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

Paulo Gaio, Melisa Gualdrón-López, Allysson Cramer, Lisia Esper, José Evaldo Rodrigues de Menezes Filho, Jader Santos Cruz, Mauro Martins Teixeira, Fabiana Simão Machado

Clinical immunology (Orlando, Fla.) 2022 Jan

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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. Copyright © 2021 Elsevier Inc. All rights reserved.

Citation

Paulo Gaio, Melisa Gualdrón-López, Allysson Cramer, Lisia Esper, José Evaldo Rodrigues de Menezes Filho, Jader Santos Cruz, Mauro Martins Teixeira, Fabiana Simão Machado. SOCS2 expression in hematopoietic and non-hematopoietic cells during Trypanosoma cruzi infection: Correlation with immune response and cardiac dysfunction. Clinical immunology (Orlando, Fla.). 2022 Jan;234:108913