Anti-BTNL2 polyclonal antibody [PE]

Hyperlipidemia-related mechanisms have been associated with damage to the cardiovascular disease (CVD). Here, we discuss potential explanations for the higher prevalence of hyperlipidemia in the Jing and Han populations. Although genetic and environmental factors are the triggers, the search for the ethnic and gender related factors that explain the increased susceptibility of hyperlipidemia is a promising area for research. Ethnicity and gender differences could be the major confounding variable to prove genetic associations. Despite that, we investigated the ethnic and sex-specific association between the butyrophilin-like 2 gene (BTNL2) rs9268480 single nucleotide polymorphism (SNP) and several environmental factors with serum lipid profiles in the Jing and Han populations. Genotypes of the rs9268480 SNP, clinical and biochemical measurements were characterized in a total of 2503 subjects (1148 Jing and 1355 Han). Jing populations had higher serum total cholesterol (TC), triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C) levels and lower apolipoprotein (Apo) A1 levels and the ratio of ApoA1 to ApoB than in Han. The frequency of susceptibility alleles of rs9268480 C > T were significantly different between the two populations (20.86% vs. 18.16%; P = 0.016), and between males and females in Jing (17.18% vs. 24.65%; P < 0.001) and Han (16.57% vs. 19.88%; P = 0.026) populations. The minor T allele carriers of BTNL2 rs9268480 SNP was a risk allele for dyslipidemia, especially higher serum TG levels in ethnic and sexually dimorphic subgroup. These results suggested that the genetic variant of rs9268480 C > T and several environmental factors were associated with hyperlipidemia, and there may be a ethnic- and/or sex-specific association of this SNP.

Background- The HLA-DRB1*01 allele of the human leukocyte antigen has been associated with acute coronary syndrome. Genome-wide association studies have revealed associations with human leukocyte antigen and non-human leukocyte antigen genes of 3 major histocompatibility complex gene classes but not at allelic level. Methods and Results- We conducted a large-scale genetic analysis on a case-control cohort comprising 5376 acute coronary syndrome cases and 4852 unrelated controls from 4 populations of 2 European countries. We analyzed the risk candidate allele of HLA-DRB1*01 by genomic real-time polymerase chain reaction together with high-density single nucleotide polymorphisms of the major histocompatibility complex to precisely identify risk loci for acute coronary syndrome with effective clinical implications. We found a risk haplotype for the disease containing single nucleotide polymorphisms from BTNL2 and HLA-DRA genes and the HLA-DRB1*01 allele. The association of the haplotype appeared in 3 of the 4 populations, and the direction of the effect was consistent in the fourth. Coronary samples from subjects homozygous for the disease-associated haplotype showed higher BTNL2 mRNA levels (r=0.760; P < 0.00001).We localized, with immunofluorescence staining, BTNL2 in CD68-positive macrophages of the coronary artery plaques. In homozygous cases, BTNL2 blocking, in T-cell stimulation assays, enhanced CD4(+)FOXP3(+) regulatory T cell proliferation significantly (blocking versus nonblocking; P < 0.05). Conclusions- In cases with the risk haplotype for acute coronary syndrome, these results suggest involvement of enhanced immune reactions. BTNL2 may have an inhibitory effect on FOXP3(+) T cell proliferation, especially in patients homozygous for the risk alleles. Clinical Trial Registration- [GRAPHICS] ; Unique Identifier: NCT00417534.