However, polymorphic analyses of the TNFB gene and Tau-a microsatellite between the HLA-B and TNF genes indicate that the pathogenic gene of BD is not the HLA-B51 gene itself but another gene located around the HLA-B gene.
The specific proliferative response of TCR gamma delta + lymphocytes elicited by the 4 peptides can be used as a laboratory test for the diagnosis of BD.
In order to investigate the influence of the MICB gene, located about 120 kb centromeric of the HLA-B gene, on the susceptibility to BD, (CA/TG) dinucleotide repeat microsatellite polymorphism in intron 1 of the MICB gene was investigated among 77 Japanese patients with BD, 60 randomly selected controls and 28 HLA-B51-positive unrelated healthy controls.
The fact that different HLA-B51 subtypes are associated with BD could suggest that common motifs shared by HLA-B51-related alleles are involved in the susceptibility to BD or, in the light of recent studies, that a mutation causing the susceptibility to BD occurred in the B*5101 haplotype, close to HLA-B gene, before the divergence of B*5108 from the B*5101 allele.
This result suggests that the MICB gene itself is not responsible for the development of BD, and that the candidate gene(s) for BD is located between the MICA and HLA-C genes.
This result suggests that the MICB gene itself is not responsible for the development of BD, and that the candidate gene(s) for BD is located between the MICA and HLA-C genes.
Seventy-one Turkish patients with BD, diagnosed according to the International Study Group for Behçet's Disease criteria, were studied and compared with 600 healthy controls to determine not only frequencies of HLA-A, B, and DR antigens but also whether BD shows any distinct linkage disequilibrium (LD) patterns.
These findings suggest that homozygosity or heterozygosity for factor V Leiden is not always associated with occurrence of venous thrombosis in BD, but it may be a contributing risk factor for venous thromboembolic events in these patients.
In stratification analysis on the confounding effect of MIC-A009 on HLA-B*51 association and vice versa, Behçet's disease was distinctively associated only with HLA-B*51.
Here, eight polymorphic microsatellite markers, distributed over a 900-kb region surrounding the HLA-B locus, were subjected to association analysis for Behçet disease.
The results of this mapping study, and the results of an earlier study of ours, suggest that MICA is a strong candidate gene for the development of Behçet disease.
This study revealed in Greek patients a strong association of BD with a particular MICA-TM allele, MICA-A6, providing insight into the molecular mechanism underlying the development of BD.
Reactivity of eosinophils to the monoclonal antibody against CCR3 and the chemotaxis to eotaxin were slightly reduced in this patient as compared with healthy controls or a patient with Behçet disease homozygous for the common allele, while CCR3 mRNA level was not different.
Since the B51 antigen has been recently identified to comprise nine alleles, B*5101-B*5109, we performed HLA-B51 allele genotyping by the polymerase chain reaction-sequencing based typing (PCR-SBT) method as well as serological HLA-A and -B typing among 21 Italian patients with Behçet's disease in order to investigate whether there is any correlation of one particular B51-associated allele with Behcet's disease.