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Interleukin-18, interleukin-12B and interferon-γ gene polymorphisms in Brazilian patients with rheumatoid arthritis: a pilot study

Polymorphisms in interleukin (IL)‐18, IL‐12 and interferon (IFN)‐γ genes are associated with different levels of cytokines expression and have been associated with rheumatoid arthritis (RA). IL‐18 +105 A/C, IL‐12B +1188 A/C and IFN‐γ +874 T/A polymorphisms were analyzed by restriction fragment lengt...

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Published in:Tissue antigens 2015-10, Vol.86 (4), p.276-278
Main Authors: Angelo, H. D., Gomes Silva, I. I. F., Oliveira, R. D. R., Louzada-Júnior, P., Donadi, E. A., Crovella, S., Maia, M. M. D., de Souza, P. R. E., Sandrin-Garcia, P.
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container_title Tissue antigens
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creator Angelo, H. D.
Gomes Silva, I. I. F.
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description Polymorphisms in interleukin (IL)‐18, IL‐12 and interferon (IFN)‐γ genes are associated with different levels of cytokines expression and have been associated with rheumatoid arthritis (RA). IL‐18 +105 A/C, IL‐12B +1188 A/C and IFN‐γ +874 T/A polymorphisms were analyzed by restriction fragment length polymorphism‐polymerase chain reaction (PCR) and amplification refractory mutation system PCR from 90 RA patients and 186 healthy individuals. There were significant differences to IL‐18 +105 A/C polymorphism between the RA and control groups (odds ratio = 3.77; P 
doi_str_mv 10.1111/tan.12645
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D. ; Gomes Silva, I. I. F. ; Oliveira, R. D. R. ; Louzada-Júnior, P. ; Donadi, E. A. ; Crovella, S. ; Maia, M. M. D. ; de Souza, P. R. E. ; Sandrin-Garcia, P.</creator><creatorcontrib>Angelo, H. D. ; Gomes Silva, I. I. F. ; Oliveira, R. D. R. ; Louzada-Júnior, P. ; Donadi, E. A. ; Crovella, S. ; Maia, M. M. D. ; de Souza, P. R. E. ; Sandrin-Garcia, P.</creatorcontrib><description>Polymorphisms in interleukin (IL)‐18, IL‐12 and interferon (IFN)‐γ genes are associated with different levels of cytokines expression and have been associated with rheumatoid arthritis (RA). IL‐18 +105 A/C, IL‐12B +1188 A/C and IFN‐γ +874 T/A polymorphisms were analyzed by restriction fragment length polymorphism‐polymerase chain reaction (PCR) and amplification refractory mutation system PCR from 90 RA patients and 186 healthy individuals. There were significant differences to IL‐18 +105 A/C polymorphism between the RA and control groups (odds ratio = 3.77; P &lt; 0.0001). Individual carriers of the variant allele C had a 3.77‐fold increased risk of for RA (P = 0.0032). No association was observed for IL‐12B and IFN‐γ polymorphisms. 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There were significant differences to IL‐18 +105 A/C polymorphism between the RA and control groups (odds ratio = 3.77; P &lt; 0.0001). Individual carriers of the variant allele C had a 3.77‐fold increased risk of for RA (P = 0.0032). No association was observed for IL‐12B and IFN‐γ polymorphisms. Our finds suggest a possible role for IL‐18 polymorphism in the RA susceptibility in studied population.