{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T14:51:49Z","timestamp":1790434309180,"version":"4.1.0"},"reference-count":69,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2013,9,1]],"date-time":"2013-09-01T00:00:00Z","timestamp":1377993600000},"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":[[2013,9,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Loss-of-function mutations in the Fas death receptor or its ligand result in a lymphoproliferative syndrome and exacerbate clinical disease in most lupus-prone strains of mice. One exception is mice injected with 2,6,10,14-tetramethylpentadecane (TMPD), a hydrocarbon oil commonly known as pristane, which induces systemic lupus erythematosus\u2013like disease. Although Fas\/Fas ligand (FasL) interactions have been strongly implicated in the activation-induced cell death of both lymphocytes and other APCs, FasL can also trigger the production of proinflammatory cytokines. FasL is a transmembrane protein with a matrix metalloproteinase cleavage site in the ectodomain. Matrix metalloproteinase cleavage inactivates membrane-bound FasL and releases a soluble form reported to have both antagonist and agonist activity. To better understand the impact of FasL cleavage on both the proapoptotic and proinflammatory activity of FasL, its cleavage site was deleted through targeted mutation to produce the deleted cleavage site (\u0394CS) mouse line. \u0394CS mice express higher levels of membrane-bound FasL than do wild-type mice and fail to release soluble FasL. To determine to what extent FasL promotes inflammation in lupus mice, TMPD-injected FasL-deficient and \u0394CS BALB\/c mice were compared with control TMPD-injected BALB\/c mice. We found that FasL deficiency significantly reduced the early inflammatory exudate induced by TMPD injection. In contrast, \u0394CS mice developed a markedly exacerbated disease profile associated with a higher frequency of splenic neutrophils and macrophages, a profound change in anti-nuclear Ab specificity, and markedly increased proteinuria and kidney pathology compared with controls. These results demonstrate that FasL promotes inflammation in TMPD-induced autoimmunity, and its cleavage limits FasL proinflammatory activity.<\/jats:p>","DOI":"10.4049\/jimmunol.1300341","type":"journal-article","created":{"date-parts":[[2013,8,6]],"date-time":"2013-08-06T05:33:19Z","timestamp":1375767199000},"page":"2104-2114","source":"Crossref","is-referenced-by-count":22,"title":["Overexpression of Membrane-Bound Fas Ligand (CD95L) Exacerbates Autoimmune Disease and Renal Pathology in Pristane-Induced Lupus"],"prefix":"10.1093","volume":"191","author":[{"given":"Lukas","family":"Bossaller","sequence":"first","affiliation":[{"name":"Division of Infectious Diseases and Immunology, University of Massachusetts Medical School , Worcester, MA 01605"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vijay A K","family":"Rathinam","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases and Immunology, University of Massachusetts Medical School , Worcester, MA 01605"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ramon","family":"Bonegio","sequence":"additional","affiliation":[{"name":"Renal Section, Department of Medicine, Boston University Medical Center , Boston, MA 02118"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ping-I","family":"Chiang","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases and Immunology, University of Massachusetts Medical School , Worcester, MA 01605"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patricia","family":"Busto","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Department of Medicine, University of Massachusetts Medical School , Worcester, MA 01605"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adam R","family":"Wespiser","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases and Immunology, University of Massachusetts Medical School , Worcester, MA 01605"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel R","family":"Caffrey","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases and Immunology, University of Massachusetts Medical School , Worcester, MA 01605"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Quan-Zhen","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Immunology and Medicine, University of Texas Southwestern Medical Center , Dallas, TX 75390"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chandra","family":"Mohan","sequence":"additional","affiliation":[{"name":"Department of Immunology and Medicine, University of Texas Southwestern Medical Center , Dallas, TX 75390"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katherine A","family":"Fitzgerald","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases and Immunology, University of Massachusetts Medical School , Worcester, MA 01605"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eicke","family":"Latz","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases and Immunology, University of Massachusetts Medical School , Worcester, MA 01605"},{"name":"Institute of Innate Immunity, University of Bonn , 53127 Bonn,","place":["Germany"]},{"name":"German Center for Neurodegenerative Diseases , 53127 Bonn,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ann","family":"Marshak-Rothstein","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Department of Medicine, University of Massachusetts Medical School , Worcester, MA 01605"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2013,9,1]]},"reference":[{"key":"2025032405251115300_r1","doi-asserted-by":"crossref","first-page":"314","DOI":"10.1038\/356314a0","article-title":"Lymphoproliferation disorder in mice explained by defects in Fas antigen that mediates apoptosis","volume":"356","author":"Watanabe-Fukunaga","year":"1992","journal-title":"Nature"},{"key":"2025032405251115300_r2","doi-asserted-by":"crossref","first-page":"1449","DOI":"10.1126\/science.7533326","article-title":"The Fas death factor","volume":"267","author":"Nagata","year":"1995","journal-title":"Science"},{"key":"2025032405251115300_r3","doi-asserted-by":"crossref","first-page":"444","DOI":"10.1038\/373444a0","article-title":"Fas(CD95)\/FasL interactions required for programmed cell death after T-cell activation","volume":"373","author":"Ju","year":"1995","journal-title":"Nature"},{"key":"2025032405251115300_r4","doi-asserted-by":"crossref","first-page":"6217","DOI":"10.4049\/jimmunol.167.11.6217","article-title":"Fas ligand engagement of resident peritoneal macrophages in vivo induces apoptosis and the production of neutrophil chemotactic factors","volume":"167","author":"Hohlbaum","year":"2001","journal-title":"J. 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