Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

The rapid and robust immunoregulatory cytokine response of Va14Ja18 natural T (iNKT) cells to glycolipid Ags determines their diverse functions. Unlike conventional T cells, iNKT lymphocyte ontogeny absolutely requires NF-kappa B signaling. However, the precise role of NF-kappa B in iNKT cell function and the identity of upstream signals that activate NF-kappa B in this T cell subset remain unknown. Using mice in which iNKT cell ontogeny has been rescued despite inhibition of NF-kappa B signaling, we demonstrate that iNKT cell function requires NF-kappa B in a lymphocyte-intrinsic manner. Furthermore, the ontogeny of functional iNKT cells requires signaling through protein kinase C theta, which is dispensable for conventional T lymphocyte development. The unique requirement of protein kinase C theta implies that signals emanating from the TCR activate NF-kappa B during iNKT cell development and function. Thus, we conclude that NF-kappa B signaling plays a crucial role at distinct levels of iNKT cell biology.

Original publication

DOI

10.4049/jimmunol.172.8.4667

Type

Journal article

Journal

Journal of immunology (Baltimore, Md. : 1950)

Publication Date

04/2004

Volume

172

Pages

4667 - 4671

Addresses

Department of Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.

Keywords

Killer Cells, Natural, Hybridomas, Animals, Mice, Inbred C57BL, Mice, Knockout, Mice, Isoenzymes, Protein Kinase C, Galactosylceramides, NF-kappa B, Receptors, Antigen, T-Cell, alpha-beta, Antigens, CD1, Cytokines, Lymphocyte Activation, Signal Transduction, Cell Differentiation, Antigen Presentation, Antigens, CD1d