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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). [ABSTRACT FROM AUTHOR]

We analyzed the possible association between human leukocyte antigen-G ( HLA-G) genetic variants, supposed to regulate HLA-G expression, and the susceptibility to develop rheumatoid arthritis ( RA) as well as its clinical manifestations. The 5′upstream regulatory region ( 5′URR) and 3′untranslated region ( 3′UTR) regions of the HLA-G gene were screened in 127 RA patients and 128 controls: 10 5′ URR and 3 3′ UTR HLA-G polymorphisms as well as two haplotypes were associated with risk for RA development, while a polymorphism in the 5′ URR showed an association with the degree of disease activity. These findings, although the number of cases analyzed is limited and the P-values are modest, indicate a possible association between HLA-G gene polymorphisms and susceptibility to develop RA disease and its severity. [ABSTRACT FROM AUTHOR]

The article discusses research that indicates an association between variations in the SLC30A6 gene that can modulate the zinc function of the transporter ZNT6 and the development of rheumatoid arthritis and its clinical and laboratory forms. Topics include the study design and the extraction and analyses of genomic data. The implications of the link between the A/A genotype from SLC30A6 and low susceptibility to severity of RA are also discussed.