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Critical Reviews™ in Immunology
IF: 1.352 5-Year IF: 3.347 SJR: 0.657 SNIP: 0.55 CiteScore™: 2.19

ISSN Print: 1040-8401
ISSN Online: 2162-6472

Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.v21.i1-3.120
12 pages

CD14+ Monocytes as Dendritic Cell Precursors: Diverse Maturation-Inducing Pathways Lead to Common Activation of NF-kB/RelB

Gary K. Koski
Division of Basic Sciences, Center for Cancer Research, National Cancer Institute at Frederick, Frederick MD 21702-1201
Lyudmila A. Lyakh
Division of Basic Sciences, Center for Cancer Research, National Cancer Institute at Frederick, Frederick MD 21702-1201
Peter A. Cohen
Center for Surgery Research, NE6-307, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, USA
Nancy R. Rice
Division of Basic Sciences, Center for Cancer Research, National Cancer Institute at Frederick, Frederick MD 21702-1201

ABSTRACT

Dendritic cells are extremely potent antigen-presenting cells that are primarily responsible for the sensitization of naive T cells to protein antigen in vivo. For this reason, dendritic cells are the focus of intense study. Despite this interest, relatively little information is available on the signal transduction pathways that regulate the development and activity of these cells. The last several years, however, have seen a steady accumulation of data regarding methods to cultivate large numbers of DC, the characterization of attendant signals that drive DC development from various precursor cells, and the induction of nuclear transcription factors that presumably direct alterations in gene expression that regulate aspects of DC development. In this review, we briefly summarize some of these findings, with emphasis on monocyte-derived dendritic cells and a discussion of two distinct types of signaling pathways that appear to regulate the final maturation of DC: one pathway calcium-dependent and cyclosporine A-sensitive, the other pathway CsA-insensitive. Although evidence suggests these signaling pathways are quite divergent in their upstream components, they both appear to activate NF-kB nuclear factors, particularly RelB.


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