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Genetic susceptibility factors, parasite strain, and an adequate modulation of the immune system seem to be crucial for disease progression after  Trypanosoma cruzi  infection. HLA-G and its murine functional homolog Qa2 have well-recognized immunomodulatory properties. We evaluated the  HLA-G  3′ untranslated region (3′UTR) polymorphic sites (associated with mRNA stability and target for microRNA binding) and HLA-G tissue expression (heart, colon, and esophagus) in patients presenting Chagas disease, stratified according to the major clinical variants. Further, we investigated the transcriptional levels of Qa2 and other pro- and anti-inflammatory genes in affected mouse tissues during  T. cruzi  experimental acute and early chronic infection induced by the CL strain. Chagas disease patients exhibited differential  HLA-G  3′UTR susceptibility allele/genotype/haplotype patterns, according to the major clinical variant (digestive/cardiac/mixed/indeterminate). HLA-G constitutive expression on cardiac muscle and colonic cells was decreased in Chagasic tissues; however, no difference was observed for Chagasic and non-Chagasic esophagus tissues. The transcriptional levels of  Qa2  and other anti and proinflammatory ( CTLA-4, PDCD1, IL-10, INF-γ , and  NOS-2 ) genes were induced only during the acute  T. cruzi  infection in BALB/c and C57BL/6 mice. We present several lines of evidence indicating the role of immunomodulatory genes and molecules in human and experimental  T. cruzi  infection.

Human Leucocyte Antigen-G (HLA-G) and Its Murine Functional Homolog Qa2 in theTrypanosoma cruziInfection