The role of KIR2DL3/HLA-C*0802 in Brazilian patients with rheumatoid vasculitis
Autor(a) principal: | |
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Data de Publicação: | 2015 |
Outros Autores: | , , , , , , |
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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USP-19 |
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Clinics |
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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 |
_version_ |
1800222762132832256 |