SOCS2 expression in hematopoietic and non-hematopoietic cells during Trypanosoma cruzi infection Correlation with immune response and cardiac dysfunction

SOCS2 expression in hematopoietic and non-hematopoietic cells during Trypanosoma cruzi infection : Correlation with immune response and cardiac dysfunction

Copyright © 2021 Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 234(2022) vom: 01. Jan., Seite 108913
1. Verfasser: Gaio, Paulo (VerfasserIn)
Weitere Verfasser: Gualdrón-López, Melisa, Cramer, Allysson, Esper, Lisia, de Menezes Filho, José Evaldo Rodrigues, Cruz, Jader Santos, Teixeira, Mauro Martins, Machado, Fabiana Simão
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2022
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Cardiac function Chagas disease Immunorregulation SOCS2 Trypanosoma cruzi Socs2 protein, mouse Suppressor of Cytokine Signaling Proteins
Beschreibung
Zusammenfassung:Copyright © 2021 Elsevier Inc. All rights reserved.
Chagas disease has a complex pathogenesis wherein the host immune response is essential for controlling its development. Suppressor of cytokine signaling(SOCS)2 is a crucial protein that regulates cytokine production. In this study, SOCS2 deficiency resulted in an initial imbalance of IL12- and IL-10-producing neutrophils and dendritic cells (DCs), which caused a long-lasting impact reducing inflammatory neutrophils and DCs, and tolerogenic DCs at the peak of acute disease. A reduced number of inflammatory and pro-resolving macrophages, and IL17A-producing CD4+ T cells, and increased lymphocyte apoptosis was found in SOCS2-deficient mice. Electrocardiogram analysis of chimeric mice showed that WT mice that received SOCS2 KO bone marrow transplantation presented increased heart dysfunction. Taken together, the results demonstrated that SOCS2 is a crucial regulator of the immune response during Trypanosoma cruzi infection, and suggest that a SOCS2 genetic polymorphism, or failure of its expression, may increase the susceptibility of cardiomyopathy development in Chagasic patients
Beschreibung:Date Completed 25.02.2022
Date Revised 25.02.2022
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2021.108913