Authors: Wan, Y.; Bramson, J.

Source: Current Pharmaceutical Design, Volume 7, Number 11, 1 July 2001 , pp. 977-992(16)

Publisher: Bentham Science Publishers

Abstract:

Over the last several years, it has become increasingly clear that dendritic cells (DC) are not only critical for the initiation of T cell immunity, but these cells also determine the course of the subsequent immune response (i.e. tolerance vs. immunity, Th1 vs Th2). However, the mechanisms by which DC can influence the final outcome of a given immune response remain to be understood. Currently, the ability of DC to direct immunity has been linked to: (1) hematopoeitic lineage, (2) maturation stage, and (3) environmental stimuli. While the literature supports each possibility, one common feature of all three hypotheses is that immunological outcome is directly correlated to the profile of DC-derived cytokines. A review of the existing scientific literature strongly suggests that the capacity of DC to orchestrate the immune responses is not an intrinsic quality of the cell, but rather it is the result of environmental stimulation which is reflected in their cytokine and chemokine production.

Keywords: Cytokines; Imune Regulation; Dendritic; IL-12; Paracrine Effects; TNF A; Plasmacytoid; Chemokines; Chemokine receptor Expreesion; NKT Cells

Document Type: Review article

DOI: http://dx.doi.org/10.2174/1381612013397627

Publication date: 2001-07-01

More about this publication?

• Current Pharmaceutical Design publishes timely in-depth reviews covering all aspects of current research in rational drug design. Each issue is devoted to a single major therapeutic area. A Guest Editor who is an acknowledged authority in a therapeutic field has solicits for each issue comprehensive and timely reviews from leading researchers in the pharmaceutical industry and academia.
  
  Each thematic issue of Current Pharmaceutical Design covers all subject areas of major importance to modern drug design, including: medicinal chemistry, pharmacology, drug targets and disease mechanism.

Related content

• In this: publication
• By this: publisher
• In this Subject: Pharmacology
• By this author: Wan, Y. ;  Bramson, J.

Website © Publishing Technology. Article copyright remains with the publisher, society or author(s) as specified within the article.

• Terms and conditions
• Privacy policy
• Information for advertisers