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=== Role in tissue homeostasis === Every tissue harbors its own specialized population of resident macrophages, which entertain reciprocal interconnections with the stroma and functional tissue.<ref>{{cite journal | vauthors = Okabe Y, Medzhitov R | title = Tissue-specific signals control reversible program of localization and functional polarization of macrophages | journal = Cell | volume = 157 | issue = 4 | pages = 832–844 | date = May 2014 | pmid = 24792964 | pmc = 4137874 | doi = 10.1016/j.cell.2014.04.016 }}</ref><ref>{{cite journal | vauthors = Gosselin D, Link VM, Romanoski CE, Fonseca GJ, Eichenfield DZ, Spann NJ, Stender JD, Chun HB, Garner H, Geissmann F, Glass CK | title = Environment drives selection and function of enhancers controlling tissue-specific macrophage identities | journal = Cell | volume = 159 | issue = 6 | pages = 1327–1340 | date = December 2014 | pmid = 25480297 | pmc = 4364385 | doi = 10.1016/j.cell.2014.11.023 }}</ref> These resident macrophages are sessile (non-migratory), provide essential growth factors to support the physiological function of the tissue (e.g. macrophage-neuronal crosstalk in the guts),<ref>{{cite journal | vauthors = Muller PA, Koscsó B, Rajani GM, Stevanovic K, Berres ML, Hashimoto D, Mortha A, Leboeuf M, Li XM, Mucida D, Stanley ER, Dahan S, Margolis KG, Gershon MD, Merad M, Bogunovic M | title = Crosstalk between muscularis macrophages and enteric neurons regulates gastrointestinal motility | journal = Cell | volume = 158 | issue = 2 | pages = 300–313 | date = July 2014 | pmid = 25036630 | pmc = 4149228 | doi = 10.1016/j.cell.2014.04.050 }}</ref> and can actively protect the tissue from inflammatory damage.<ref>{{cite journal | vauthors = Uderhardt S, Martins AJ, Tsang JS, Lämmermann T, Germain RN | title = Resident Macrophages Cloak Tissue Microlesions to Prevent Neutrophil-Driven Inflammatory Damage | journal = Cell | volume = 177 | issue = 3 | pages = 541–555.e17 | date = April 2019 | pmid = 30955887 | pmc = 6474841 | doi = 10.1016/j.cell.2019.02.028 }}</ref>
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