{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,3]],"date-time":"2026-11-03T17:13:59Z","timestamp":1793726039745,"version":"4.6.1"},"reference-count":22,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2005,12,12]],"date-time":"2005-12-12T00:00:00Z","timestamp":1134345600000},"content-version":"vor","delay-in-days":3267,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Arthritis &amp; Rheumatism"],"published-print":{"date-parts":[[1997,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p><jats:italic>Objective<\/jats:italic>. To determine whether clinical heterogeneity in patients with giant cell arteritis (GCA) is correlated with different patterns in the tissue\u2010specific inflammatory response.<\/jats:p><jats:p><jats:italic>Methods<\/jats:italic>. Twenty\u2010three patients with typical histomorphologic findings of GCA were grouped according to the presence or absence of jaw claudication and\/or visual abnormalities, fever, concomitant polymyalgia rheumatica (PMR), and histologic evidence of giant cell formation. The inflammatory response in temporal artery biopsy specimens was characterized by semiquantification of cytokine messenger RNA (mRNA) transcripts using reverse transcriptase\u2010polymerase chain reaction, followed by oligonucleotide hybridization with cytokine\u2010specific probes. Clinical patterns were then correlated with profiles of tissue cytokines.<\/jats:p><jats:p><jats:italic>Results<\/jats:italic>. Inflammatory cytokines were expressed in all temporal artery tissues. In situ synthesis of interleukin\u20102 (IL\u20102), interferon\u2010\u03b3 (IFN\u03b3), and IL\u20101\u03b2 mRNA, but not of IL\u201010 and IL\u201012 mRNA, distinguished different patterns of inflammation, and these patterns correlated with clinical manifestations of the disease. Patients with evidence of ischemic symptoms, indicated by jaw claudication and\/or visual symptoms, typically expressed higher concentrations of IFN\u03b3 mRNA (<jats:italic>P<\/jats:italic> = 0.008) and IL\u20101\u03b2 mRNA (<jats:italic>P<\/jats:italic> = 0.02). Presence of fever was correlated with lower copy numbers of IFN\u03b3 (<jats:italic>P<\/jats:italic> = 0.02). Formation of giant cells in the granulomatous infiltrates was associated with the local synthesis of IFN\u03b3 mRNA (<jats:italic>P<\/jats:italic> = 0.003). Tissue from GCA patients with concomitant PMR contained higher levels of IL\u20102 mRNA transcripts (<jats:italic>P<\/jats:italic> = 0.001).<\/jats:p><jats:p><jats:italic>Conclusion<\/jats:italic>. Variations in the clinical presentation of GCA were correlated with cytokine mRNA expression in the affected temporal arteries. Differences in the effector functions of tissue\u2010infiltrating T cells distinguished disease patterns in which either local ischemic symptoms or systemic involvement was dominant, or in which there was co\u2010occurrence of PMR. Definition of different patterns of inflammation in GCA might, therefore, facilitate the design of differentiated therapeutic approaches.<\/jats:p>","DOI":"10.1002\/art.1780400105","type":"journal-article","created":{"date-parts":[[2007,2,14]],"date-time":"2007-02-14T12:15:56Z","timestamp":1171455356000},"page":"19-26","source":"Crossref","is-referenced-by-count":159,"title":["Disease patterns and tissue cytokine profiles in giant cell arteritis"],"prefix":"10.1002","volume":"40","author":[{"given":"Cornelia M.","family":"Weyand","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Naomi","family":"Tetzlaff","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johannes","family":"Bj\u00f6rnsson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander","family":"Brack","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian","family":"Younge","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J\u00f6rg J.","family":"Goronzy","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2005,12,12]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-88-2-162"},{"key":"e_1_2_1_3_2","doi-asserted-by":"crossref","first-page":"471","DOI":"10.1016\/S0307-742X(21)00600-7","article-title":"Giant cell arteritis and polymyalgia rheumatica","volume":"11","author":"Hunder GG","year":"1985","journal-title":"Clin Rheum Dis"},{"key":"e_1_2_1_4_2","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-122-7-199504010-00004"},{"key":"e_1_2_1_5_2","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.2.5212.1562"},{"key":"e_1_2_1_6_2","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-121-7-199410010-00003"},{"key":"e_1_2_1_7_2","doi-asserted-by":"publisher","DOI":"10.1002\/art.1780370411"},{"key":"e_1_2_1_8_2","doi-asserted-by":"crossref","first-page":"1027","DOI":"10.1016\/S0889-857X(21)00483-X","article-title":"Giant cell arteritis as an antigen driven disease","volume":"21","author":"Weyand CM","year":"1995","journal-title":"Rheum Dis Clin North Am"},{"key":"e_1_2_1_9_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI117428"},{"key":"e_1_2_1_10_2","doi-asserted-by":"publisher","DOI":"10.1002\/art.1780330804"},{"key":"e_1_2_1_11_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.155.1.168"},{"key":"e_1_2_1_12_2","doi-asserted-by":"publisher","DOI":"10.1002\/eji.1830200807"},{"key":"e_1_2_1_13_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.167.2.598"},{"key":"e_1_2_1_14_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.iy.07.040189.001045"},{"key":"e_1_2_1_15_2","first-page":"1925","article-title":"Interferon gamma producing T cells in giant cell vasculitis represent a minority of tissue infiltrating cells and are located distant from the site of pathology","volume":"148","author":"Wagner AD","year":"1996","journal-title":"Am J Pathol"},{"key":"e_1_2_1_16_2","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-108-4-595"},{"key":"e_1_2_1_17_2","doi-asserted-by":"publisher","DOI":"10.1016\/0167-5699(93)90230-I"},{"key":"e_1_2_1_18_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.iy.13.040195.001343"},{"key":"e_1_2_1_19_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199301143280207"},{"key":"e_1_2_1_20_2","doi-asserted-by":"publisher","DOI":"10.1016\/1074-7613(95)90154-X"},{"key":"e_1_2_1_21_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116125"},{"key":"e_1_2_1_22_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.179.3.951"},{"key":"e_1_2_1_23_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.81.16.5214"}],"container-title":["Arthritis &amp; 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