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Downmodulation of CD18 and CD86 on Macrophages and VLA-4 on Lymphocytes in Experimental Tuberculosis
Article first published online: 24 JAN 2002
DOI: 10.1046/j.1365-3083.2001.00996.x
1365-3083/asset/cover.gif?v=1&s=851263375540b207304bed4ad505b46ca5c4242b "Scandinavian Journal of Immunology")
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How to Cite
Bonato, V. L. D., Medeiros, A. I., Lima, V. M. F., Dias, A. R., Faccioli, L. H. and Silva, C. L. (2001), Downmodulation of CD18 and CD86 on Macrophages and VLA-4 on Lymphocytes in Experimental Tuberculosis. Scandinavian Journal of Immunology, 54: 564–573. doi: 10.1046/j.1365-3083.2001.00996.x
Publication History
- Issue published online: 24 JAN 2002
- Article first published online: 24 JAN 2002
- (Received 23 April 2001; Accepted in revised form 6 August 2001)
- Abstract
- Article
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- Cited By
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.