Molecular genotyping for the major histocompatibility complex (MHC) class II loci, HLA-DRB1, -DQB1 and -DQA1, in 100 patients with relapsing/remitting multiple sclerosis (MS) demonstrated an association with the HLA-DR2, DQw6-associated alleles DRB1*1501, DQB1*0602 and DQA1*0102, thereby extending this finding among MS patients in several countries to an Australian population. Analysis by the relative predispositional effect (RPE) method provided no evidence for a second susceptibility allele at either DQA1 or DQB1. However, our data and that of others suggest a negative association with DQA1*0101. Associations were found with DQB1 alleles sharing sequence homology with DQB1*0602, with DQB1 alleles encoding leucine at residue 26 (Leu 26), with DQA1 alleles encoding glutamine at residue 34 (Gln 34) and with Leu 26 plus Gln 34 alleles, but each was shown by two-loci linkage analysis to be secondary to the DRB1*1501, DQB1*0602, DQA1*0102 association. The recently reported negative association with DQA1 alleles encoding phenylalanine at amino acid 25, leucine at amino acid 69 and arginine at amino acid 52 was not found in this study, although there was a trend towards reduced phenylalanine at amino acid 25. The determination at a molecular level of an explanation for the world-wide association with these alleles remains elusive despite major advances in MHC typing.

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Forty-four patients with inflammatory demyelinating polyneuritis (22 with Landry-Guillain-Barré syndrome, 6 with subacute polyneuritis, and 16 with chronic relapsing polyneuritis) were typed for genetic markers in and around the HLA region of chromosome 6. Patients with chronic relapsing polyneuritis showed a definite association with HLA-AW30 and AW31 and probable associations with HLA-B8, HLA-DW3, and glyoxalase I. No significant associations were demonstrated with the Landry-Guillain-Barré syndrome although an increase in glyoxalase I was significant if combined with the results of typing in chronic relapsing polyneuritis. The total patient group showed significant increases in HLA-AW30, HLA-AW31, and HLA-DW3. The results support the view that HLA-linked genetic factors influence susceptibility to chronic relapsing polyneuritis and may contribute to the differences in clinical patterns observed in inflammatory demyelination of the peripheral nervous system.