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We investigated this issue using the mice model of cardiotoxin (CTX)-induced myoinjury, with or without estrogen level adjustment.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      CTX injection i.m. (tibialis anterior, TA) was performed for preparing mice myoinjury model. Injection s.c. of 17\u03b2-estradiol (E\n                      <jats:sub>2<\/jats:sub>\n                      ) or estrogen receptor antagonist 4-OHT, or ovariectomy (OVX), was used to change estrogen level of animal models in vivo. Serum E\n                      <jats:sub>2<\/jats:sub>\n                      level was evaluated by ELISA. Gene levels of estrogen receptor (ERs) and cytokines\/chemokines in inflamed muscle were monitored by qPCR. Inflammatory infiltration was observed by immunofluorescence. Macrophage and T cell phenotypes were analyzed by FACS. Immunoblotting was used to assess protein levels of ERs and immunomolecules in C\n                      <jats:sub>2<\/jats:sub>\n                      C\n                      <jats:sub>12<\/jats:sub>\n                      myotubes treated with E\n                      <jats:sub>2<\/jats:sub>\n                      or 4-OHT, in the presence of IFN-\u03b3.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We monitored the increased serum E\n                      <jats:sub>2<\/jats:sub>\n                      level and the upregulated ER\u03b2 in regenerated myofibres after myotrauma. The absence of estrogen in vivo resulted in the more severe muscle inflammatory infiltration, involving the recruitment of monocyte\/macrophage and CD4\n                      <jats:sup>+<\/jats:sup>\n                      T cells, and the heightened proinflammatory (M1) macrophage. Moreover, estrogen signaling loss led to Treg cells infiltration decrease, Th1 response elevation in inflamed muscle, and the markedly expression upregulation of immunomolecules in IFN-\u03b3-stimulated C\n                      <jats:sub>2<\/jats:sub>\n                      C\n                      <jats:sub>12<\/jats:sub>\n                      myotubes in vitro.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our data suggest that estrogen is a positive intervention factor for muscle inflammatory response, through its effects on controlling intramuscular infiltration and phenotypes of monocytes\/macrophages, on affecting accumulation and function of Treg cells, and on suppressing Th1 response in inflamed muscle. Our findings also imply an inhibition effect of estrogen on the intrinsic immune behaviors of muscle cells.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s13395-019-0205-2","type":"journal-article","created":{"date-parts":[[2019,7,29]],"date-time":"2019-07-29T04:03:02Z","timestamp":1564372982000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":57,"title":["Estrogen signaling effects on muscle-specific immune responses through controlling the recruitment and function of macrophages and T cells"],"prefix":"10.1186","volume":"9","author":[{"given":"Zhao Hong","family":"Liao","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tao","family":"Huang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiang Wei","family":"Xiao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rui Cai","family":"Gu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun","family":"Ouyang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gang","family":"Wu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hua","family":"Liao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2019,7,29]]},"reference":[{"key":"205_CR1","doi-asserted-by":"publisher","first-page":"134","DOI":"10.3109\/08830185.2015.1018417","volume":"34","author":"L Mirandola","year":"2015","unstructured":"Mirandola L, Wade R, Verma R, Pena C, Hosiriluck N, Figueroa JA, et al. 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