期刊
IMMUNOLOGICAL REVIEWS
卷 277, 期 1, 页码 158-173出版社
WILEY
DOI: 10.1111/imr.12537
关键词
apoptosis/autophagy; autoimmunity; dendritic cells; monocytes/macrophages; phagocytosis; toll-like receptors/pattern recognition receptors
类别
资金
- National Institute of Diabetes and Digestive and Kidney Diseases [DK072201]
- National Institute of Allergy and Infectious Diseases [AI123284, AI127658]
- Burroughs Wellcome Fund
- Leukemia and Lymphoma Society
Apoptosis is an important component of normal tissue physiology, and the prompt removal of apoptotic cells is equally essential to avoid the undesirable consequences of their accumulation and disintegration. Professional phagocytes are highly specialized for engulfing apoptotic cells. The recent ability to track cells that have undergone apoptosis in situ has revealed a division of labor among the tissue resident phagocytes that sample them. Macrophages are uniquely programmed to process internalized apoptotic cell-derived fatty acids, cholesterol and nucleotides, as a reflection of their dominant role in clearing the bulk of apoptotic cells. Dendritic cells carry apoptotic cells to lymph nodes where they signal the emergence and expansion of highly suppressive regulatory CD4 T cells. A broad suppression of inflammation is executed through distinct phagocyte-specific mechanisms. A clever induction of negative regulatory nodes is notable in dendritic cells serving to simultaneously shut down multiple pathways of inflammation. Several of the genes and pathways modulated in phagocytes in response to apoptotic cells have been linked to chronic inflammatory and autoimmune diseases such as atherosclerosis, inflammatory bowel disease and systemic lupus erythematosus. Our collective understanding of old and new phagocyte functions after apoptotic cell phagocytosis demonstrates the enormity of ways to mediate immune suppression and enforce tissue homeostasis.
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