Análisis de la expresión y funcionalidad del receptor de IL-7 y su asociación con la respuesta celular T específica para Trypanosoma cruzi en pacientes con enfermedad de chagas crónica

The severity of Chagas heart disease is associated with a process of immune T-cell exhaustion. IL-7 plays an important role in T-cell maintenance and function. In this study, we evaluated whether the ability of T cells to produce IFN-? in response to Trypanosoma cruzi was associated with the express...

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Autor principal: Natale, María Ailén
Otros Autores: Albareda, María Cecilia
Formato: Tesis doctoral acceptedVersion
Lenguaje:Español
Publicado: Facultad de Farmacia y Bioquímica 2019
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Acceso en línea:http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgraafa&cl=CL1&d=HWA_2959
http://repositoriouba.sisbi.uba.ar/gsdl/collect/posgraafa/index/assoc/HWA_2959.dir/2959.PDF
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Sumario:The severity of Chagas heart disease is associated with a process of immune T-cell exhaustion. IL-7 plays an important role in T-cell maintenance and function. In this study, we evaluated whether the ability of T cells to produce IFN-? in response to Trypanosoma cruzi was associated with the expression and function of IL-7R. Patients possessing T. cruzi-specific IFN-?-producing cells had higher levels of memory T cells capable of modulating the alpha chain of IL-7R and an efficient response to IL-7 compared to that in patients lacking parasite-specific T-cell responses. Modulation of IL-7R was inversely associated with serum IL-6 levels and positively associated with serum IL-8 levels. Circulating IL-21 and IL-27 levels were not associated with the frequency of IFN-? producing cells but were reduced in less severe clinical forms of the disease. The expression and function of the IL-27R were associated with the magnitude of T. cruzi-specific T-cell responses. In vitro stimulation of PBMCs with IL-7 or IL-27 enhanced IFN-? production in IFN-? producers but not in IFN-? non-producers. The alterations of the IL-7/IL-7R axis might be responsible of the loss of T. cruzi-specific T cells during the chronic infection.