DISTRIBUTIONS OF HLA CLASS-II ALLELES IN AUTOANTIBODY SUBSETS AMONG NORWEGIAN PATIENTS WITH SYSTEMIC LUPUS-ERYTHEMATOSUS

In order to find potential correlations between HLA class II alleles a nd anti-SS-A,-SS-B, -Sm and anti-snRNP responses among Norwegian patie nts with systemic lupus erythematosus (SLE), HLA-DRB1, -DRB30101, -DQ A1 and -DQB1 alleles were determined by DNA typing 50 patients and 108 controls. HLA distributions were analysed in the following autoantibo dy subgroups: anti-SS-A with SS-B, anti-SS-A without -SS-B, anti-snRNP without -Sm, anti-SS-A without -snRNP and anti-snRNP without -SS-A. T he autoantibodies were detected by EIA (enzyme immunuassay). Patients with anti-SSA and -SS-B had significantly increased frequencies of DRB 103, DRB3*0101, DQA1*0501, DQB1*0201 (in linkage disequilibrium) vers us controls and versus patients without anti-SS-A and SS-B. No differe nces in HLA distribution were found when the group with anti-SS-A alon e was compared to the group with anti-SS-A and concomitant -SS-B. Comp aring the groups with and without anti-SS-A and -SS-B, the highest RR were found for the alleles DRB103, DRB3*0101, DQB1*0501,DQB1*0201 (in linkage disequilibrium) with RR: 16.8, 5.0, 19.6, 10.3, respectively, P < 0.05). RR for DQw2/DQw6 heterozygotes was 3.5 (Ns.), and RR for c ases having DQ alpha molecules with glutamine in position 34 and DQ be ta molecules with leucine in position 26 on both chains was 6.3 (P < 0 .05). No HLA associations were observed in the group with anti-snRNP w ithout concomitant -Sm or without concomitant -SS-A. These results sho w that production of anti-SS-A and -SS-B is associated to the HLA alle les DRB103, DRB3*0101, DQA1*0501, DQB1*0201, and that this haplotype shows stronger correlation to these responses than DQw2/DQw6 heterozyg osity or HLA molecules having glutamine in position 34 (DQ alpha) and leucine in position 26 (DQ beta). The failure to observe any correlati on with DRB115,16 (DR2) in the group with anti-SS-A alone may demonst rate ethnic differences concerning this response. The failure to ident ify any HLA associations for the anti-snRNP response may reflect the h eterogeneity of the molecules that constitute this antigen.