Downmodulation of CD18 and CD86 on Macrophages and VLA-4 on Lymphocytes in Experimental Tuberculosis

Authors

  • V. L. D. Bonato,

    1. Centre for Tuberculosis Research, Department of Biochemistry and Immunology, School of Medicine of Ribeirão Preto, University of São Paulo; and
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  • A. I. Medeiros,

    1. Centre for Tuberculosis Research, Department of Biochemistry and Immunology, School of Medicine of Ribeirão Preto, University of São Paulo; and
    2. Department of Clinical Analysis, Toxicology and Bromatology, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Brazil
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  • V. M. F. Lima,

    1. Centre for Tuberculosis Research, Department of Biochemistry and Immunology, School of Medicine of Ribeirão Preto, University of São Paulo; and
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  • A. R. Dias,

    1. Centre for Tuberculosis Research, Department of Biochemistry and Immunology, School of Medicine of Ribeirão Preto, University of São Paulo; and
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  • L. H. Faccioli,

    1. Department of Clinical Analysis, Toxicology and Bromatology, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Brazil
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  • C. L. Silva

    1. Centre for Tuberculosis Research, Department of Biochemistry and Immunology, School of Medicine of Ribeirão Preto, University of São Paulo; and
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Dr C. L. Silva, Centre for Tuberculosis Research, Department of Biochemistry and Immunology, School of Medicine of Ribeirão Preto, University of São Paulo, Avenida Bandeirantes 3900, 14049–900, Ribeirão Preto, SP, Brazil. E-mail: clsilva@fmrp.usp.br

Abstract

Development and evaluation of new vaccines and immunotherapy against tuberculosis demand a better understanding of the immune mechanisms in this disease. Costimulatory signals and intercellular contact seem to be pivotal in determining whether recognition of antigen by T cells leads to activation or anergy. In this paper, we show that virulent M. tuberculosis H37Rv downmodulates the ex vivo expression of CD18 and CD86 on peritoneal macrophages and VLA-4 on lymphocytes but does not disturb the in vitro production of interleukin (IL)-12 and interferon (IFN)-γ after intraperitoneal infection. In addition, splenocytes from infected mice produce IL-10, while the expression of cell surface receptors is unchanged. The interplay among IL-12, IFN-γ and IL-10 in vivo and the downmodulation of cell-surface receptors during the infection at the inflammatory site may contribute to the explanation of the maintenance of infection.

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