Accuri C6 Flow Cytometer System
Originally published online as doi:10.1189/jlb.1003476 on February 13, 2004

Published online before print February 13, 2004
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(Journal of Leukocyte Biology. 2004;75:874-883.)
© 2004 by Society for Leukocyte Biology

Cross-regulation of CD86 by CD80 differentially regulates T helper responses from Mycobacterium tuberculosis secretory antigen-activated dendritic cell subsets

Mumtaz Yaseen Balkhi, Vinoth K. Latchumanan, Balwan Singh, Pawan Sharma and Krishnamurthy Natarajan1

Immunology Group, International Center for Genetic Engineering and Biotechnology, Aruna Asaf Ali Marg, New Delhi, India

1Correspondence: Immunology Group, International Center for Genetic Engineering and Biotechnology, Aruna Asaf Ali Marg, New Delhi-110-067, India. E-mail: natrajan{at}icgeb.res.in

We report that stimulation of Mycobacterium tuberculosis secretory antigen- and tumor necrosis factor {alpha}-matured BALB/c mouse bone marrow dendritic cells (BMDCs) with anti-CD80 monoclonal antibody up-regulated CD86 levels on the cell surface. Coculture of these BMDCs with naïve, allogeneic T cells now down-regulated T helper cell type 1 (Th1) responses and up-regulated suppressor responses. Similar results were obtained with splenic CD11c+/CD8a– DCs but not to the same extent with CD11c+/CD8a+ DCs. Following coculture with T cells, only BMDCs and CD11c+/CD8a– DCs and not CD11c+/CD8a+ DCs displayed increased levels of surface CD86, and further, coculturing these DCs with a fresh set of T cells attenuated Th1 responses and increased suppressor responses. Not only naïve but even antigen-specific recall responses of the Th1-committed cells were modulated by DCs expressing up-regulated surface CD86. Further analyses showed that stimulation with anti-CD80 increased interleukin (IL)-10 and transforming growth factor-ß-1 levels with a concomitant reduction in IL-12p40 and interferon-{gamma} levels from BMDCs and CD11c+/CD8a– DCs and to a lesser extent, from CD11c+/CD8a+ DCs. These results suggest that cross-talk between costimulatory molecules differentially regulates their relative surface densities leading to modulation of Th responses initiated from some DC subsets, and Th1-committed DCs such as CD11c+/CD8a+ DCs may not allow for such modulation. Cognate antigen-presenting cell (APC):T cell interactions then impart a level of polarization on APCs mediated via cross-regulation of costimulatory molecules, which govern the nature of subsequent Th responses.

Key Words: MTSA • Th1 response • polarization • co-stimulation • cross-talk




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