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               <mods:name>
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                  <mods:namePart>Castano-Nunez, Angel</mods:namePart>
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                  <mods:namePart>Montes-Cano, Marco-Antonio</mods:namePart>
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                  <mods:namePart>Garcia-Lozano, Jose-Raul</mods:namePart>
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               <mods:name>
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                  <mods:namePart>Ortego-Centeno, Norberto</mods:namePart>
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               <mods:name>
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                  <mods:namePart>Garcia-Hernandez, Francisco-Jose</mods:namePart>
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                  <mods:namePart>Espinosa, Gerard</mods:namePart>
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                  <mods:namePart>Grana-Gil, Genaro</mods:namePart>
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                  <mods:namePart>Sanchez-Burson, Juan</mods:namePart>
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               <mods:name>
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                  <mods:namePart>Julia Benique, Maria Rosa</mods:namePart>
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               <mods:name>
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                  <mods:namePart>Solans, Roser</mods:namePart>
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               <mods:name>
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                  <mods:namePart>Blanco, Ricardo</mods:namePart>
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               <mods:name>
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                  <mods:namePart>Barnosi-Marin, Ana-Celia</mods:namePart>
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                  <mods:namePart>Gomez de la Torre, Ricardo</mods:namePart>
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               <mods:name>
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                  <mods:namePart>Fanlo Mateo, Patricia</mods:namePart>
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                  <mods:namePart>Rodriguez-Carballeira, Monica</mods:namePart>
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                  <mods:namePart>Rodriguez-Rodriguez, Luis</mods:namePart>
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                  <mods:namePart>Camps, Teresa</mods:namePart>
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                  <mods:namePart>Castaneda, Santos</mods:namePart>
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               <mods:name>
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                     <mods:roleTerm type="text">author</mods:roleTerm>
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                  <mods:namePart>Alegre-Sancho, Juan-Jose</mods:namePart>
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                  <mods:namePart>Martin, Javier</mods:namePart>
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               <mods:name>
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                     <mods:roleTerm type="text">author</mods:roleTerm>
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                  <mods:namePart>Gonzalez-Escribano, Maria-Francisca</mods:namePart>
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                  <mods:dateAccessioned encoding="iso8601">2024-09-10T13:08:58Z</mods:dateAccessioned>
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                  <mods:dateIssued encoding="iso8601">2019-11-29</mods:dateIssued>
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               <mods:identifier type="citation">Castano-Nunez A, Montes-Cano MA, Garcia-Lozano JR, Ortego-Centeno N, Garcia-Hernandez FJ, Espinosa G, et al. Association of Functional Polymorphisms of KIR3DL1/DS1 With Behcet's Disease. Front Immunol. 2019 Nov 29;10:2755.</mods:identifier>
               <mods:identifier type="doi">10.3389/fimmu.2019.02755</mods:identifier>
               <mods:identifier type="issn">1664-3224</mods:identifier>
               <mods:identifier type="journal">Frontiers in Immunology</mods:identifier>
               <mods:identifier type="other">http://hdl.handle.net/20.500.13003/12964</mods:identifier>
               <mods:identifier type="pubmedID">31849952</mods:identifier>
               <mods:identifier type="pui">L630179342</mods:identifier>
               <mods:identifier type="scopus">2-s2.0-85076837491</mods:identifier>
               <mods:identifier type="uri">https://hdl.handle.net/20.500.12105/22720</mods:identifier>
               <mods:identifier type="wos">502780300001</mods:identifier>
               <mods:abstract>Behcet's disease (BD) is an immune-mediated vasculitis related to imbalances between the innate and adaptive immune response. Infectious agents or environmental factors may trigger the disease in genetically predisposed individuals. HLA-B51 is the genetic factor stronger associated with the disease, although the bases of this association remain elusive. NK cells have also been implicated in the etiopathogenesis of BD. A family of NK receptors, Killer-cell Immunoglobulin-like Receptor (KIR), with a very complex organization, is very important in the education and control of the NK cells by the union to their ligands, most of them, HLA class I molecules. This study aimed to investigate the contribution of certain KIR functional polymorphisms to the susceptibility to BD. A total of 466 BD patients and 444 healthy individuals were genotyped in HLA class I (A, B, and C). The set of KIR genes and the functional variants of KIR3DL1/DS1 and KIR2DS4 were also determined. Frequency of KIR3DL1*004 was lower in patients than in controls (0.15 vs. 0.20, P = 0.005, Pc = 0.015; OR = 0.70; 95% CI 0.54-0.90) in both B51 positive and negative individuals. KIR3DL1*004, which encodes a misfolded protein, is included in a common telomeric haplotype with only one functional KIR gene, KIR3DL2. Both, KIR3DL1 and KIR3DL2 sense pathogen-associated molecular patterns but they have different capacities to eliminate them. The education of the NK cells depending on the HLA, the balance of KIR3DL1/KIR3DL2 licensed NK cells and the different capacities of these receptors to eliminate pathogens could be involved in the etiopathogenesis of BD.</mods:abstract>
               <mods:language>
                  <mods:languageTerm authority="rfc3066">eng</mods:languageTerm>
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               <mods:accessCondition type="useAndReproduction"/>
               <mods:subject>
                  <mods:topic>Behcet's disease</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>HLA</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>KIR</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>NK cells</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Functional polymorphisms</mods:topic>
               </mods:subject>
               <mods:titleInfo>
                  <mods:title>Association of Functional Polymorphisms of KIR3DL1/DS1 With Behcet's Disease</mods:title>
               </mods:titleInfo>
               <mods:genre>research article</mods:genre>
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