{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:59:06Z","timestamp":1787018346057,"version":"build-2736575974"},"reference-count":23,"publisher":"American Society for Clinical Investigation","issue":"2","funder":[{"DOI":"10.13039\/501100007423","name":"Duchenne Parent Project","doi-asserted-by":"crossref","award":["B51I180002,000"],"award-info":[{"award-number":["B51I180002,000"]}],"id":[{"id":"10.13039\/501100007423","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2020,1,30]]},"abstract":"<jats:p>\n                    Dystrophic muscle is characterized by chronic injury and a steady recruitment of inflammatory Ly6C\n                    <jats:sup>hi<\/jats:sup>\n                    monocytes. Recent studies have identified the spleen as the dominant reservoir of these cells during chronic inflammation. Here, we investigated the contribution of splenic Ly6C\n                    <jats:sup>hi<\/jats:sup>\n                    monocytes to dystrophic muscle pathology. Using the\n                    <jats:italic>mdx<\/jats:italic>\n                    mouse model of muscular dystrophy, we show that Ly6C\n                    <jats:sup>hi<\/jats:sup>\n                    monocytes accumulate in great numbers in the spleen over the course of the disease. The chemokine receptor CCR2 was upregulated on Ly6C\n                    <jats:sup>hi<\/jats:sup>\n                    monocytes in\n                    <jats:italic>mdx<\/jats:italic>\n                    spleen before disease onset, thereby enabling their recruitment to dystrophic muscle. Splenectomy performed before disease onset significantly reduced the number of Ly6C\n                    <jats:sup>hi<\/jats:sup>\n                    monocytes infiltrating dystrophic limb muscle. Moreover, in the absence of splenic Ly6C\n                    <jats:sup>hi<\/jats:sup>\n                    monocytes there was a significant reduction in dystrophic muscle inflammation and necrosis, along with improved regeneration during early disease. However, during late disease, a lack of splenic Ly6C\n                    <jats:sup>hi<\/jats:sup>\n                    monocytes adversely affected muscle fiber repair, due to a delay in the phenotypic shift of proinflammatory F4\/80\n                    <jats:sup>+<\/jats:sup>\n                    Ly6C\n                    <jats:sup>hi<\/jats:sup>\n                    CD206\n                    <jats:sup>lo<\/jats:sup>\n                    to antiinflammatory F4\/80\n                    <jats:sup>+<\/jats:sup>\n                    Ly6C\n                    <jats:sup>lo<\/jats:sup>\n                    CD206\n                    <jats:sup>+<\/jats:sup>\n                    macrophages. Overall, we show that the spleen is an indispensable source of Ly6C\n                    <jats:sup>hi<\/jats:sup>\n                    monocytes in muscular dystrophy and that splenic monocytes are critical players in both muscle fiber injury and repair.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.130807","type":"journal-article","created":{"date-parts":[[2019,12,24]],"date-time":"2019-12-24T12:01:30Z","timestamp":1577188890000},"source":"Crossref","is-referenced-by-count":46,"title":["Splenic Ly6Chi monocytes are critical players in dystrophic muscle injury and repair"],"prefix":"10.1172","volume":"5","author":[{"given":"Giuseppe","family":"Rizzo","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rosanna","family":"Di Maggio","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anna","family":"Benedetti","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jacopo","family":"Morroni","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0938-5360","authenticated-orcid":true,"given":"Marina","family":"Bouche","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Biliana","family":"Lozanoska-Ochser","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"232","published-online":{"date-parts":[[2020,1,30]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(02)07815-7"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1126\/scitranslmed.aaa7322"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.pmrj.2009.04.010"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-8966(01)00198-5"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1080\/21675511.2015.1010966"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1002\/path.5016"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2018.10.005"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/j.it.2011.05.001"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1038\/nri.2017.42"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1126\/science.1175202"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1172\/JCI62636"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20111009"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.111.061986"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/nri.2016.150"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2016.10.026"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1097\/NEN.0b013e3182a7f0b8"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20171274"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20170689"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.15252\/emmm.201403967"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1096\/fj.201600619R"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajpath.2013.12.020"},{"issue":"18","key":"B22","doi-asserted-by":"crossref","DOI":"10.1172\/jci.insight.121549","article-title":"Chronic infection stunts macrophage heterogeneity and disrupts immune-mediated myogenesis","volume":"3","author":"Jin","year":"2018","journal-title":"JCI Insight"},{"key":"B23","doi-asserted-by":"publisher","DOI":"10.1016\/j.ebiom.2017.01.001"}],"container-title":["JCI Insight"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/insight.jci.org\/articles\/view\/130807\/files\/pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T12:19:22Z","timestamp":1779193162000},"score":1,"resource":{"primary":{"URL":"https:\/\/insight.jci.org\/articles\/view\/130807"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2020,1,30]]},"references-count":23,"journal-issue":{"issue":"2","published-online":{"date-parts":[[2020,1,30]]},"published-print":{"date-parts":[[2020,1,30]]}},"alternative-id":["10.1172\/jci.insight.130807"],"URL":"https:\/\/doi.org\/10.1172\/jci.insight.130807","relation":{},"ISSN":["2379-3708"],"issn-type":[{"value":"2379-3708","type":"electronic"}],"subject":[],"published":{"date-parts":[[2020,1,30]]},"article-number":"e130807"}}