PMID- 31681306 OWN - NLM STAT- MEDLINE DCOM- 20201109 LR - 20240421 IS - 1664-3224 (Electronic) IS - 1664-3224 (Linking) VI - 10 DP - 2019 TI - Dendritic Cells as Sensors, Mediators, and Regulators of Ischemic Injury. PG - 2418 LID - 10.3389/fimmu.2019.02418 [doi] LID - 2418 AB - Dendritic cells (DCs) are highly specialized, bone marrow (BM)-derived antigen-processing and -presenting cells crucial to the induction, integration and regulation of innate, and adaptive immunity. They are stimulated by damage-associated molecular patterns (DAMPS) via pattern recognition receptors to promote inflammation and initiate immune responses. In addition to residing within the parenchyma of all organs as part of the heterogeneous mononuclear phagocyte system, DCs are an abundant component of the inflammatory cell infiltrate that appears in response to ischemia reperfusion injury (IRI). They can play disparate roles in the pathogenesis of IRI since their selective depletion has been found to be protective, deleterious, or of no benefit in mouse models of IRI. In addition, administration of DC generated and manipulated ex vivo can protect organs from IRI by suppressing inflammatory cytokine production, limiting the capacity of DCs to activate NKT cells, or enhancing regulatory T cell function. Few studies however have investigated specific signal transduction mechanisms underlying DC function and how these affect IRI. Here, we address current knowledge of the role of DCs in regulation of IRI, current gaps in understanding and prospects for innovative therapeutic intervention at the biological and pharmacological levels. CI - Copyright (c) 2019 Dai, Thomson and Rogers. FAU - Dai, Helong AU - Dai H AD - Department of Urological Organ Transplantation, The Second Xiangya Hospital of Central South University, Changsha, China. AD - Clinical Research Center for Organ Transplantation of Hunan Province, Changsha, China. FAU - Thomson, Angus W AU - Thomson AW AD - Department of Surgery, Thomas E. Starzl Transplantation Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States. AD - Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States. FAU - Rogers, Natasha M AU - Rogers NM AD - Department of Surgery, Thomas E. Starzl Transplantation Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States. AD - Center for Transplant and Renal Research, Westmead Institute for Medical Research, Westmead, NSW, Australia. AD - Renal Division, Westmead Hospital, Westmead, NSW, Australia. AD - Westmead Clinical School, University of Sydney, Camperdown, NSW, Australia. LA - eng GR - R01 AI118777/AI/NIAID NIH HHS/United States GR - R21 AI137799/AI/NIAID NIH HHS/United States GR - U19 AI131453/AI/NIAID NIH HHS/United States GR - U01 AI136779/AI/NIAID NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't PT - Review DEP - 20191015 PL - Switzerland TA - Front Immunol JT - Frontiers in immunology JID - 101560960 RN - 0 (Biomarkers) SB - IM MH - Animals MH - Biomarkers MH - Cell Communication MH - Cell Plasticity/immunology MH - Dendritic Cells/*immunology/*metabolism MH - *Disease Susceptibility MH - Humans MH - Hypoxia/genetics/immunology/metabolism MH - *Immunity MH - *Immunomodulation MH - Ischemia/*etiology/*metabolism MH - Ischemic Preconditioning MH - Organ Specificity MH - Phenotype MH - Reperfusion Injury/etiology/metabolism/pathology PMC - PMC6803430 OTO - NOTNLM OT - dendritic cells OT - heart OT - ischemic injury OT - kidney OT - liver EDAT- 2019/11/05 06:00 MHDA- 2020/11/11 06:00 PMCR- 2019/01/01 CRDT- 2019/11/05 06:00 PHST- 2019/08/13 00:00 [received] PHST- 2019/09/27 00:00 [accepted] PHST- 2019/11/05 06:00 [entrez] PHST- 2019/11/05 06:00 [pubmed] PHST- 2020/11/11 06:00 [medline] PHST- 2019/01/01 00:00 [pmc-release] AID - 10.3389/fimmu.2019.02418 [doi] PST - epublish SO - Front Immunol. 2019 Oct 15;10:2418. doi: 10.3389/fimmu.2019.02418. eCollection 2019.