{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T19:33:55Z","timestamp":1789760035405,"version":"4.0.1"},"reference-count":54,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2009,9,1]],"date-time":"2009-09-01T00:00:00Z","timestamp":1251763200000},"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":[[2009,9,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Because IL-1\u03b2 plays an important role in inflammation in human and murine arthritis, we investigated the contribution of the inflammasome components ASC, NALP-3, IPAF, and caspase-1 to inflammatory arthritis. We first studied the phenotype of ASC-deficient and wild-type mice during Ag-induced arthritis (AIA). ASC\u2212\/\u2212 mice showed reduced severity of AIA, decreased levels of synovial IL-1\u03b2, and diminished serum amyloid A levels. In contrast, mice deficient in NALP-3, IPAF, or caspase-1 did not show any alteration of joint inflammation, thus indicating that ASC associated effects on AIA are independent of the classical NALP-3 or IPAF inflammasomes. Because ASC is a ubiquitous cytoplasmic protein that has been implicated in multiple cellular processes, we explored other pathways through which ASC may modulate inflammation. Ag-specific proliferation of lymph node and spleen cells from ASC-deficient mice was significantly decreased in vitro, as was the production of IFN-\u03b3, whereas IL-10 production was enhanced. TCR ligation by anti-CD3 Abs in the presence or absence of anti-CD28 Abs induced a reduction in T cell proliferation in ASC\u2212\/\u2212 T cells compared with wild-type ones. In vivo lymph node cell proliferation was also significantly decreased in ASC\u2212\/\u2212 mice, but no effects on apoptosis were observed either in vitro or in vivo in these mice. In conclusion, these results strongly suggest that ASC modulates joint inflammation in AIA through its effects on cell-mediated immune responses but not via its implication in inflammasome formation.<\/jats:p>","DOI":"10.4049\/jimmunol.0802173","type":"journal-article","created":{"date-parts":[[2009,8,28]],"date-time":"2009-08-28T20:44:23Z","timestamp":1251492263000},"page":"4003-4012","source":"Crossref","is-referenced-by-count":72,"title":["Inflammatory Role of ASC in Antigen-Induced Arthritis Is Independent of Caspase-1, NALP-3, and IPAF"],"prefix":"10.1093","volume":"183","author":[{"given":"Laeticia","family":"Kolly","sequence":"first","affiliation":[{"name":"Service of Rheumatology, D\u00e9partement de l\u2019Appareil Locomoteur"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mahir","family":"Karababa","sequence":"additional","affiliation":[{"name":"Service of Rheumatology, D\u00e9partement de l\u2019Appareil Locomoteur"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leo A B","family":"Joosten","sequence":"additional","affiliation":[{"name":"Rheumatology Research and Advanced Therapeutics, Department of Rheumatology, Radboud University Nijmegen Medical Centre , Nijmegen,","place":["The Netherlands"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sharmal","family":"Narayan","sequence":"additional","affiliation":[{"name":"Service of Rheumatology, D\u00e9partement de l\u2019Appareil Locomoteur"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roberto","family":"Salvi","sequence":"additional","affiliation":[{"name":"Service of Rheumatology, D\u00e9partement de l\u2019Appareil Locomoteur"},{"name":"Service of Endocrinology, Centre Hospitalier Universitaire Vaudois and University of Lausanne"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Virginie","family":"P\u00e9trilli","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, University of Lausanne , Lausanne,","place":["Switzerland"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jurg","family":"Tschopp","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, University of Lausanne , Lausanne,","place":["Switzerland"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wim B","family":"van den Berg","sequence":"additional","affiliation":[{"name":"Rheumatology Research and Advanced Therapeutics, Department of Rheumatology, Radboud University Nijmegen Medical Centre , Nijmegen,","place":["The Netherlands"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander Kai-Lik","family":"So","sequence":"additional","affiliation":[{"name":"Service of Rheumatology, D\u00e9partement de l\u2019Appareil Locomoteur"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nathalie","family":"Busso","sequence":"additional","affiliation":[{"name":"Service of Rheumatology, D\u00e9partement de l\u2019Appareil Locomoteur"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2009,9,15]]},"reference":[{"key":"2026012811223743300_R1","first-page":"8749","article-title":"Interleukin 1 induces leukocyte infiltration and cartilage proteoglycan degradation in the synovial joint.","volume-title":"Proc. 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