Journal
ANNUAL REVIEW OF IMMUNOLOGY, VOL 31
Volume 31, Issue -, Pages 743-791Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev-immunol-020711-074929
Keywords
Toll-like receptors; MyD88; autoimmunity; colitis; costimulatory molecules; A20
Categories
Funding
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [P01AI078869] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [T32DK007007, P30DK042086, P30DK026743, R01DK095693, R01DK071939] Funding Source: NIH RePORTER
- NIAID NIH HHS [P01 AI078869] Funding Source: Medline
- NIDDK NIH HHS [P30 DK026743, R01 DK095693, T32 DK007007, P30 DK042086, R01 DK071939] Funding Source: Medline
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Dendritic cells (DCs) are specialized sentinels responsible for coordinating adaptive immunity. This function is dependent upon coupled sensitivity to environmental signs of inflammation and infection to cellular maturation-the programmed alteration of DC phenotype and function to enhance immune cell activation. Although DCs are thus well equipped to respond to pathogens, maturation triggers are not unique to infection. Given that immune cells are exquisitely sensitive to the biological functions of DCs, we now appreciate that multiple layers of suppression are required to restrict the environmental sensitivity, cellular maturation, and even life span of DCs to prevent aberrant immune activation during the steady state. At the same time, steady-state DCs are not quiescent but rather perform key functions that support homeostasis of numerous cell types. Here we review these functions and molecular mechanisms of suppression that control steady-state DC maturation. Corruption of these steady-state operatives has diverse immunological consequences and pinpoints DCs as potent drivers of autoimmune and inflammatory disease.
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