{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,28]],"date-time":"2025-10-28T18:29:21Z","timestamp":1761676161679,"version":"3.40.3"},"reference-count":31,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2005,9,1]],"date-time":"2005-09-01T00:00:00Z","timestamp":1125532800000},"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":[[2005,9,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>One hundred ten to 120-kDa fragments of fibronectin (FNf), generated by proteases released in the course of tissue injury and inflammation, stimulate monocytes to produce proinflammatory cytokines, promote mononuclear leukocytes (MNL) transendothelial migration, up-regulate monocyte CD11b and CD86 expression, and induce monocyte-derived dendritic cell differentiation. To investigate whether the proinflammatory consequences of FNf are offset by responses that can suppress proliferation of activated T lymphocytes, we investigated the effect of FNf-treated MNL on autologous T lymphocytes induced to proliferate by substrate-immobilized anti-CD3. FNf-stimulated MNL suppressed anti-CD3-induced T cell proliferation through both contact-dependent and contact-independent mechanisms. Contact-independent suppression was mediated, at least in part, by IL-10 and TGF-\u03b2 released by the FNf-stimulated MNL. After 24\u201348 h exposure to FNf, activated T cells and monocytes formed clusters displaying CD25, CD14, CD3, and CD4 that were not dissociable by chelation of divalent cations. Killing monocytes with l-leucine methyl ester abolished these T cell-monocyte clusters and the ability of the FNf-stimulated MNL to suppress anti-CD3 induced T cell proliferation. Thus, in addition to activating MNL and causing them to migrate to sites of injury, FNf appears to induce suppressor monocytes.<\/jats:p>","DOI":"10.4049\/jimmunol.175.5.3347","type":"journal-article","created":{"date-parts":[[2014,4,24]],"date-time":"2014-04-24T13:44:04Z","timestamp":1398347044000},"page":"3347-3353","source":"Crossref","is-referenced-by-count":8,"title":["Monocytes Stimulated by 110-kDa Fibronectin Fragments Suppress Proliferation of Anti-CD3-Activated T Cells"],"prefix":"10.1093","volume":"175","author":[{"given":"Holly H","family":"Birdsall","sequence":"first","affiliation":[{"name":"Research Center for AIDS and HIV Infections, Immunology Research Laboratory at the Michael E. DeBakey Veterans Affairs Medical Center , Houston, TX 77030"},{"name":"Department of Otorhinolaryngology , Houston, TX 77030"},{"name":"Department of Immunology , Houston, TX 77030"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wendy J","family":"Porter","sequence":"additional","affiliation":[{"name":"Research Center for AIDS and HIV Infections, Immunology Research Laboratory at the Michael E. DeBakey Veterans Affairs Medical Center , Houston, TX 77030"},{"name":"Department of Otorhinolaryngology , Houston, TX 77030"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"JoAnn","family":"Trial","sequence":"additional","affiliation":[{"name":"Research Center for AIDS and HIV Infections, Immunology Research Laboratory at the Michael E. DeBakey Veterans Affairs Medical Center , Houston, TX 77030"},{"name":"Department of Medicine at Baylor College of Medicine , Houston, TX 77030"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Roger D","family":"Rossen","sequence":"additional","affiliation":[{"name":"Research Center for AIDS and HIV Infections, Immunology Research Laboratory at the Michael E. DeBakey Veterans Affairs Medical Center , Houston, TX 77030"},{"name":"Department of Immunology , Houston, TX 77030"},{"name":"Department of Medicine at Baylor College of Medicine , Houston, TX 77030"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2005,9,1]]},"reference":[{"first-page":"419","volume-title":"J. Clin. Invest.","year":"1999","key":"2025032808421235500_R1"},{"first-page":"331","volume-title":"J. Leukocyte Biol.","year":"1991","key":"2025032808421235500_R2"},{"first-page":"1310","volume-title":"J. Clin. 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