{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T12:49:17Z","timestamp":1777639757060,"version":"3.51.4"},"reference-count":27,"publisher":"Wiley","license":[{"start":{"date-parts":[[2012,1,1]],"date-time":"2012-01-01T00:00:00Z","timestamp":1325376000000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81271924"],"award-info":[{"award-number":["81271924"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"name":"National Center for Clinical Laboratories, Beijing","award":["81271924"],"award-info":[{"award-number":["81271924"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clinical and Developmental Immunology"],"published-print":{"date-parts":[[2012]]},"abstract":"<jats:p>In the present study, the CA III and IV autoantibodies, CA activity, antioxidant enzymes and cytokines in rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), diabetes, hypertensive renal disease, and heart failure were investigated. The anti-CA III antibody titers in patients with RA, SLE, and type 1 diabetes (T1D) were significantly higher than that in control groups (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M1\"><mml:mrow><mml:mi>P<\/mml:mi><mml:mo>&lt;<\/mml:mo><mml:mn>0.05<\/mml:mn><\/mml:mrow><\/mml:math>). The anti-CA IV antibody titers in patients with RA, SLE, type 1 diabetic nephropathy (T1DN), and heart failure were significantly higher than that in control groups (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M2\"><mml:mrow><mml:mi>P<\/mml:mi><mml:mo>&lt;<\/mml:mo><mml:mn>0.05<\/mml:mn><\/mml:mrow><\/mml:math>) while anti-CA IV antibody could suppress the total CA activity. The SOD and GPx levels in patients with RA, SLE, and T1DN were significantly lower than that in control groups (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M3\"><mml:mrow><mml:mi>P<\/mml:mi><mml:mo>&lt;<\/mml:mo><mml:mn>0.05<\/mml:mn><\/mml:mrow><\/mml:math>). IL-6, IL-17, IFN-<jats:italic>\u03b3<\/jats:italic>, and TNF-<jats:italic>\u03b1<\/jats:italic>levels were significantly higher in SLE group compared with the control group (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M4\"><mml:mrow><mml:mi>P<\/mml:mi><mml:mo>&lt;<\/mml:mo><mml:mn>0.05<\/mml:mn><\/mml:mrow><\/mml:math>). Weak but significant correlations were found between anti-CA III antibodies and ESR in RA (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M5\"><mml:mrow><mml:mi>r<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>0.403<\/mml:mn><\/mml:mrow><\/mml:math>,<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M6\"><mml:mrow><mml:mi>P<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>0.013<\/mml:mn><\/mml:mrow><\/mml:math>) and SLE patients (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M7\"><mml:mrow><mml:mi>r<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>0.397<\/mml:mn><\/mml:mrow><\/mml:math>,<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M8\"><mml:mrow><mml:mi>P<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>0.007<\/mml:mn><\/mml:mrow><\/mml:math>). These results suggested that the generation of CA III and IV autoantibodies, antioxidant enzymes, and cytokines might influence each other and CA autoantibodies might affect the normal physiology function of CA.<\/jats:p>","DOI":"10.1155\/2012\/354594","type":"journal-article","created":{"date-parts":[[2012,9,16]],"date-time":"2012-09-16T21:02:05Z","timestamp":1347829325000},"page":"1-6","source":"Crossref","is-referenced-by-count":39,"title":["Carbonic Anhydrases III and IV Autoantibodies in Rheumatoid Arthritis, Systemic Lupus Erythematosus, Diabetes, Hypertensive Renal Disease, and Heart Failure"],"prefix":"10.1155","volume":"2012","author":[{"given":"Chengeng","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Clinical Laboratory, Xuanwu Hospital, Capital Medical University, 45 Changchun Road, Beijing 100053, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yue","family":"Wei","sequence":"additional","affiliation":[{"name":"Department of Oncology, Dongfang Hospital, Beijing University of Chinese Medicine, Beijing 100078, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jianmin","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Clinical Immune, Xiangya School of Medicine, Central South University, Changsha 410078, Hunan, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Langan","family":"Pi","sequence":"additional","affiliation":[{"name":"Department of Clinical Immune, Xiangya School of Medicine, Central South University, Changsha 410078, Hunan, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jianjun","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Clinical Immune, Xiangya School of Medicine, Central South University, Changsha 410078, Hunan, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Peichang","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of 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