{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T02:52:23Z","timestamp":1777431143961,"version":"3.51.4"},"reference-count":28,"publisher":"American Society for Microbiology","issue":"12","license":[{"start":{"date-parts":[[2012,12,1]],"date-time":"2012-12-01T00:00:00Z","timestamp":1354320000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Clin Vaccine Immunol"],"published-print":{"date-parts":[[2012,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Psoriasis vulgaris is considered a chronic inflammatory disease, but its immunopathogenesis has not been well understood. The tumor necrosis factor alpha-induced protein 3 (TNFAIP3) gene functions in negative-feedback regulation of inflammation, and its single nucleotide polymorphism is associated with psoriasis. However, the relationship between the expression level of the TNFAIP3 gene in immune cells and psoriasis is not known so far. In the present study, TNFAIP3 mRNA expression levels in peripheral blood mononuclear cells from 44 patients with psoriasis vulgaris and 30 healthy controls were determined using real-time reverse transcription-PCR analysis. We found that expression of TNFAIP3 mRNA in all patients negatively correlated with the psoriatic area and severity index (PASI) (\n            <jats:italic>r<\/jats:italic>\n            = \u22120.5126;\n            <jats:italic>P<\/jats:italic>\n            = 0.0004) as well as with the percentage of body surface area affected by psoriasis (\n            <jats:italic>r<\/jats:italic>\n            = \u22120.5013;\n            <jats:italic>P<\/jats:italic>\n            = 0.0005). Patients were divided into mild and severe groups based on the mean PASI score. Expression of TNFAIP3 mRNA in the mild group was higher than that in the severe group (\n            <jats:italic>P<\/jats:italic>\n            = 0.0064). Moreover, compared with that in healthy controls, the expression of TNFAIP3 mRNA in the mild group was significantly upregulated (\n            <jats:italic>P<\/jats:italic>\n            = 0.0004), but the expression of TNFAIP3 mRNA in the severe group was not. These results suggest that the expression level of TNFAIP3 plays an important role in the pathology of psoriasis vulgaris and that the loss of upregulation of TNFAIP3 expression may contribute to the severity of psoriasis vulgaris.\n          <\/jats:p>","DOI":"10.1128\/cvi.00500-12","type":"journal-article","created":{"date-parts":[[2012,10,12]],"date-time":"2012-10-12T00:44:38Z","timestamp":1350002678000},"page":"1938-1942","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":27,"title":["Expression of Tumor Necrosis Factor Alpha-Induced Protein 3 mRNA in Peripheral Blood Mononuclear Cells Negatively Correlates with Disease Severity in Psoriasis Vulgaris"],"prefix":"10.1128","volume":"19","author":[{"given":"Xuebing","family":"Jiang","sequence":"first","affiliation":[{"name":"Institute of Immunology, School of Medicine, Shandong University, Jinan, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hongqing","family":"Tian","sequence":"additional","affiliation":[{"name":"Shandong Provincial Institute of Dermatology and Venereology, Shandong Academy of Medical Science, Jinan, China"},{"name":"Shandong Provincial Hospital for Skin Diseases, Jinan, Shandong Province, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yuchen","family":"Fan","sequence":"additional","affiliation":[{"name":"Department of Hepatology, Qilu Hospital of Shandong University, Jinan, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jie","family":"Chen","sequence":"additional","affiliation":[{"name":"Institute of Immunology, School of Medicine, Shandong University, Jinan, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yonghong","family":"Song","sequence":"additional","affiliation":[{"name":"Shandong Blood Center, Jinan, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shurong","family":"Wang","sequence":"additional","affiliation":[{"name":"Shandong