{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T15:24:55Z","timestamp":1781105095931,"version":"3.54.1"},"reference-count":31,"publisher":"National Academy of Sciences","issue":"34","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2006,8,22]]},"abstract":"\n Rats and mice with a lower capacity to produce reactive oxygen species (ROS) because of allelic polymorphisms in the\n Ncf1<\/jats:italic>\n gene (which encodes neutrophil cytosolic factor 1) are more susceptible to develop severe arthritis. These data suggest that ROS are involved in regulating the immune response. We now show that the lower capacity to produce ROS is associated with an increased number of reduced thiol groups (\u2212SH) on T cell membrane surfaces. Artificially increasing the number of reduced thiols on T cells from animals with arthritis-protective\n Ncf1<\/jats:italic>\n alleles by glutathione treatment lowered the threshold for T cell reactivity and enhanced proliferative responses\n in vitro<\/jats:italic>\n and\n in vivo<\/jats:italic>\n . Importantly, T cells from immunized congenic rats with an E3-derived Ncf1 allele (DA.\n \n Ncf1\n E3<\/jats:sup>\n <\/jats:italic>\n rats) that cannot transfer arthritis to rats with an arthritis-associated Dark Agouti (DA)-derived mutated Ncf1 allele (DA.\n \n Ncf1\n DA<\/jats:sup>\n <\/jats:italic>\n rats) became arthritogenic after increasing cell surface thiol levels. This finding was confirmed by the reverse experiment, in which oxidized T cells from DA.\n \n Ncf1\n DA<\/jats:sup>\n <\/jats:italic>\n rats induced less severe arthritis compared with controls. Therefore, we conclude that ROS production as controlled by\n Ncf1<\/jats:italic>\n is important in regulating surface redox levels of T cells and thereby suppresses autoreactivity and arthritis development.\n <\/jats:p>","DOI":"10.1073\/pnas.0604571103","type":"journal-article","created":{"date-parts":[[2006,8,14]],"date-time":"2006-08-14T20:34:00Z","timestamp":1155587640000},"page":"12831-12836","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":211,"title":["T cell surface redox levels determine T cell reactivity and arthritis susceptibility"],"prefix":"10.1073","volume":"103","author":[{"given":"Kyra A.","family":"Gelderman","sequence":"first","affiliation":[{"name":"Medical Inflammation Research, Biomedical Center I11, Lund University, SE-221 84 Lund, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Malin","family":"Hultqvist","sequence":"additional","affiliation":[{"name":"Medical Inflammation Research, Biomedical Center I11, Lund University, SE-221 84 Lund, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jens","family":"Holmberg","sequence":"additional","affiliation":[{"name":"Medical Inflammation Research, Biomedical Center I11, Lund University, SE-221 84 Lund, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter","family":"Olofsson","sequence":"additional","affiliation":[{"name":"Medical Inflammation Research, Biomedical Center I11, Lund University, SE-221 84 Lund, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rikard","family":"Holmdahl","sequence":"additional","affiliation":[{"name":"Medical Inflammation Research, Biomedical Center I11, Lund University, SE-221 84 Lund, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2006,8,22]]},"reference":[{"key":"e_1_3_4_1_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9343(00)00481-2"},{"key":"e_1_3_4_2_2","doi-asserted-by":"publisher","DOI":"10.1186\/ar1447"},{"key":"e_1_3_4_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/ng1058"},{"key":"e_1_3_4_4_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0403831101"},{"key":"e_1_3_4_5_2","doi-asserted-by":"publisher","DOI":"10.1002\/jlb.67.2.210"},{"key":"e_1_3_4_6_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.176.2.1172"},{"key":"e_1_3_4_7_2","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2005.7.964"},{"key":"e_1_3_4_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.abb.2004.11.015"},{"key":"e_1_3_4_9_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.2434516100"},{"key":"e_1_3_4_10_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.175.4.2158"},{"key":"e_1_3_4_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0968-0004(03)00057-4"},{"key":"e_1_3_4_12_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.0022-202X.2005.23851.x"},{"key":"e_1_3_4_13_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.022630299"},{"key":"e_1_3_4_14_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.164.4.2170"},{"key":"e_1_3_4_15_2","doi-asserted-by":"crossref","first-page":"1354","DOI":"10.4049\/jimmunol.160.3.1354","volume":"160","author":"Lahdenpohja N.","year":"1998","unstructured":"N. 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