TY - JOUR
T1 - Comprehensive analysis of polymorphisms in the HLA-G 5′ upstream regulatory and 3′ untranslated regions in Brazilian patients with systemic lupus erythematosus
AU - Catamo, E.
AU - Addobbati, C.
AU - Segat, L.
AU - Sotero Fragoso, T.
AU - Tavares Dantas, A.
AU - de Ataide Mariz, H.
AU - Ferreira da Rocha Junior, L.
AU - Branco Pintoduarte, A. L.
AU - Coelho, A. V C
AU - de Moura, R. R.
AU - Polesello, V.
AU - Crovella, S.
AU - Sandrin Garcia, P.
PY - 2015/6/1
Y1 - 2015/6/1
N2 - This study aims to comprehensively analyze human leucocyte antigen (HLA)-G polymorphisms association with susceptibility to systemic lupus erythematosus (SLE) development and clinical manifestations. The HLA-G 5′ upstream regulatory region (URR), 3′ untranslated region (UTR) and a cytosine deletion at exon 3 (ΔC, HLA-G*0105N allele) were analyzed in 114 SLE patients and 128 healthy controls from North East Brazil. The +3003T>C (rs1707) C allele and the HG010101c extended HLA-G allele were significantly more frequent in SLE patients than healthy controls (+3003C allele frequency: 12% in SLE patients vs 6% in controls; odds ratio (OR), 2.10, 95% confidence interval (CI), 1.06-4.28, P=0.026; HG010101c frequency: 11.8% in SLE patients and 6.3% in controls; OR, 2.14, 95% CI, 1.01-4.51, P=0.046) and were associated with susceptibility for disease development. Other polymorphisms were associated with different clinical manifestations. Although HLA-G role in SLE disease is far from being elucidated yet, our association study results along with a systematic review and meta-analysis suggest that HLA-G might be able to slightly modulate the complex SLE phenotype (pooled OR, 1.14, 95% CI, 1.02-1.27, P=0.021).
AB - This study aims to comprehensively analyze human leucocyte antigen (HLA)-G polymorphisms association with susceptibility to systemic lupus erythematosus (SLE) development and clinical manifestations. The HLA-G 5′ upstream regulatory region (URR), 3′ untranslated region (UTR) and a cytosine deletion at exon 3 (ΔC, HLA-G*0105N allele) were analyzed in 114 SLE patients and 128 healthy controls from North East Brazil. The +3003T>C (rs1707) C allele and the HG010101c extended HLA-G allele were significantly more frequent in SLE patients than healthy controls (+3003C allele frequency: 12% in SLE patients vs 6% in controls; odds ratio (OR), 2.10, 95% confidence interval (CI), 1.06-4.28, P=0.026; HG010101c frequency: 11.8% in SLE patients and 6.3% in controls; OR, 2.14, 95% CI, 1.01-4.51, P=0.046) and were associated with susceptibility for disease development. Other polymorphisms were associated with different clinical manifestations. Although HLA-G role in SLE disease is far from being elucidated yet, our association study results along with a systematic review and meta-analysis suggest that HLA-G might be able to slightly modulate the complex SLE phenotype (pooled OR, 1.14, 95% CI, 1.02-1.27, P=0.021).
KW - Human leukocyte antigen-G
KW - mRNA stability
KW - Polymorphisms
KW - Systemic lupus erythematosus
UR - http://www.scopus.com/inward/record.url?scp=84929042723&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84929042723&partnerID=8YFLogxK
U2 - 10.1111/tan.12545
DO - 10.1111/tan.12545
M3 - Article
C2 - 25762019
AN - SCOPUS:84929042723
VL - 85
SP - 458
EP - 465
JO - Tissue Antigens
JF - Tissue Antigens
SN - 0001-2815
IS - 6
ER -