Blood Center, Jinan, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Faliang","family":"Zhu","sequence":"additional","affiliation":[{"name":"Institute of Immunology, School of Medicine, Shandong University, Jinan, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chun","family":"Guo","sequence":"additional","affiliation":[{"name":"Institute of Immunology, School of Medicine, Shandong University, Jinan, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lining","family":"Zhang","sequence":"additional","affiliation":[{"name":"Institute of Immunology, School of Medicine, Shandong University, Jinan, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yongyu","family":"Shi","sequence":"additional","affiliation":[{"name":"Institute of Immunology, School of Medicine, Shandong University, Jinan, China"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"crossref","first-page":"681","DOI":"10.1084\/jem.192.5.681","article-title":"Blockade of T lymphocyte costimulation with cytotoxic T lymphocyte-associated antigen 4-immunoglobulin (CTLA4Ig) reverses the cellular pathology of psoriatic plaques, including the activation of keratinocytes, dendritic cells, and endothelial cells","volume":"192","author":"Abrams JR","year":"2000","unstructured":"AbramsJR . 2000. Blockade of T lymphocyte costimulation with cytotoxic T lymphocyte-associated antigen 4-immunoglobulin (CTLA4Ig) reverses the cellular pathology of psoriatic plaques, including the activation of keratinocytes, dendritic cells, and endothelial cells. J. Exp. Med. 192: 681\u2013 694.","journal-title":"J. Exp. Med."},{"key":"e_1_3_2_3_2","doi-asserted-by":"crossref","first-page":"253","DOI":"10.1038\/ng.766","article-title":"Association of a functional variant downstream of TNFAIP3 with systemic lupus erythematosus","volume":"43","author":"Adrianto I","year":"2011","unstructured":"AdriantoI . 2011. Association of a functional variant downstream of TNFAIP3 with systemic lupus erythematosus. Nat. Genet. 43: 253\u2013 258.","journal-title":"Nat. Genet."},{"key":"e_1_3_2_4_2","doi-asserted-by":"crossref","first-page":"1085","DOI":"10.1111\/j.1365-2133.2010.09990.x","article-title":"Elevation of serum epidermal growth factor and interleukin 1 receptor antagonist in active psoriasis vulgaris","volume":"163","author":"Anderson KS","year":"2010","unstructured":"AndersonKS . 2010. Elevation of serum epidermal growth factor and interleukin 1 receptor antagonist in active psoriasis vulgaris. Br. J. Dermatol. 163: 1085\u2013 1089.","journal-title":"Br. J. Dermatol."},{"key":"e_1_3_2_5_2","doi-asserted-by":"crossref","first-page":"273","DOI":"10.1155\/MI.2005.273","article-title":"Serum levels of TNF-alpha, IFN-gamma, IL-6, IL-8, IL-12, IL-17, and IL-18 in patients with active psoriasis and correlation with disease severity","volume":"2005","author":"Arican O","year":"2005","unstructured":"AricanO AralM SasmazS CiragilP . 2005. Serum levels of TNF-alpha, IFN-gamma, IL-6, IL-8, IL-12, IL-17, and IL-18 in patients with active psoriasis and correlation with disease severity. Mediators Inflamm. 2005: 273\u2013 279.","journal-title":"Mediators Inflamm."},{"key":"e_1_3_2_6_2","doi-asserted-by":"crossref","first-page":"499","DOI":"10.2337\/db06-0946","article-title":"Tag polymorphisms at the A20 (TNFAIP3) locus are associated with lower gene expression and increased risk of coronary artery disease in type 2 diabetes","volume":"56","author":"Boonyasrisawat W","year":"2007","unstructured":"BoonyasrisawatW . 2007. Tag polymorphisms at the A20 (TNFAIP3) locus are associated with lower gene expression and increased risk of coronary artery disease in type 2 diabetes. Diabetes 56: 499\u2013 505.","journal-title":"Diabetes"},{"key":"e_1_3_2_7_2","doi-asserted-by":"crossref","first-page":"483","DOI":"10.1038\/leu.2009.234","article-title":"A20 is targeted by promoter methylation, deletion and inactivating mutation in MALT lymphoma","volume":"24","author":"Chanudet E","year":"2010","unstructured":"ChanudetE . 