The role of KIR2DL3/HLA-C*0802 in Brazilian patients with rheumatoid vasculitis

Detalhes bibliográficos
Autor(a) principal: Nishimura, Wester Eidi
Data de Publicação: 2015
Outros Autores: Sachetto, Zoraida, Costallat, Lilian Teresa Lavras, Yazbek, Michel Alexandre, Londe, Ana Carolina Santos, Guariento, Edilaine Gildo, Marques, Silvia Barbosa Dutra, Bertolo, Manoel Barros
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Clinics
Texto Completo: https://www.revistas.usp.br/clinics/article/view/101071
Resumo: OBJECTIVES: Rheumatoid arthritis is a polygenically controlled systemic autoimmune disease. Rheumatoid vasculitis is an important extra-articular phenotype of rheumatoid arthritis that can result in deep cutaneous ulcers. The objective of this study was to establish a correlation between the frequency of major histocompatibility complex class I/II alleles and killer immunoglobulin-like receptor genotypes in patients with cutaneous rheumatoid vasculitis. METHODS: Using the Scott & Bacon 1984 criteria to diagnose rheumatoid vasculitis and after excluding any other causes such as diabetes, atherosclerosis, adverse drug reactions, infection, and smoking, patients who met the criteria were selected. All of the selected rheumatoid vasculitis patients presented deep cutaneous ulcers. Identification of the major histocompatibility complex class I/II and killer immunoglobulin-like receptor genotypes was performed by polymerase chain reaction assays of samples collected from the 23 rheumatoid vasculitis patients as well as from 80 controls (40 non-rheumatoid vasculitis RA control patients and 40 healthy volunteers). RESULTS: An association between the presence of the HLA-DRB1*1402 and HLA-DRB1*0101 alleles and cutaneous lesions in rheumatoid vasculitis patients and a correlation between the inhibitor KIR2DL3 and the HLA-C*0802 ligand in rheumatoid vasculitis patients were found. CONCLUSION: An association was found between the presence of the HLA-DRB1*1402 and HLA-DRB1*0101 alleles and the development of cutaneous lesions in rheumatoid vasculitis patients. Additionally, the HLA-C*0802 ligand protects these individuals from developing cutaneous lesions.
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spelling The role of KIR2DL3/HLA-C*0802 in Brazilian patients with rheumatoid vasculitis OBJECTIVES: Rheumatoid arthritis is a polygenically controlled systemic autoimmune disease. Rheumatoid vasculitis is an important extra-articular phenotype of rheumatoid arthritis that can result in deep cutaneous ulcers. The objective of this study was to establish a correlation between the frequency of major histocompatibility complex class I/II alleles and killer immunoglobulin-like receptor genotypes in patients with cutaneous rheumatoid vasculitis. METHODS: Using the Scott & Bacon 1984 criteria to diagnose rheumatoid vasculitis and after excluding any other causes such as diabetes, atherosclerosis, adverse drug reactions, infection, and smoking, patients who met the criteria were selected. All of the selected rheumatoid vasculitis patients presented deep cutaneous ulcers. Identification of the major histocompatibility complex class I/II and killer immunoglobulin-like receptor genotypes was performed by polymerase chain reaction assays of samples collected from the 23 rheumatoid vasculitis patients as well as from 80 controls (40 non-rheumatoid vasculitis RA control patients and 40 healthy volunteers). RESULTS: An association between the presence of the HLA-DRB1*1402 and HLA-DRB1*0101 alleles and cutaneous lesions in rheumatoid vasculitis patients and a correlation between the inhibitor KIR2DL3 and the HLA-C*0802 ligand in rheumatoid vasculitis patients were found. CONCLUSION: An association was found between the presence of the HLA-DRB1*1402 and HLA-DRB1*0101 alleles and the development of cutaneous lesions in rheumatoid vasculitis patients. Additionally, the HLA-C*0802 ligand protects these individuals from developing cutaneous lesions. Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo2015-06-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://www.revistas.usp.br/clinics/article/view/10107110.6061/clinics/2015(06)04Clinics; Vol. 70 No. 6 (2015); 408-412Clinics; v. 70 n. 6 (2015); 408-412Clinics; Vol. 70 Núm. 6 (2015); 408-4121980-53221807-5932reponame:Clinicsinstname:Universidade de São Paulo (USP)instacron:USPenghttps://www.revistas.usp.br/clinics/article/view/101071/99730Copyright (c) 2015 Clinicsinfo:eu-repo/semantics/openAccessNishimura, Wester Eidi Sachetto, Zoraida Costallat, Lilian Teresa Lavras Yazbek, Michel Alexandre Londe, Ana Carolina Santos Guariento, Edilaine Gildo Marques, Silvia Barbosa Dutra Bertolo, Manoel Barros 2015-07-28T15:24:28Zoai:revistas.usp.br:article/101071Revistahttps://www.revistas.usp.br/clinicsPUBhttps://www.revistas.usp.br/clinics/oai||clinics@hc.fm.usp.br1980-53221807-5932opendoar:2015-07-28T15:24:28Clinics - Universidade de São Paulo (USP)false
