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Review |
Mark A. Wallet and Pradip Sen, PhD, Department of Microbiology and Immunology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599.
Roland Tisch, PhD, Department of Microbiology and Immunology, and Lineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599.
Reprint Requests: Roland Tisch, PhD, Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, 804 Mary Ellen Jones Bldg., CB7290, Chapel Hill, NC 27599;Tel 919-966-7020; Fax 919-962-8103; Email: rmtisch{at}med.unc.edu
The paradigm of tolerogenic/immature versus inflammatory/mature dendritic cells has dominated the recent literature regarding the role of these antigen-presenting cells in mediating immune homeostasis or self-tolerance and response to pathogens, respectively. This issue is further complicated by the identification of distinct subtypes of dendritic cells that exhibit different antigen-presenting cell effector functions. The discovery of pathogen-associated molecular patterns and toll-like receptors provides the mechanistic basis for dendritic cell recognition of specific pathogens and induction of appropriate innate and adaptive immune responses. Only recently has insight been gained into how dendritic cells contribute to establishing and/or maintaining immunological tolerance to self. Soluble and cellular mediators have been reported to effectively regulate the function of dendritic cells by inducing several outcomes ranging from non-inflammatory dendritic cells that lack the ability to induce T lymphocyte activation to dendritic cells that actively suppress T lymphocyte responses. A thorough discussion of these stimuli and their outcomes is essential to understanding the potential for modulating dendritic cell function in the treatment of inflammatory disease conditions.
Key Words: Dendritic cells • Immunoregulation • Tolerance • IL-10 • Apoptosis • TGF-ß • CTLA-4 • CD200
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