{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,29]],"date-time":"2026-07-29T22:28:46Z","timestamp":1785364126234,"version":"3.55.0"},"reference-count":47,"publisher":"American Society for Microbiology","issue":"4","license":[{"start":{"date-parts":[[2018,3,26]],"date-time":"2018-03-26T00:00:00Z","timestamp":1522022400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2018,4,1]],"date-time":"2018-04-01T00:00:00Z","timestamp":1522540800000},"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":["J Clin Microbiol"],"published-print":{"date-parts":[[2018,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Naturally occurring functional variants (rs148314165 and rs200820567, collectively referred to as TT&gt;A) reduce the expression of the tumor necrosis factor alpha-induced protein 3 (\n            <jats:italic>TNFAIP3<\/jats:italic>\n            ) gene, a negative regulator of NF-\u03baB signaling, and predispose individuals to autoimmune disease. In this analysis, we conducted a genetic association study of the TT&gt;A variants in 1,209 controls and 150 patients with brucellosis, an infectious disease, and further assessed the role of the variants in brucellosis. Our data demonstrated that the TT&gt;A variants were correlated with cases of brucellosis (\n            <jats:italic>P<\/jats:italic>\n            = 0.002; odds ratio [OR] = 0.34) and with individuals who had a positive serum agglutination test (SAT) result (titer of &gt;1\/160) (\n            <jats:italic>P<\/jats:italic>\n            = 4.2 \u00d7 10\n            <jats:sup>\u22126<\/jats:sup>\n            ; OR = 0.23). A functional study demonstrated that brucellosis patients carrying the protective allele (A) showed significantly lower expression levels of the TNFAIP3 gene in their peripheral blood mononuclear cells and showed increased NF-\u03baB signaling. Monocytes from individuals carrying the A allele that were stimulated with\n            <jats:named-content content-type=\"genus-species\">Brucella abortus<\/jats:named-content>\n            had lower mRNA levels of TNFAIP3 and produced more interleukin-10 (IL-10), IL-6, and IL-1\u03b2 than those from TT allele carriers. These data showed that autoimmune disease-associated risk variants, TT&gt;A, of the TNFAIP3 locus play a protective role in the pathogenesis of brucellosis. Our findings suggest that a disruption of the normal function of the TNFAIP3 gene might serve as a therapeutic target for the treatment of brucellosis.\n          <\/jats:p>","DOI":"10.1128\/jcm.01363-17","type":"journal-article","created":{"date-parts":[[2018,1,18]],"date-time":"2018-01-18T11:26:04Z","timestamp":1516274764000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":3,"title":["An Autoimmune Disease-Associated Risk Variant in the\n            <i>TNFAIP3<\/i>\n            Gene Plays a Protective Role in Brucellosis That Is Mediated by the NF-\u03baB Signaling Pathway"],"prefix":"10.1128","volume":"56","author":[{"given":"Lixin","family":"Lou","sequence":"first","affiliation":[{"name":"Department of Infectious Diseases, The First Hospital of Jilin University, Jilin, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wanguo","family":"Bao","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases, The First Hospital of Jilin University, Jilin, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xianjun","family":"Liu","sequence":"additional","affiliation":[{"name":"The Bethune Institute of Epigenetic Medicine, The First Hospital of Jilin University, Jilin, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hongxiao","family":"Song","sequence":"additional","affiliation":[{"name":"Department of Translational Medicine, The First Hospital, Jilin University, Jilin, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yang","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases, The First Hospital of Jilin University, Jilin, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kaiyu","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases, The First Hospital of Jilin University, Jilin, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wenjing","family":"Gao","sequence":"additional","affiliation":[{"name":"The Bethune Institute of Epigenetic Medicine, The First Hospital of Jilin University, Jilin, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haijun","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Translational Medicine, The First Hospital, Jilin University, Jilin, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhengkun","family":"Tu","sequence":"additional","affiliation":[{"name":"Department of Translational Medicine, The First Hospital, Jilin University, Jilin, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shaofeng","family":"Wang","sequence":"additional","affiliation":[{"name":"The Bethune Institute of Epigenetic Medicine, The First Hospital of Jilin University, Jilin, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra050570"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0378-1135(02)00223-7"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1286-4579(00)01350-2"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1615\/CritRevImmunol.v26.i5.30"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2016.12.012"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1038\/gene.2010.64"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1007\/s00011-012-0455-5"},{"key":"e_1_3_3_9_2","first-page":"566","article-title":"Pathway analysis of genome-wide association studies on rheumatoid arthritis","volume":"31","author":"Song GG","year":"2013","unstructured":"Song GG, Bae SC, Lee YH. 2013. 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