Objective To investigate the relationship between human leukocyte antigen(HLA)-B51 and Behcet′s disease (BD) with uveities. Methods HLA-A and HLA-B antigen of 27 pateints with BD and 30 healthy persons were detected by microly mphocyte toxicity asssay. HLA-B51 allele (HLA-B5101-B5107) in BD patients with positive HLA-B51 antigen and the controls was detected by polymerase chain reaction-sequence specific primer(PCR-SSP). Results The positive rate of HLA-B51 was 63% and 16.7% in BD patients and the controls, respectively (χ2=12.9, P＜0.001, Pc＜0.05,RR=8.5). Uveities was found in 11 out of 27 BD patients with uveitis. No relativity was found between HLA-B51 and uveitis in BD patients(RR=2.07,χ2=0.759,P＞0.25),and weak association was found between HLA=B5101 and uveitis (RR=2.67, χ2=1.395, P＞0.10). Conclusions HLA-B51 might be a susceptible gene for BD, and there was a weak association between HLA-B51(HLA-B5101) and BD patients with uveitis.(Chin J Ocul Fundus Dis，2004，20：203-205)
Eighteen male patients and 10 female patients with Bt.Behccedil;et's disease were addressed to study the influences of sex factor on Behccedil;et's disease. It was found that recurrences of uveitis were more frequent in malepatients than in females,and that male patients were worse than females in prognosis due to the high severity of retinal vasculitis and the low sensitivity to treatment.It is pressumed that the sex hormone may, at least in part,contribute to the diffrenees between the male and female patients. （Chin J Ocul Fundus Dis,1994,10:143-145）
Behcet's Disease (BD) is a multisystem vasculitis characterized by disease alternated with recurrent episodes and remissions, involving genital, oral, ocular uvea, cutaneous, and articular manifestations. The nuclear factor (NF)-κB signaling pathway paly an important role in the BD progression. It encompasses diverse gene, protein, and cellular regulatory mechanisms operating across various levels, alongside microbiological and experimental studies involving animals and cells. At the protein research findings, activation of the NF-κB pathway in BD patients is marked by elevated plasma levels of soluble CD40 ligand, which stimulates neutrophils to release reactive oxygen species and extracellular traps, thereby promoting inflammation. At the cellular research findings, macrophages in BD patients polarize towards classically activated macrophages phenotype through the NF-κB pathway, exacerbating the inflammatory response. The activation of NF-κB is associated with increased expression of anti-apoptotic proteins in T cells, leading to prolonged inflammation. Microbiological investigations reveal that the decreased gut microbiota diversity in BD patients compromises intestinal barrier integrity. NF-κB pathway involvement in regulating neutrophil and type 1 helper T cell (Th) 1/Th17 cell function worsens inflammation. Genetically, BD patients exhibit polymorphisms in immune regulatory genes, which contribute to inflammation through the NF-κB pathway. Mutations in NF-κB-associated genes elevate the risk of BD, while mutations in the endogenous inhibitor A20 lead to abnormal NF-κB activity, sustaining inflammation. Animal experiments and in vitro experiments corroborate the efficacy of NF-κB inhibitors in attenuating inflammation. Targeting upstream inflammatory factors within the NF-κB pathway yields positive outcomes in BD patients. In summary, the NF-κB signaling pathway plays a pivotal role in the development of BD. Developing NF-κB inhibitors may open new avenues for treating BD. Further research is necessary to comprehensively elucidate the precise mechanisms by which NF-κB operates in the pathogenesis of BD, as well as its potential clinical applications in therapy.