Abstract
The aim of this study was to investigate the influence of killer cell immunoglobulin-like receptor (KIR) genes and their human leucocyte antigen (HLA) ligands in the susceptibility of chronic Chagas disease. This case-control study enrolled 131 serologically-diagnosed Chagas disease patients (59 men and 72 women, mean age of 60.4 ± 9.8 years) treated at the University Hospital of Londrina and the Chagas Disease Laboratory of the State University of Maringa. A control group was formed of 165 healthy individuals - spouses of patients or blood donors from the Regional Blood Bank in Maringa (84 men and 81 women, with a mean age of 59.0 ± 11.4 years). Genotyping of HLA and KIR was performed by PCR-SSOP. KIR2DS2-C1 in the absence of KIR2DL2 (KIR2DS2+/2DL2-/C1+) was more frequent in Chagas patients (P = 0.020; Pc = 0.040; OR = 2.14) and, in particular, those who manifested chronic chagasic cardiopathy—CCC (P = 0.0002; Pc = 0.0004; OR = 6.64; 95% CI = 2.30–18.60) when compared to the control group, and when CCC group was compared to the patients without heart involvement (P = 0.010; Pc = 0.020; OR = 3.97). The combination pair KIR2DS2+/2DL2-/KIR2DL3+/C1+ was also positively associated with chronic chagasic cardiopathy. KIR2DL2 and KIR2DS2 were related to immunopathogenesis in Chagas disease. The combination of KIR2DS2 activating receptor with C1 ligand, in the absence of KIR2DL2, may be related to a risk factor in the chronic Chagas disease and chronic chagasic cardiopathy.
Highlights
Chagas disease, caused by the flagellate parasite Trypanosoma cruzi, currently affects around 6 million to 7 million people worldwide and about 25 million have the potential risk of becoming infected [1]
chagasic cardiopathy patients (CCC) presented a lower frequency of KIR2DL2 when compared to the control group (31.8% vs. 53.3%; P = 0.017; OR = 0.41; 95% confidence interval (95% CI) = 0.20–0.83); significance was lost after Bonferroni correction (Pc = 0.27)
CCD: chronic Chagas disease patients, NC: without heart involvement patients, CCC: chronic chagasic cardiopathy patients. a P = 0.017; Pc = 0.27; OR = 0.41; 95% CI = 0.20–0.83 (CCC vs Controls) doi:10.1371/journal.pntd.0003753.t002
Summary
Chagas disease, caused by the flagellate parasite Trypanosoma cruzi, currently affects around 6 million to 7 million people worldwide and about 25 million have the potential risk of becoming infected [1]. The disease is endemic and its development occurs in acute and chronic phases. The latter may present in different clinical forms, indeterminate, cardiac and/or digestive, with the chronic cardiac form being the most serious [2]. This variation in pathological manifestation has been reported to be related to the complexity of parasite and to differences in host immune response, such as the ability to control parasitaemia, the strength of inflammatory reactions, and the induction of autoimmune-like responses [3,4,5,6,7]. The precise pathogenic mechanism of Chagas' heart disease is not completely elucidated [7, 8]
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