کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8648459 | 1570692 | 2018 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Human leukocyte antigen-G 3' untranslated region polymorphisms are associated with asthma severity
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شناسی مولکولی
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چکیده انگلیسی
Asthma is a genetically complex chronic inflammatory airway disorder, and according to disease pathogenesis, clinical manifestations may vary according to asthma severity. A gene region close to the human leukocyte antigen-G (HLA-G) gene was identified as an independent susceptibility marker for asthma. Considering that the HLA-G immune checkpoint molecule may modulate inflammation, we evaluated the diversity of the HLA-G 3â² untranslated region (3â²UTR) in asthmatic patients stratified according to disease severity. We evaluate the entire HLA-G 3â²UTR segment in 115 Brazilian patients stratified into mild (n=29), moderate (n=21) and severe asthmatics (n=65), and in 116 healthy individuals. HLA-G 3â²UTR typing was performed using Sanger sequencing. The multiple comparisons among patients stratified according to disease severity revealed several associations; however, after Bonferroni's correction, the following results remained significant: i) the +3010C and +3142G alleles were overrepresented in mild asthma patients when compared to controls; ii) the +3010G and +3142C alleles were overrepresented in severe asthma patients in comparison to patients with mild asthma. In conclusion, the +3010C/G and +3142C/G HLA-G 3â²UTR variation sites were differentially associated according to asthma severity.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular Immunology - Volume 101, September 2018, Pages 500-506
Journal: Molecular Immunology - Volume 101, September 2018, Pages 500-506
نویسندگان
Cinthia C. Alves, LuÃsa K.P. Arruda, FabÃola R. Oliveira, Juliana D. Massaro, Beatriz J. Aquino, Michelle A. Paz, Erick C. Castelli, Celso T. Mendes-Junior, Eduardo A. Donadi,