RIIa and RIII activate cellular responses upon triggering, whereas RIIb is inhibitory. A balanced action of these opposing signaling systems determines cellular response. In Trypanosoma cruzi infection, few studies have been conducted in humans. Previous data showed that asymptomatic patients presented higher expression of CD64 in monocytes and higher frequency of CD16+ monocytes (VITELLI et al.;2004). Aims: To evaluate ex-vivo FcgR expression and the impact of T. cruzi antigens stimulation on FcgR expression on different leukocyte populations from chagasic patients.Methodology: Peripheral blood from infected and non infected individualswas assayed by flow cytometry. Whole blood was also cultured for 5 hours in the presence of trypomastigote antigens before immune staining. Results: In peripheral leucocytes, we verified lower expression of CD16 on neutrophils and monocytes. T.cruzi antigen stimulation induced decrease of all FcgRs expression on neutrophils from non infected and infected individuals, mainly in cardiac patients. In monocytes, an increase of CD16 expression was observed in asymptomatic patients and a decrease in CD32 was verified incardiac patients. In lymphocytes, antigen stimulation induced consistentdecrease of CD16 expression in all groups, especially in cardiac patients. Conclusions: Antigen stimulation was able to induce robust decay in FcgR expression in different leukocyte populations. This down-regulation, predominant in cardiac patients, could be consequent to internalization or cleavage of ligant/receptor complex, acting as important element triggering immunological events related to severe clinical manifestations.