We have located links that may give you full text access.
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Review
DLL4 + dendritic cells: Key regulators of Notch Signaling in effector T cell responses.
Pharmacological Research : the Official Journal of the Italian Pharmacological Society 2016 November
Dendritic cells (DCs) are critical regulators of adaptive immune responses. DCs can elicit primary T cell responses at low DC:T cell ratios through their expression of high levels of antigen-presenting molecules and costimulatory molecules. DCs are important for induction of functionally diverse T cell subsets such as CD4+ T helper (Th)1 and Th17 cells and effector CD8+ T cells able to reside in epithelial tissues. Recent studies begin illuminating the underlying mechanism by which DCs regulate specialized T cell subsets. DCs are composed of subsets that differ in their phenotype, localization and function. DCs expressing high levels of DLL4 (DLL4+ DCs), which is a member of Notch ligand family, are newly discovered cells that have greater ability than DLL4- DCs to promote the generation of Th1 and Th17 CD4+ T cells. DLL4 derived from DLL4+ DCs is also important for promoting the differentiation and expansion of effector CD8+ T cells. Experimental studies have demonstrated that selective deletion of DLL4 in DCs causes impaired antitumor immunity. In contrast, blocking DLL4 leads to dramatic reduction of inflammatory T cell responses and their-mediated tissue damage. We will discuss emerging functional specialization within the DLL4+ DC compartment, DLL4+ DC biology and the impact of pharmacological modulation of DLL4 to control inflammatory disorders.
Full text links
Related Resources
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app