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10.1016/j.phrs.2016.09.001

http://scihub22266oqcxt.onion/10.1016/j.phrs.2016.09.001
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C5571445!5571445!27639599
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suck abstract from ncbi


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pmid27639599      Pharmacol+Res 2016 ; 113 (Pt A): 449-57
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  • DLL4+ Dendritic Cells: Key Regulators of Notch Signaling in Effector T Cell Responses #MMPMID27639599
  • Meng L; Hu S; Wang J; He S; Zhang Y
  • Pharmacol Res 2016[Nov]; 113 (Pt A): 449-57 PMID27639599show ga
  • 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.
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