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Immunogenetic Profile Of Egyptian Children With Juvenile Rheumatoid Arthritis

1Abd Al-Rehiem G. Ads, 2Farha A. El-Chennawi, 1Mohamed I. Abd El-Hamid, 3Mostafa A. Abo-Farrag and 1Azza M. Hassan

Departments of 1Microbiology, and 3Pediatric Faculty of Medicine, Tanta University, Tanta and department of 2Clinical Pathology, Faculty of Medicine, Mansoura University, Mansoura, Egypt.

The aim of the present study is to analyze the immunogenetic features of juvenile rheumatoid arthritis (JRA) in Egyptian children and to investigate the role of human leukocytic antigen (HLA) class I and II alleles as well as T cell receptors (TCRs) polymorphism in susceptibility to JRA. Subjects were 25 Egyptian patients with JRA and 20 controls were included in this study. Rheumatoid factor (RF) was performed using latex test, while antinuclear antibodies (ANA) were estimated by immunofluorescent assay. For HLA-class I typing, lymphocyte cytotoxicity technique was performed, while for HLA class II typing; DR, DQA, and DQB as well as TCRVB6.1 polymorphism DNA techniques were used.   We studied two groups of patients with JRA having different disease prognosis and course; pauciarticular and polyarticular groups. Each JRA subset was characterized by a distinct distribution of HLA class I and class II alleles. In pauciarticular group and its early onset subset, there were positive associations with HLA-A2, B5, DRB 1*0801 and 1301, DQA1*01 as well as DQB 1*02, while in late onset subset there was positive association with HLA-B27. In polyarticular group and its seronegative subset, the significant positive associations were mainly with HLA-B13, DRB1 *01 and *0801 as well as DQA1 *01. DRB1 *0401 was the only HLA allele that was significantly frequent in seropositive subset. Unique protective effect of HLA-DRRB 1*1001 was observed in JRA patients. TCRVB6.1 polymorphism was not associated with any of JRA groups except in those with or without chronic iridocyclitis, ANA or both. Immunogenetic profile of JRA in Egyptian children appears to be somewhat different from that reported for other populations and the role of TCRVB6.1 polymorphism needs to be reevaluated.