SIGN IN   Advanced Search

Browse Illustration
Diacylglycerol Kinases Put the Brakes on Immune Function

Diacylglycerol kinases (DGKs) are emerging as key negative regulators of immune function, particularly in T cells. DGKs consume diacylglycerol to produce phosphatidic acid. Because both diacylglycerol and phosphatidic acid are important activators of signaling molecules, DGKs have the potential to modulate a number of signaling pathways, and this certainly seems to be the case in T cell function. Studies of T cell signaling demonstrate that DGKs inhibit T cell receptor signaling and thus may serve an important role in limiting the immune response. Other studies have examined the molecular basis of anergy, a state of T cell unresponsiveness that is an important postdevelopmental control over the immune response to self antigens. Two groups have suggested that DGK activity lies at the heart of the anergic phenotype. In addition, DGK activity may limit the response of macrophages and dendritic cells to intracellular pathogens. An overall picture is emerging in which the capacity of DGKs to modulate membrane signaling lipids is used to keep a tight rein on immune responses.

Rate this Resource:
1 = not useful, 5 = very useful

Please be the first to rate this resource.

Subscribe and
View Resource


Resource Type: Bibliography, Diagram, Illustration, Journal article/Issue, Review
Audience Level: Undergraduate upper division 15-16, Graduate, Professional (degree program)

Author and Copyright

Authors and Editors: Binks W. Wattenberg of University of Louisville, Daniel M. Raben of Department of Biological Chemistry, The Johns Hopkins School of Medicine
Publisher: American Association for the Advancement of Science
Format: application/pdf, image/gif, image/jpeg, text/html
Copyright and other restrictions: Yes
Cost: Yes


» Sign In or register to post comments.

STKE/Science Signaling



Triple A S National Science Foundation Naitonal Science Digital Library Pathway
Funded by the individual BEN Collaborators and grants from the
National Science Foundation [DUE 0085840 / DUE 0226185 / DUE 0532797 / DUE 0734995]

This website is a National Science Digital Library (NSDL) Pathway.
Copyright © 2019. American Association for the Advancement of Science. All Rights Reserved.