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https://www.arca.fiocruz.br/handle/icict/13950
TISSUE FACTOR EXPRESSION BY MYELOID CELLS CONTRIBUTES TO PROTECTIVE IMMUNE RESPONSE AGAINST MYCOBACTERIUM TUBERCULOSIS INFECTION.
Author
Affilliation
University of Texas Health Science Center at Tyler. Department of Pulmonary Immunology. Tyler, TX, USA
University of Texas Health Science Center at Tyler. Department of Pulmonary Immunology. Tyler, TX, USA
University of Texas Health Science Center at Tyler. Department of Cellular and Molecular Biology. Tyler, TX, USA
University of Texas Health Science Center at Tyler. Department of Pulmonary Immunology. Tyler, TX, USA
University of Texas Health Science Center at Tyler. Department of Pulmonary Immunology. Tyler, TX, USA
University of Texas Health Science Center at Tyler. Department of Pulmonary Immunology. Tyler, TX, USA
University of Texas Health Science Center at Tyler. Department of Pulmonary Immunology. Tyler, TX, USA
University of Texas Health Science Center at Tyler. Department of Cellular and Molecular Biology. Tyler, TX, USA
University of Texas Health Science Center at Tyler. Department of Pulmonary Immunology. Tyler, TX, USA
Frederick National Laboratory for Cancer Research. Clinical Research Directorate/Clinical Monitoring Research Program. Leidos Biomedical Research, Inc. Frederick, MD, USA
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Laboratório Integrado de Microbiologia e Imunoregulação. Salvador, BA, Brasil / Brazilian Institute for Tuberculosis Research. Research Center. Salvador, BA, Brasil
The University of North Carolina at Chapel Hill School of Medicine. Department of Medicine. NC, USA
University of Texas Health Science Center at Tyler. Department of Cellular and Molecular Biology. Tyler, TX, USA
University of Texas Health Science Center at Tyler. Department of Pulmonary Immunology. Tyler, TX, USA
University of Texas Health Science Center at Tyler. Department of Pulmonary Immunology. Tyler, TX, USA
University of Texas Health Science Center at Tyler. Department of Cellular and Molecular Biology. Tyler, TX, USA
University of Texas Health Science Center at Tyler. Department of Pulmonary Immunology. Tyler, TX, USA
University of Texas Health Science Center at Tyler. Department of Pulmonary Immunology. Tyler, TX, USA
University of Texas Health Science Center at Tyler. Department of Pulmonary Immunology. Tyler, TX, USA
University of Texas Health Science Center at Tyler. Department of Pulmonary Immunology. Tyler, TX, USA
University of Texas Health Science Center at Tyler. Department of Cellular and Molecular Biology. Tyler, TX, USA
University of Texas Health Science Center at Tyler. Department of Pulmonary Immunology. Tyler, TX, USA
Frederick National Laboratory for Cancer Research. Clinical Research Directorate/Clinical Monitoring Research Program. Leidos Biomedical Research, Inc. Frederick, MD, USA
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Laboratório Integrado de Microbiologia e Imunoregulação. Salvador, BA, Brasil / Brazilian Institute for Tuberculosis Research. Research Center. Salvador, BA, Brasil
The University of North Carolina at Chapel Hill School of Medicine. Department of Medicine. NC, USA
University of Texas Health Science Center at Tyler. Department of Cellular and Molecular Biology. Tyler, TX, USA
University of Texas Health Science Center at Tyler. Department of Pulmonary Immunology. Tyler, TX, USA
Abstract
Tissue factor (TF) is a transmembrane glycoprotein that plays an essential role in hemostasis by activating coagulation. TF is also expressed by monocytes/macrophages as part of the innate immune response to infections. In the current study, we determined the role of TF expressed by myeloid cells during Mycobacterium tuberculosis (M. tb) infection by using mice lacking the TF gene in myeloid cells (TF(Δ) ) and human monocyte derived macrophages (MDMs). We found that during M. tb infection, a deficiency of TF in myeloid cells was associated with reduced inducible nitric oxide synthase (iNOS) expression, enhanced arginase 1 (Arg1) expression, enhanced IL-10 production and reduced apoptosis in infected macrophages, which augmented M. tb growth. Our results demonstrate that a deficiency of TF in myeloid cells promotes M2-like phenotype in M .tb infected macrophages. A deficiency in TF expression by myeloid cells was also associated with reduced fibrin deposition and increased matrix metalloproteases (MMP)-2 and MMP-9 mediated inflammation in M. tb infected lungs. Our studies demonstrate that TF expressed by myeloid cells has newly recognized abilities to polarize macrophages and to regulate M. tb growth
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