Interplay of Cytokines and Microbial Signals in Regulation of CD1d Expression and NKT Cell Activation

In this study we show that like MHC class I and class II molecules, cell surface CD1d expression on APC is regulated and affects T cell activation under physiological conditions. Although IFN-gamma alone is sufficient for optimum expression of MHC, CD1d requires two signals, one provided by IFN-gamm...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2005-09, Vol.175 (6), p.3584-3593
Main Authors: Skold, Markus, Xiong, Xiaowei, Illarionov, Petr A, Besra, Gurdyal S, Behar, Samuel M
Format: Article
Language:English
Subjects:
Animals
Antigen-Presenting Cells - immunology
Antigens, Bacterial - physiology
Antigens, CD1 - genetics
Antigens, CD1 - immunology
Antigens, CD1d
Bacterial Infections - immunology
Cytokines - physiology
Gene Expression Regulation - immunology
Interferon gamma Receptor
Interferon-gamma - physiology
Killer Cells, Natural - immunology
Killer Cells, Natural - metabolism
Lymphocyte Activation - immunology
Macrophages - immunology
Macrophages - metabolism
Mice
Mice, Knockout
Receptors, Interferon - deficiency
T-Cell Antigen Receptor Specificity
Tumor Necrosis Factor-alpha - physiology
Up-Regulation
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Summary:In this study we show that like MHC class I and class II molecules, cell surface CD1d expression on APC is regulated and affects T cell activation under physiological conditions. Although IFN-gamma alone is sufficient for optimum expression of MHC, CD1d requires two signals, one provided by IFN-gamma and a second mediated by microbial products or by the proinflammatory cytokine TNF. IFN-gamma-dependent CD1d up-regulation occurs on macrophages following infection with live bacteria or exposure to microbial products in vitro and in vivo. APC expressing higher CD1d levels more efficiently activate NKT cell hybridomas and primary NKT cells independently of whether the CD1d-restricted TCR recognizes foreign or self-lipid Ags. Our findings support a model in which CD1d induction regulates NKT cell activation.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.175.6.3584