{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T08:47:24Z","timestamp":1790153244626,"version":"4.0.1"},"reference-count":59,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T00:00:00Z","timestamp":1782864000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Systemic sclerosis (SSc) is a severe autoimmune disease characterized by immune dysregulation, fibrosis, and substantial morbidity and mortality. Although type I interferon-related pathways have been implicated in SSc, the contribution of Toll-like receptor 7 (TLR7) and its downstream signaling, including the transcription factor interferon regulatory factor 7 (IRF7) and effector molecules such as CCL2 and CCL12, to disease pathogenesis remains unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We used a bleomycin (BLM)-induced mouse model of SSc. Male wild-type (WT),\n                      <jats:italic>Tlr7<\/jats:italic>\n                      -deficient (\n                      <jats:italic>\n                        Tlr7\n                        <jats:sup>\u2212<\/jats:sup>\n                        \/\n                        <jats:sup>\u2212<\/jats:sup>\n                      <\/jats:italic>\n                      ), and\n                      <jats:italic>Irf7<\/jats:italic>\n                      -deficient (\n                      <jats:italic>\n                        Irf7\n                        <jats:sup>\u2212<\/jats:sup>\n                        \/\n                        <jats:sup>\u2212<\/jats:sup>\n                      <\/jats:italic>\n                      ) mice (10\u201312 weeks old) received daily subcutaneous BLM (2.5 mg\/kg\/day) for 4 weeks. In a separate experiment, BLM-treated WT mice were treated with the CCR2 antagonist (RS504393). Disease features were evaluated by histopathology, ELISA, flow cytometry, western blotting, RT-qPCR, and Olink proteomics.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      BLM-treated\n                      <jats:italic>\n                        Tlr7\n                        <jats:sup>\u2212<\/jats:sup>\n                        \/\n                        <jats:sup>\u2212<\/jats:sup>\n                      <\/jats:italic>\n                      and\n                      <jats:italic>\n                        Irf7\n                        <jats:sup>\u2212<\/jats:sup>\n                        \/\n                        <jats:sup>\u2212<\/jats:sup>\n                      <\/jats:italic>\n                      mice showed less body weight loss, reduced pulmonary interstitial inflammation, fewer inflammatory monocytes in the spleen, lower pulmonary type I interferon-related gene expression, and lower serum anti-topoisomerase I autoantibody (anti-Scl-70) levels. Pharmacologic CCR2 antagonism attenuated BLM-induced body weight loss, lung injury, and reduced dermal collagen deposition.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>These findings support a pathogenic role for TLR7-IRF7-IFN-I signaling in anti-Scl-70 autoantibody production and pulmonary inflammation in experimental SSc, and suggest that downstream chemokine pathways may represent therapeutic targets.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1823229","type":"journal-article","created":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T06:33:56Z","timestamp":1782887636000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":2,"title":["TLR7 signaling aggravates lung inflammation associated with increased anti-Scl-70 autoantibody production in murine bleomycin-induced systemic sclerosis"],"prefix":"10.3389","volume":"17","author":[{"given":"Jefferson Fernandes","family":"Evangelista","sequence":"first","affiliation":[{"name":"Division of Comparative Pathology, Tulane National Biomedical Center","place":["Covington, LA, United States"]},{"name":"Department of Microbiology and Immunology, Tulane University School of Medicine","place":["New Orleans, LA, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ana Karina","family":"Nisperuza Vidal","sequence":"additional","affiliation":[{"name":"Division of Comparative Pathology, Tulane National Biomedical Center","place":["Covington, LA, United States"]},{"name":"Department of Microbiology and Immunology, Tulane University School of Medicine","place":["New Orleans, LA, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Donghua","family":"Xu","sequence":"additional","affiliation":[{"name":"Division of Comparative Pathology, Tulane 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