2010. A20 is targeted by promoter methylation, deletion and inactivating mutation in MALT lymphoma. Leukemia 24: 483\u2013 487.","journal-title":"Leukemia"},{"key":"e_1_3_2_8_2","doi-asserted-by":"crossref","first-page":"8217","DOI":"10.1074\/jbc.R800032200","article-title":"A20: central gatekeeper in inflammation and immunity","volume":"284","author":"Coornaert B","year":"2009","unstructured":"CoornaertB CarpentierI BeyaertR . 2009. A20: central gatekeeper in inflammation and immunity. J. Biol. Chem. 284: 8217\u2013 8221.","journal-title":"J. Biol. Chem."},{"key":"e_1_3_2_9_2","doi-asserted-by":"crossref","first-page":"7718","DOI":"10.4049\/jimmunol.0803313","article-title":"A20 negatively regulates T cell receptor signaling to NF-kappaB by cleaving Malt1 ubiquitin chains","volume":"182","author":"D\u00fcwel M","year":"2009","unstructured":"D\u00fcwelM . 2009. A20 negatively regulates T cell receptor signaling to NF-kappaB by cleaving Malt1 ubiquitin chains. J. Immunol. 182: 7718\u2013 7728.","journal-title":"J. Immunol."},{"key":"e_1_3_2_10_2","doi-asserted-by":"crossref","first-page":"201","DOI":"10.1038\/gene.2009.11","article-title":"Genome-wide association scan yields new insights into the immunopathogenesis of psoriasis","volume":"10","author":"Elder JT","year":"2009","unstructured":"ElderJT . 2009. Genome-wide association scan yields new insights into the immunopathogenesis of psoriasis. Genes Immun. 10: 201\u2013 209.","journal-title":"Genes Immun."},{"key":"e_1_3_2_11_2","doi-asserted-by":"crossref","first-page":"2495","DOI":"10.1002\/ijc.25579","article-title":"Sustained NF-kappaB activity in chronic lymphocytic leukemia is independent of genetic and epigenetic alterations in the TNFAIP3 (A20) locus","volume":"128","author":"Frenzel LP","year":"2011","unstructured":"FrenzelLP . 2011. Sustained NF-kappaB activity in chronic lymphocytic leukemia is independent of genetic and epigenetic alterations in the TNFAIP3 (A20) locus. Int. J. Cancer 128: 2495\u2013 2500.","journal-title":"Int. J. Cancer"},{"key":"e_1_3_2_12_2","doi-asserted-by":"crossref","first-page":"1019","DOI":"10.1111\/j.1365-4632.2008.03753.x","article-title":"A comparison between BSA, PASI, PLASI and SAPASI as measures of disease severity and improvement by therapy in patients with psoriasis","volume":"47","author":"Henseler T","year":"2008","unstructured":"HenselerT Schmitt-RauK . 2008. A comparison between BSA, PASI, PLASI and SAPASI as measures of disease severity and improvement by therapy in patients with psoriasis. Int. J. Dermatol. 47: 1019\u2013 1023.","journal-title":"Int. J. Dermatol."},{"key":"e_1_3_2_13_2","doi-asserted-by":"crossref","first-page":"845","DOI":"10.1111\/j.1365-2230.2011.04131.x","article-title":"The role of inflammatory markers in assessing disease severity and response to treatment in patients with psoriasis treated with etanercept","volume":"36","author":"Kanelleas A","year":"2011","unstructured":"KanelleasA . 2011. The role of inflammatory markers in assessing disease severity and response to treatment in patients with psoriasis treated with etanercept. Clin. Exp. Dermatol. 36: 845\u2013 850.","journal-title":"Clin. Exp. Dermatol."},{"key":"e_1_3_2_14_2","doi-asserted-by":"crossref","first-page":"4520","DOI":"10.4049\/jimmunol.1001051","article-title":"Cutting edge: TCR ligation triggers digital activation of NF-kappaB","volume":"185","author":"Kingeter LM","year":"2010","unstructured":"KingeterLM PaulS MaynardSK CartwrightNG SchaeferBC . 2010. Cutting edge: TCR ligation triggers digital activation of NF-kappaB. J. Immunol. 185: 4520\u2013 4524.","journal-title":"J. Immunol."},{"key":"e_1_3_2_15_2","doi-asserted-by":"crossref","first-page":"17971","DOI":"10.1016\/S0021-9258(19)37138-8","article-title":"Transcriptional activation of the tumor necrosis factor alpha-inducible zinc finger protein, A20, is mediated by kappa B elements","volume":"267","author":"Krikos A","year":"1992","unstructured":"KrikosA LahertyCD DixitVM . 