{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T15:12:20Z","timestamp":1791299540733,"version":"4.1.0"},"reference-count":49,"publisher":"Oxford University Press (OUP)","issue":"11","license":[{"start":{"date-parts":[[2005,12,1]],"date-time":"2005-12-01T00:00:00Z","timestamp":1133395200000},"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":[[2005,12,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Systemic lupus erythematosus (SLE), which is characterized by the increased production of autoantibodies and defective T cell responses, can be induced in mice by immunization with a human anti-DNA mAb that expresses a major Id, designated 16\/6Id. A peptide based on the sequence of the CDR1 of the 16\/6Id (human CDR1 (hCDR1)) ameliorated the clinical manifestations of SLE and down-regulated, ex vivo, the 16\/6Id-induced T cell proliferation. In this study, we examined the mechanism responsible for the hCDR1-induced modulation of T cell functions related to the pathogenesis of SLE. We found that injection of hCDR1 into BALB\/c mice concomitant with their immunization with 16\/6Id resulted in a marked elevation of TGF-\u03b2 secretion 10 days later. Addition of TGF-\u03b2 suppressed the 16\/6Id-stimulated T cell proliferation similarly to hCDR1. In addition, we provide evidence that one possible mechanism underlying the hCDR1- and TGF\u03b2-induced inhibition of T cell proliferation is by down-regulating the expression, and therefore the functions, of a pair of key cell adhesion receptors, LFA-1 (\u03b1L\u03b22) and CD44, which operate as accessory molecules in mediating APC-T cell interactions. Indeed, T cells of mice treated with hCDR1 showed a TGF-\u03b2-induced suppression of adhesion to the LFA-1 and CD44 ligands, hyaluronic acid and ICAM-1, respectively, induced by stromal cell-derived factor-1\u03b1 and PMA. The latter suppression is through the inhibition of ERK phosphorylation. Thus, the down-regulation of SLE-associated responses by hCDR1 treatment may be due to the effect of the up-regulated TGF-\u03b2 on the expression and function of T cell adhesion receptors and, consequently, on T cell stimulation, adhesion, and proliferation.<\/jats:p>","DOI":"10.4049\/jimmunol.175.11.7255","type":"journal-article","created":{"date-parts":[[2014,4,21]],"date-time":"2014-04-21T01:05:46Z","timestamp":1398042346000},"page":"7255-7263","source":"Crossref","is-referenced-by-count":29,"title":["The Inhibition of Autoreactive T Cell Functions by a Peptide Based on the CDR1 of an Anti-DNA Autoantibody Is via TGF-\u03b2-Mediated Suppression of LFA-1 and CD44 Expression and Function"],"prefix":"10.1093","volume":"175","author":[{"given":"Uri","family":"Sela","sequence":"first","affiliation":[{"name":"Department of Immunology, Weizmann Institute of Science , Rehovot ,","place":["Israel"]},{"name":"Assaf-Harofeh Medical Center and Sakler Faculty of Medicine, Tel-Aviv University , Tel-Aviv ,","place":["Israel"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nora","family":"Mauermann","sequence":"additional","affiliation":[{"name":"Department of Immunology, Weizmann Institute of Science , Rehovot ,","place":["Israel"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rami","family":"Hershkoviz","sequence":"additional","affiliation":[{"name":"Assaf-Harofeh Medical Center and Sakler Faculty of Medicine, Tel-Aviv University , Tel-Aviv ,","place":["Israel"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Heidy","family":"Zinger","sequence":"additional","affiliation":[{"name":"Department of Immunology, Weizmann Institute of Science , Rehovot ,","place":["Israel"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Molly","family":"Dayan","sequence":"additional","affiliation":[{"name":"Department of Immunology, Weizmann Institute of Science , Rehovot ,","place":["Israel"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liora","family":"Cahalon","sequence":"additional","affiliation":[{"name":"Department of Immunology, Weizmann Institute of Science , Rehovot ,","place":["Israel"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jian Ping","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Immunology, Weizmann Institute of Science , Rehovot ,","place":["Israel"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Edna","family":"Mozes","sequence":"additional","affiliation":[{"name":"Department of Immunology, Weizmann Institute of Science , Rehovot ,","place":["Israel"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ofer","family":"Lider","sequence":"additional","affiliation":[{"name":"Department of Immunology, Weizmann Institute of Science , Rehovot ,","place":["Israel"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2005,12,1]]},"reference":[{"key":"2025032706015931400_R1","first-page":"69","volume-title":"Dubois\u2019 Lupus Erythematosus","year":"1993"},{"key":"2025032706015931400_R2","first-page":"2260","volume-title":"Proc. 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