The association of Takayasu arteritis with Amerindian and Asian HLA-DRB1 alleles (DRB1*1602 and DRB1*1001) in the Colombian mestizo patients reported here, and with HLA-B*3906 previously reported in Mexicans, suggest the possibility that some HLA and disease associations are markers for ethnicity of a population carrying a disease gene which is present in an admixed population with the disease.
The purposes of this study were to examine the TNFR2 polymorphism in Japanese patients with SLE and to investigate its association with other autoimmune diseases accompanied by vasculitis, mixed connective tissue disease, Buerger's disease, and Takayasu's arteritis.
Studies both in Mexican and Asian populations suggest that residues at positions 63 (glutamic acid) and 67 (serine) of the HLA-B molecule could be the genetic markers for TA.
P-selectin may play a significant role in the inflammatory and thrombotic responses associated with intractable TA, presumably by inducing platelet-leukocyte interactions.
We previously revealed that one of the human leukocyte antigen-linked susceptibility genes for Takayasu's arteritis (TA) was mapped between TNFA and MICB loci and that -63T allele of NFKBIL1, which is between TNFA and MICB loci, was associated with rheumatoid arthritis (RA) in the Japanese population.
We previously revealed that one of the human leukocyte antigen-linked susceptibility genes for Takayasu's arteritis (TA) was mapped between TNFA and MICB loci and that -63T allele of NFKBIL1, which is between TNFA and MICB loci, was associated with rheumatoid arthritis (RA) in the Japanese population.
We previously revealed that one of the human leukocyte antigen-linked susceptibility genes for Takayasu's arteritis (TA) was mapped between TNFA and MICB loci and that -63T allele of NFKBIL1, which is between TNFA and MICB loci, was associated with rheumatoid arthritis (RA) in the Japanese population.
Sera from AAECA-positive patients with TA, compared with sera from AAECA-negative patients with TA and that from controls, induced increased expression of E-selectin (mean +/- SD 0.833 +/- 0.063 versus 0.217 +/- 0.081 and 0.221 +/- 0.101 optical density [OD] units, respectively) and vascular cell adhesion molecule 1 (0.620 +/- 0.144 versus 0.165 +/- 0.005 and 0.177 +/- 0.055 OD units, respectively) and increased production of interleukin-4 (IL-4) (6.8 +/- 2.4 versus 1.2 +/- 1.6 and 1.3 +/- 2.5 pg/ml, respectively), IL-6 (24.3 +/- 2.4 versus 4.5 +/- 6.7 and 5.9 +/- 5.1 pg/ml, respectively), and IL-8 (36.8 +/- 10.3 versus 10.1 +/- 6.7 and 7.8 +/- 2.1 pg/ml, respectively).
Sera from AAECA-positive patients with TA, compared with sera from AAECA-negative patients with TA and that from controls, induced increased expression of E-selectin (mean +/- SD 0.833 +/- 0.063 versus 0.217 +/- 0.081 and 0.221 +/- 0.101 optical density [OD] units, respectively) and vascular cell adhesion molecule 1 (0.620 +/- 0.144 versus 0.165 +/- 0.005 and 0.177 +/- 0.055 OD units, respectively) and increased production of interleukin-4 (IL-4) (6.8 +/- 2.4 versus 1.2 +/- 1.6 and 1.3 +/- 2.5 pg/ml, respectively), IL-6 (24.3 +/- 2.4 versus 4.5 +/- 6.7 and 5.9 +/- 5.1 pg/ml, respectively), and IL-8 (36.8 +/- 10.3 versus 10.1 +/- 6.7 and 7.8 +/- 2.1 pg/ml, respectively).
The frequencies of IL12B 1188 C allele (p = 0.03, OR = 1.7) and CC genotype (p = 0.007, OR = 3.7) were both higher in TA patients than in control subjects.
The polymorphism of IL-12 as well as IL-6 and IL-2 genes may contribute to susceptibility and pathogenesis of TA by altering cytokine production and inducing inflammation.