1992. Transcriptional activation of the tumor necrosis factor alpha-inducible zinc finger protein, A20, is mediated by kappa B elements. J. Biol. Chem. 267: 17971\u2013 17976.","journal-title":"J. Biol. Chem."},{"key":"e_1_3_2_16_2","doi-asserted-by":"crossref","first-page":"7001","DOI":"10.4049\/jimmunol.1000324","article-title":"African-derived genetic polymorphisms in TNFAIP3 mediate risk for autoimmunity","volume":"184","author":"Lodolce JP","year":"2010","unstructured":"LodolceJP . 2010. African-derived genetic polymorphisms in TNFAIP3 mediate risk for autoimmunity. J. Immunol. 184: 7001\u2013 7009.","journal-title":"J. Immunol."},{"key":"e_1_3_2_17_2","doi-asserted-by":"crossref","first-page":"145","DOI":"10.1016\/S0923-1811(96)00562-2","article-title":"Role of increased production of monocytes TNF-alpha, IL-1beta and IL-6 in psoriasis: relation to focal infection, disease activity and responses to treatments","volume":"14","author":"Mizutani H","year":"1997","unstructured":"MizutaniH OhmotoY MizutaniT MurataM ShimizuM . 1997. Role of increased production of monocytes TNF-alpha, IL-1beta and IL-6 in psoriasis: relation to focal infection, disease activity and responses to treatments. J. Dermatol. Sci. 14: 145\u2013 153.","journal-title":"J. Dermatol. Sci."},{"key":"e_1_3_2_18_2","doi-asserted-by":"crossref","first-page":"199","DOI":"10.1038\/ng.311","article-title":"Genome-wide scan reveals association of psoriasis with IL-23 and NF-kappaB pathways","volume":"41","author":"Nair RP","year":"2009","unstructured":"NairRP . 2009. Genome-wide scan reveals association of psoriasis with IL-23 and NF-kappaB pathways. Nat. Genet. 41: 199\u2013 204.","journal-title":"Nat. Genet."},{"key":"e_1_3_2_19_2","doi-asserted-by":"crossref","first-page":"3","DOI":"10.1016\/j.sder.2010.03.001","article-title":"New insights in the immunologic basis of psoriasis","volume":"29","author":"Nograles KE","year":"2010","unstructured":"NogralesKE DavidoviciB KruegerJG . 2010. New insights in the immunologic basis of psoriasis. Semin. Cutan. Med. Surg. 29: 3\u2013 9.","journal-title":"Semin. Cutan. Med. Surg."},{"key":"e_1_3_2_20_2","doi-asserted-by":"crossref","first-page":"3","DOI":"10.1111\/j.1468-3083.2011.04410.x","article-title":"The concept of psoriasis as a systemic inflammation: implications for disease management","volume":"26","author":"Reich K","year":"2012","unstructured":"ReichK . 2012. The concept of psoriasis as a systemic inflammation: implications for disease management. J. Eur. Acad. Dermatol. Venereol. 26(Suppl 2):3\u201311.","journal-title":"J. Eur. Acad. Dermatol. Venereol."},{"key":"e_1_3_2_21_2","first-page":"25","article-title":"An association study of single nucleotide polymorphisms of the FOXP3 intron-1 and the risk of psoriasis vulgaris","volume":"49","author":"Song QH","year":"2012","unstructured":"SongQH . 2012. An association study of single nucleotide polymorphisms of the FOXP3 intron-1 and the risk of psoriasis vulgaris. Indian J. Biochem. Biophys. 49: 25\u2013 35.","journal-title":"Indian J. Biochem. Biophys."},{"key":"e_1_3_2_22_2","doi-asserted-by":"publisher","DOI":"10.1038\/nm1721"},{"key":"e_1_3_2_23_2","doi-asserted-by":"crossref","first-page":"415","DOI":"10.1016\/j.cell.2008.03.026","article-title":"TIPE2, a negative regulator of innate and adaptive immunity that maintains immune homeostasis","volume":"133","author":"Sun H","year":"2008","unstructured":"SunH . 2008. TIPE2, a negative regulator of innate and adaptive immunity that maintains immune homeostasis. Cell 133: 415\u2013 426.","journal-title":"Cell"},{"key":"e_1_3_2_24_2","doi-asserted-by":"crossref","first-page":"645","DOI":"10.1111\/j.1365-2230.2009.03704.x","article-title":"Serum cytokines and growth factor levels in Japanese patients with psoriasis","volume":"35","author":"Takahashi H","year":"2010","unstructured":"TakahashiH TsujiH HashimotoY Ishida-YamamotoA IizukaH . 