{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T11:08:01Z","timestamp":1779188881126,"version":"3.51.4"},"reference-count":32,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2012,9,28]],"date-time":"2012-09-28T00:00:00Z","timestamp":1348790400000},"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; Rheumatism"],"published-print":{"date-parts":[[2012,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>To analyze the mechanism for the therapeutic effects of tumor necrosis factor \u03b1 (TNF\u03b1) inhibition in a murine model of systemic lupus erythematosus.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We used the (NZB \u00d7 NZW)F<jats:sub>1<\/jats:sub> (NZB\/NZW) mouse model of interferon\u2010\u03b1\u2013induced lupus nephritis and treated mice with TNF receptor type II (TNFRII) Ig after TNF\u03b1 expression was detected in the kidneys. Autoantibodies were measured by enzyme\u2010linked immunosorbent assay (ELISA), and autoantibody\u2010 forming cells were determined using an enzyme\u2010linked immunospot assay. Activation of splenocytes was analyzed by flow cytometry. Kidneys were harvested and analyzed using flow cytometry, immunohistochemistry, ELISA, Western blotting, and real\u2010time polymerase chain reaction.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>TNFRII Ig treatment stabilized nephritis and markedly prolonged survival. Autoantibody production and systemic immune activation were not inhibited, but the renal response to glomerular immune complex deposition was attenuated. This was associated with decreases in renal production of chemokines, renal endothelial cell activation, interstitial F4\/80<jats:sup>high<\/jats:sup> macrophage accumulation, tubular damage, and oxidative stress. In contrast, perivascular lymphoid aggregates containing B cells, T cells, and dendritic cells accumulated unabated.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Our data suggest that TNF\u03b1 is a critical cytokine that amplifies the response of the nephron to immune complex deposition, but that it has less influence on the response of the systemic vasculature to inflammation.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.34553","type":"journal-article","created":{"date-parts":[[2012,9,30]],"date-time":"2012-09-30T18:14:59Z","timestamp":1349028899000},"page":"3399-3408","source":"Crossref","is-referenced-by-count":35,"title":["Anti\u2013tumor necrosis factor \u03b1 treatment of interferon\u2010\u03b1\u2013induced murine lupus nephritis reduces the renal macrophage response but does not alter glomerular immune complex formation"],"prefix":"10.1002","volume":"64","author":[{"given":"Ramalingam","family":"Bethunaickan","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ranjit","family":"Sahu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zheng","family":"Liu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yi 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