{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,11,23]],"date-time":"2023-11-23T22:59:53Z","timestamp":1700780393806},"reference-count":36,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2005,12,9]],"date-time":"2005-12-09T00:00:00Z","timestamp":1134086400000},"content-version":"vor","delay-in-days":5790,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Arthritis &amp; Rheumatism"],"published-print":{"date-parts":[[1990,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The purpose of this study was to analyze T suppressor cell function in juvenile rheumatoid arthritis (JRA). JRA is a chronic inflammatory childhood disease of unknown etiology that is characterized by arthritis and immunoregulatory abnormalities. T suppressor cell precursors (CD8+, CD28\u2212) were purified from the peripheral blood of 24 JRA patients, using a combination of monoclonal antibodies. These cells were treated with histamine or concanavalin A, agents that are known to induce suppressor activity. They were also tested for their ability to inhibit the proliferative response of autologous T cells to phytohemagglutinin. In some experiments, the accumulation of intracellular cAMP following histamine treatment was also measured. Twelve of 13 patients with clinically active JRA showed abnormal histamine\u2010inducible T suppressor cell function, characterized by the failure of CD8+, CD28\u2212 T cells to mediate any detectable suppression. The failure of these cells to accumulate intracellular cAMP after histamine treatment was observed in 5 of 5 patients tested who had active disease. In contrast, 11 of 11 patients with clinically inactive JRA, 5 of 5 patients with cystic fibrosis, and 9 of 9 pediatric control subjects had normal histamine\u2010and concanavalin A\u2010inducible T suppressor cell function, and a normal cAMP response to histamine. These results suggest that patients with clinically active JRA have a reversible defect in T suppressor cell function that is associated with a failure of T suppressor cell precursors to accumulate intracellular cAMP following their exposure to selected immune stimuli.<\/jats:p>","DOI":"10.1002\/art.1780330208","type":"journal-article","created":{"date-parts":[[2007,2,14]],"date-time":"2007-02-14T23:03:53Z","timestamp":1171494233000},"page":"205-211","source":"Crossref","is-referenced-by-count":18,"title":["Abnormal t suppressor cell function in juvenile rheumatoid arthritis"],"prefix":"10.1002","volume":"33","author":[{"given":"Earl D.","family":"Silverman","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Catherine","family":"Somma","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Manzoor M.","family":"Khan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kenneth L.","family":"Melmon","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Edgar G.","family":"Engleman","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2005,12,9]]},"reference":[{"key":"e_1_2_1_2_2","first-page":"125","article-title":"Loss of suppressor T\u2010lymphocyte function in patients with systemic lupus erythematosus (SLE).","volume":"32","author":"Morimoto C","year":"1978","journal-title":"Clin Exp Immunol"},{"key":"e_1_2_1_3_2","doi-asserted-by":"crossref","first-page":"1972","DOI":"10.4049\/jimmunol.129.5.1972","article-title":"Analysis of suppressor T cell function in patients with rheumatoid arthritis: defects in production of and responsiveness to concanavalin A\u2010induced suppressor T 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