2010. Serum cytokines and growth factor levels in Japanese patients with psoriasis. Clin. Exp. Dermatol. 35: 645\u2013 649.","journal-title":"Clin. Exp. Dermatol."},{"key":"e_1_3_2_25_2","doi-asserted-by":"crossref","first-page":"1086","DOI":"10.1042\/BST0391086","article-title":"Genetic relationships between A20\/TNFAIP3, chronic inflammation and autoimmune disease","volume":"39","author":"Vereecke L","year":"2011","unstructured":"VereeckeL BeyaertR van LooG . 2011. Genetic relationships between A20\/TNFAIP3, chronic inflammation and autoimmune disease. Biochem. Soc. Trans. 39: 1086\u2013 1091.","journal-title":"Biochem. Soc. Trans."},{"key":"e_1_3_2_26_2","doi-asserted-by":"crossref","first-page":"383","DOI":"10.1016\/j.it.2009.05.007","article-title":"The ubiquitin-editing enzyme A20 (TNFAIP3) is a central regulator of immunopathology","volume":"30","author":"Vereecke L","year":"2009","unstructured":"VereeckeL BeyaertR van LooG . 2009. The ubiquitin-editing enzyme A20 (TNFAIP3) is a central regulator of immunopathology. Trends Immunol. 30: 383\u2013 391.","journal-title":"Trends Immunol."},{"key":"e_1_3_2_27_2","doi-asserted-by":"crossref","first-page":"1513","DOI":"10.1084\/jem.20092474","article-title":"Enterocyte-specific A20 deficiency sensitizes to tumor necrosis factor-induced toxicity and experimental colitis","volume":"207","author":"Vereecke L","year":"2010","unstructured":"VereeckeL . 2010. Enterocyte-specific A20 deficiency sensitizes to tumor necrosis factor-induced toxicity and experimental colitis. J. Exp. Med. 207: 1513\u2013 1523.","journal-title":"J. Exp. Med."},{"key":"e_1_3_2_28_2","doi-asserted-by":"crossref","first-page":"2009","DOI":"10.1016\/j.bcp.2010.06.044","article-title":"Expression, biological activities and mechanisms of action of A20 (TNFAIP3)","volume":"80","author":"Verstrepen L","year":"2010","unstructured":"VerstrepenL . 2010. Expression, biological activities and mechanisms of action of A20 (TNFAIP3). Biochem. Pharmacol. 80: 2009\u2013 2020.","journal-title":"Biochem. Pharmacol."},{"key":"e_1_3_2_29_2","doi-asserted-by":"crossref","first-page":"2289","DOI":"10.4049\/jimmunol.0903133","article-title":"IL-17 activates the canonical NF-kappaB signaling pathway in autoimmune B cells of BXD2 mice to upregulate the expression of regulators of G-protein signaling 16","volume":"184","author":"Xie S","year":"2010","unstructured":"XieS . 2010. IL-17 activates the canonical NF-kappaB signaling pathway in autoimmune B cells of BXD2 mice to upregulate the expression of regulators of G-protein signaling 16. J. Immunol. 184: 2289\u2013 2296.","journal-title":"J. Immunol."}],"container-title":["Clinical and Vaccine Immunology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/journals.asm.org\/doi\/pdf\/10.1128\/CVI.00500-12","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/journals.asm.org\/doi\/pdf\/10.1128\/CVI.00500-12","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,7,29]],"date-time":"2021-07-29T20:46:14Z","timestamp":1627591574000},"score":1,"resource":{"primary":{"URL":"https:\/\/journals.asm.org\/doi\/10.1128\/CVI.00500-12"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2012,12]]},"references-count":28,"journal-issue":{"issue":"12","published-print":{"date-parts":[[2012,12]]}},"alternative-id":["10.1128\/CVI.00500-12"],"URL":"https:\/\/doi.org\/10.1128\/cvi.00500-12","relation":{},"ISSN":["1556-6811","1556-679X"],"issn-type":[{"value":"1556-6811","type":"print"},{"value":"1556-679X","type":"electronic"}],"subject":[],"published":{"date-parts":[[2012,12]]},"assertion":[{"value":"2012-08-14","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2012-10-02","order":1,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2012-11-27","order":2,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}