dc.title.none.fl_str_mv The role of KIR2DL3/HLA-C*0802 in Brazilian patients with rheumatoid vasculitis
title The role of KIR2DL3/HLA-C*0802 in Brazilian patients with rheumatoid vasculitis
spellingShingle The role of KIR2DL3/HLA-C*0802 in Brazilian patients with rheumatoid vasculitis
Nishimura, Wester Eidi
title_short The role of KIR2DL3/HLA-C*0802 in Brazilian patients with rheumatoid vasculitis
title_full The role of KIR2DL3/HLA-C*0802 in Brazilian patients with rheumatoid vasculitis
title_fullStr The role of KIR2DL3/HLA-C*0802 in Brazilian patients with rheumatoid vasculitis
title_full_unstemmed The role of KIR2DL3/HLA-C*0802 in Brazilian patients with rheumatoid vasculitis
title_sort The role of KIR2DL3/HLA-C*0802 in Brazilian patients with rheumatoid vasculitis
author Nishimura, Wester Eidi
author_facet Nishimura, Wester Eidi
Sachetto, Zoraida
Costallat, Lilian Teresa Lavras
Yazbek, Michel Alexandre
Londe, Ana Carolina Santos
Guariento, Edilaine Gildo
Marques, Silvia Barbosa Dutra
Bertolo, Manoel Barros
author_role author
author2 Sachetto, Zoraida
Costallat, Lilian Teresa Lavras
Yazbek, Michel Alexandre
Londe, Ana Carolina Santos
Guariento, Edilaine Gildo
Marques, Silvia Barbosa Dutra
Bertolo, Manoel Barros
author2_role author
author
author
author
author
author
author
dc.contributor.author.fl_str_mv Nishimura, Wester Eidi
Sachetto, Zoraida
Costallat, Lilian Teresa Lavras
Yazbek, Michel Alexandre
Londe, Ana Carolina Santos
Guariento, Edilaine Gildo
Marques, Silvia Barbosa Dutra
Bertolo, Manoel Barros
description OBJECTIVES: Rheumatoid arthritis is a polygenically controlled systemic autoimmune disease. Rheumatoid vasculitis is an important extra-articular phenotype of rheumatoid arthritis that can result in deep cutaneous ulcers. The objective of this study was to establish a correlation between the frequency of major histocompatibility complex class I/II alleles and killer immunoglobulin-like receptor genotypes in patients with cutaneous rheumatoid vasculitis. METHODS: Using the Scott & Bacon 1984 criteria to diagnose rheumatoid vasculitis and after excluding any other causes such as diabetes, atherosclerosis, adverse drug reactions, infection, and smoking, patients who met the criteria were selected. All of the selected rheumatoid vasculitis patients presented deep cutaneous ulcers. Identification of the major histocompatibility complex class I/II and killer immunoglobulin-like receptor genotypes was performed by polymerase chain reaction assays of samples collected from the 23 rheumatoid vasculitis patients as well as from 80 controls (40 non-rheumatoid vasculitis RA control patients and 40 healthy volunteers). RESULTS: An association between the presence of the HLA-DRB1*1402 and HLA-DRB1*0101 alleles and cutaneous lesions in rheumatoid vasculitis patients and a correlation between the inhibitor KIR2DL3 and the HLA-C*0802 ligand in rheumatoid vasculitis patients were found. CONCLUSION: An association was found between the presence of the HLA-DRB1*1402 and HLA-DRB1*0101 alleles and the development of cutaneous lesions in rheumatoid vasculitis patients. Additionally, the HLA-C*0802 ligand protects these individuals from developing cutaneous lesions.
publishDate 2015
dc.date.none.fl_str_mv 2015-06-01
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv https://www.revistas.usp.br/clinics/article/view/101071
10.6061/clinics/2015(06)04
url https://www.revistas.usp.br/clinics/article/view/101071
identifier_str_mv 10.6061/clinics/2015(06)04
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv https://www.revistas.usp.br/clinics/article/view/101071/99730
dc.rights.driver.fl_str_mv Copyright (c) 2015 Clinics
info:eu-repo/semantics/openAccess
rights_invalid_str_mv Copyright (c) 2015 Clinics
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
dc.source.none.fl_str_mv Clinics; Vol. 70 No. 6 (2015); 408-412
Clinics; v. 70 n. 6 (2015); 408-412
Clinics; Vol. 70 Núm. 6 (2015); 408-412
1980-5322
1807-5932
reponame:Clinics
instname:Universidade de São Paulo (USP)
instacron:USP
instname_str Universidade de São Paulo (USP)
instacron_str USP
institution USP
reponame_str Clinics
collection Clinics
repository.name.fl_str_mv Clinics - Universidade de São Paulo (USP)
repository.mail.fl_str_mv ||clinics@hc.fm.usp.br
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