PMID: 11902331Mar 21, 2002Paper

Downmodulation of CD18 and CD86 on macrophages and VLA-4 on lymphocytes in experimental tuberculosis

Scandinavian Journal of Immunology
V L BonatoC L Silva

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)-gamma 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-gamma 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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Citations

May 12, 2016·Bulletin of Experimental Biology and Medicine·A V ChechushkovV A Shkurupy
Aug 26, 2016·Frontiers in Immunology·Daniel J Wikenheiser, Jason S Stumhofer
Aug 24, 2007·Brazilian Journal of Medical and Biological Research = Revista Brasileira De Pesquisas Médicas E Biológicas·V C S Flores-BatistaJ R Lapa-e-Silva

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