</description><subject>Adult</subject><subject>Alleles</subject><subject>arthritis</subject><subject>Arthritis, Rheumatoid - genetics</subject><subject>Arthritis, Rheumatoid - immunology</subject><subject>Arthritis, Rheumatoid - pathology</subject><subject>Brazil</subject><subject>Case-Control Studies</subject><subject>cytokines</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Gene Frequency</subject><subject>Genetic Predisposition to Disease</subject><subject>Humans</subject><subject>Interferon-gamma - genetics</subject><subject>Interferon-gamma - immunology</subject><subject>Interleukin-12 Subunit p40 - genetics</subject><subject>Interleukin-12 Subunit p40 - immunology</subject><subject>Interleukin-18 - genetics</subject><subject>Interleukin-18 - immunology</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Pilot Projects</subject><subject>Polymerase Chain Reaction</subject><subject>polymorphism</subject><subject>Polymorphism, Restriction Fragment Length</subject><subject>Polymorphism, Single Nucleotide</subject><subject>rheumatoid</subject><subject>Risk</subject><issn>0001-2815</issn><issn>1399-0039</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><recordid>eNp1kMtO3TAQhi1UBKeURV-g8rJIDfgS20l33EE6ompFxdLySSYcQ-IE2xGcbvtIfY8-E4YA6qazGc3om1-aD6GPlOzSVHvRuF3KZC7W0IzysswI4eU7NCOE0IwVVGyi9yHcpClXZbmBNpnkhJWKztDvcxfBtzDeWpfR4gu2_87sABtXT7sGfO-yv3_wNTjAQ9-uut4PSxu6kAB84M0v21rj8GCiBRcDvrdxif0Sxs7E3tbY-Lj0NtrwFRs82LaPOMSxXn1A641pA2y_9C308-T48vAsm387PT_cn2dVzrnIFBfFgilSMtrkpF7knLLCCMObopJMcSVSExRIXgrZEMHBVBSKRa5AirqWfAt9nnIH39-NEKLubKigbY2DfgyaqiRP0FyyhO5MaOX7EDw0evC2M36lKdFPznVyrp-dJ_bTS-y46KB-I18lJ2BvAu5tC6v_J-nL_YvXyGy6sCHCw9uF8bdaPj2qry5O9fcT-kMezYlW_BH-k5ub</recordid><startdate>201510</startdate><enddate>201510</enddate><creator>Angelo, H. 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D.</creatorcontrib><creatorcontrib>Gomes Silva, I. I. F.</creatorcontrib><creatorcontrib>Oliveira, R. D. R.</creatorcontrib><creatorcontrib>Louzada-Júnior, P.</creatorcontrib><creatorcontrib>Donadi, E. A.</creatorcontrib><creatorcontrib>Crovella, S.</creatorcontrib><creatorcontrib>Maia, M. M. D.</creatorcontrib><creatorcontrib>de Souza, P. R. E.</creatorcontrib><creatorcontrib>Sandrin-Garcia, P.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Tissue antigens</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Angelo, H. D.</au><au>Gomes Silva, I. I. F.</au><au>Oliveira, R. D. R.</au><au>Louzada-Júnior, P.</au><au>Donadi, E. 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IL‐18 +105 A/C, IL‐12B +1188 A/C and IFN‐γ +874 T/A polymorphisms were analyzed by restriction fragment length polymorphism‐polymerase chain reaction (PCR) and amplification refractory mutation system PCR from 90 RA patients and 186 healthy individuals. There were significant differences to IL‐18 +105 A/C polymorphism between the RA and control groups (odds ratio = 3.77; P &lt; 0.0001). Individual carriers of the variant allele C had a 3.77‐fold increased risk of for RA (P = 0.0032). No association was observed for IL‐12B and IFN‐γ polymorphisms. Our finds suggest a possible role for IL‐18 polymorphism in the RA susceptibility in studied population.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>26302971</pmid><doi>10.1111/tan.12645</doi><tpages>3</tpages></addata></record>
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ispartof Tissue antigens, 2015-10, Vol.86 (4), p.276-278
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language eng
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source Wiley
subjects Adult
Alleles
arthritis
Arthritis, Rheumatoid - genetics
Arthritis, Rheumatoid - immunology
Arthritis, Rheumatoid - pathology
Brazil
Case-Control Studies
cytokines
Female
Gene Expression
Gene Frequency
Genetic Predisposition to Disease
Humans
Interferon-gamma - genetics
Interferon-gamma - immunology
Interleukin-12 Subunit p40 - genetics
Interleukin-12 Subunit p40 - immunology
Interleukin-18 - genetics
Interleukin-18 - immunology
Male
Middle Aged
Pilot Projects
Polymerase Chain Reaction
polymorphism
Polymorphism, Restriction Fragment Length
Polymorphism, Single Nucleotide
rheumatoid
Risk
title Interleukin-18, interleukin-12B and interferon-γ gene polymorphisms in Brazilian patients with rheumatoid arthritis: a pilot study
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