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Evaluation of the immune response against Trypanosoma cruzi cytosolic tryparedoxin peroxidase in human natural infection
Author(s) -
Girard Magalí C.,
Acevedo Gonzalo R.,
López Lucía,
Ossowski Micaela S.,
Piñeyro María D.,
Grosso Juan P.,
Fernandez Marisa,
Hernández Vasquez Yolanda,
Robello Carlos,
Gómez Karina A.
Publication year - 2018
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/imm.12979
Subject(s) - immune system , biology , immunology , peripheral blood mononuclear cell , trypanosoma cruzi , asymptomatic , chagas disease , immunogenicity , virology , parasite hosting , medicine , biochemistry , world wide web , computer science , in vitro
Summary Trypanosoma cruzi , the aetiological agent of Chagas disease, has a highly efficient detoxification system to deal with the oxidative burst imposed by its host. One of the antioxidant enzymes involved is the cytosolic tryparedoxin peroxidase (c‐ TXNP x), which catalyses the reduction to hydrogen peroxide, small‐chain organic hydroperoxides and peroxynitrite. This enzyme is present in all parasite stages, and its overexpression renders parasites more resistant to the oxidative defences of macrophages, favouring parasite survival. This work addressed the study of the specific humoral and cellular immune response triggered by c‐ TXNP x in human natural infection. Thus, sera and peripheral blood mononuclear cells ( PBMC ) were collected from chronically infected asymptomatic and cardiac patients, and non‐infected individuals. Results showed that levels of IgG antibodies against c‐ TXNP x were low in sera from individuals across all groups. B‐cell epitope prediction limited immunogenicity to a few, small regions on the c‐ TXNP x sequence. At a cellular level, PBMC from asymptomatic and cardiac patients proliferated and secreted interferon‐ γ after c‐ TXNP x stimulation, compared with mock control. However, only proliferation was higher in asymptomatic patients compared with cardiac and non‐infected individuals. Furthermore, asymptomatic patients showed an enhanced frequency of CD 19 + CD 69 + cells upon exposure to c‐ TXNP x. Overall, our results show that c‐ TXNP x fails to induce a strong immune response in natural infection, being measurable only in those patients without any clinical symptoms. The low impact of c‐ TXNP x in the human immune response could be strategic for parasite survival, as it keeps this crucial antioxidant enzyme activity safe from the mechanisms of adaptive immune response.