Artículo

Altered distribution of peripheral blood memory B cells in humans chronically infected with Trypanosoma cruzi

Fernández, Esteban Rodrigo Icon; Olivera, Gabriela Carina Icon; Quebrada Palacio, Luz Piedad Icon; González, Mariela Natacha Icon; Hernandez Vasquez, Yolanda ; Sirena, Natalia María ; Moran, Maria Laura ; Ledesma Patiño, Oscar S. ; Postan, Miriam Icon

Otros responsables

Fecha

08/2014

Editorial

Public Library of Science

Revista

Plos One

Título del libro

Nombre del evento

Fecha del evento

Institución organizadora

ISSN

1932-6203

eISSN

ISBN

Idioma

Inglés

Tipo del evento

Clasificación temática

Resumen

Numerous abnormalities of the peripheral blood T cell compartment have been reported in human chronic Trypanosoma cruzi infection and related to prolonged antigenic stimulation by persisting parasites. Herein, we measured circulating lymphocytes of various phenotypes based on the differential expression of CD19, CD4, CD27, CD10, IgD, IgM, IgG and CD138 in a total of 48 T. cruzi-infected individuals and 24 healthy controls. Infected individuals had decreased frequencies of CD19+CD27+ cells, which positively correlated with the frequencies of CD4+CD27+ cells. The contraction of CD19 +CD27+ cells was comprised of IgG+IgD-, IgM+IgD- and isotype switched IgM-IgD- memory B cells, CD19+CD10+CD27+ B cell precursors and terminally differentiated CD19+CD27+CD138+ plasma cells. Conversely, infected individuals had increased proportions of CD19+IgG+CD27-IgD- memory and CD19+IgM+CD27-IgD+ transitional/naïve B cells. These observations prompted us to assess soluble CD27, a molecule generated by the cleavage of membrane-bound CD27 and used to monitor systemic immune activation. Elevated levels of serum soluble CD27 were observed in infected individuals with Chagas cardiomyopathy, indicating its potentiality as an immunological marker for disease progression in endemic areas. In conclusion, our results demonstrate that chronic T. cruzi infection alters the distribution of various peripheral blood B cell subsets, probably related to the CD4+ T cell deregulation process provoked by the parasite in humans.

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