{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T19:26:03Z","timestamp":1790018763706,"version":"4.0.1"},"reference-count":60,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2004,10,1]],"date-time":"2004-10-01T00:00:00Z","timestamp":1096588800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2004,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Inflammation in the kidney and other tissues (lung, and salivary and lacrimal glands) is characteristic of MRL-Faslpr mice with features of lupus. Macrophages (M\u03c6) are prominent in these tissues. Given that 1) M\u03c6 survival, recruitment, proliferation, and activation during inflammation is dependent on CSF-1, 2) M\u03c6 mediate renal resident cell apoptosis, and 3) CSF-1 is up-regulated in MRL-Faslpr mice before, and during nephritis, we hypothesized that CSF-1-deficient MRL-Faslpr mice would be protected from M\u03c6-mediated nephritis, and the systemic illness. To test this hypothesis, we compared CSF-1-deficient MRL-Faslpr with wild-type strains. Renal pathology is suppressed and function improved in CSF-1-deficient MRL-Faslpr mice. There are far fewer intrarenal M\u03c6 and T cells in CSF-1-deficient MRL-Faslpr vs wild-type kidneys. This leukocytic reduction results from suppressed infiltration, and intrarenal proliferation, but not enhanced apoptosis. The CSF-1-deficient MRL-Faslpr kidneys remain preserved as indicated by greatly reduced indices of injury (nephritogenic cytokines, tubular apoptosis, and proliferation). The renal protective mechanism in CSF-1-deficient mice is not limited to reduced intrarenal leukocytes; circulating Igs and autoantibodies, and renal Ig deposits are decreased. This may result from enhanced B cell apoptosis and fewer B cells in CSF-1-deficient MRL-Faslpr mice. Furthermore, the systemic illness including, skin, lung, and lacrimal and salivary glands pathology, lymphadenopathy, and splenomegaly are dramatically suppressed in CSF-1-deficient MRL-Faslpr as compared with wild-type mice. These results indicate that CSF-1 is an attractive therapeutic target to combat M\u03c6-, T cell-, and B cell-mediated autoimmune lupus.<\/jats:p>","DOI":"10.4049\/jimmunol.173.7.4744","type":"journal-article","created":{"date-parts":[[2014,4,21]],"date-time":"2014-04-21T02:56:23Z","timestamp":1398048983000},"page":"4744-4754","source":"Crossref","is-referenced-by-count":64,"title":["Negative Role of Colony-Stimulating Factor-1 in Macrophage, T Cell, and B Cell Mediated Autoimmune Disease in MRL-<i>Fas<\/i>\n                  <i>lpr<\/i> Mice"],"prefix":"10.1093","volume":"173","author":[{"given":"Deborah M","family":"Lenda","sequence":"first","affiliation":[{"name":"Laboratory of Molecular Autoimmune Disease, Renal Division, Brigham and Women\u2019s Hospital, Harvard University Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E Richard","family":"Stanley","sequence":"additional","affiliation":[{"name":"Department of Developmental and Molecular Biology, Albert Einstein College of Medicine , Bronx, NY 10461"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vicki R","family":"Kelley","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Autoimmune Disease, Renal Division, Brigham and Women\u2019s Hospital, Harvard University Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2004,10,1]]},"reference":[{"key":"2025032617342883900_R1","first-page":"179","volume-title":"Immunol. 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