{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T05:01:53Z","timestamp":1787806913381,"version":"build-2784847793"},"reference-count":50,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2013,12,30]],"date-time":"2013-12-30T00:00:00Z","timestamp":1388361600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Arthritis &amp; Rheumatology"],"published-print":{"date-parts":[[2014,1]]},"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To define the pathogenesis of bone marrow (BM) involvement in systemic lupus erythematosus (SLE).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Tumor necrosis factor \u03b1 (TNF\u03b1) levels, cell death, and cellular damage in BM from SLE patients, controls, and mice with pristane\u2010induced lupus were analyzed using a morphometric technique and immunohistochemistry. The pathogenesis of BM abnormalities was studied in wild\u2010type (WT), TNF\u03b1\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      , Toll\u2010like receptor\u2013deficient (TLR\u20107\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      ), interferon (IFN)\u2013\u03b1\/\u03b2\/\u03c9 receptor\u2013knockout (IFNAR\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      ), and B cell\u2013deficient (\u03bcmt) mice treated with pristane. Flow cytometry was used to examine TNF\u03b1 production (by intracellular staining) and plasma cell\/plasmablast development. CXCL12 expression was determined by quantitative polymerase chain reaction.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      BM from SLE patients exhibited striking death of niche and hematopoietic cells associated with TNF\u03b1 overproduction. BM from mice with a type I IFN\u2013mediated lupus syndrome induced by pristane showed similar abnormalities. TNF\u03b1 was produced mainly by BM neutrophils, many with phagocytosed nuclear material (lupus erythematosus cells). TNF\u03b1 production was abolished in pristane\u2010treated TLR\u20107\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      and \u03bcmt mice but was restored in \u03bcmt mice by infusing normal plasma. Pristane\u2010treated WT and IFNAR\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice developed anemia, BM hypocellularity, and extramedullary hematopoiesis, which were absent in TLR\u20107\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      and TNF\u03b1\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice. Additionally, the expression of CXCL12, which is produced by stromal cells and mediates homing of hematopoietic cells and plasmablasts, was decreased in BM from pristane\u2010treated WT mice but was normal in BM from pristane\u2010treated TNF\u03b1\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Although autoantibodies and glomerulonephritis are type I IFN dependent, lupus\u2010associated BM abnormalities were TLR\u20107 and TNF\u03b1 driven but type I IFN independent, suggesting that lupus is a disorder of innate immunity in which TLR\u20107 activation by phagocytosed nuclei causes relentless type I IFN and TNF\u03b1 production mediating glomerulonephritis and hematologic involvement, respectively.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/art.38189","type":"journal-article","created":{"date-parts":[[2013,9,11]],"date-time":"2013-09-11T05:15:51Z","timestamp":1378876551000},"page":"140-151","source":"Crossref","is-referenced-by-count":56,"title":["Toll\u2010like Receptor 7\u2013Stimulated Tumor Necrosis Factor \u03b1 Causes Bone Marrow Damage in Systemic Lupus Erythematosus"],"prefix":"10.1002","volume":"66","author":[{"given":"Haoyang","family":"Zhuang","sequence":"first","affiliation":[{"name":"University of Florida Gainesville"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuhong","family":"Han","sequence":"additional","affiliation":[{"name":"University of Florida Gainesville"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuan","family":"Xu","sequence":"additional","affiliation":[{"name":"University of Florida 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