Summary Comparison of DOA 1 and DOB1 alleles in 60 children with common acute tymphoblastic leukaemia (c-ALL) and 78 newborn infant control subjects revealed that male but not female patients had a higher frequency of DA1*0A101/'O104 and DOB1*0501 than appropriate control subjects. The results suggest a male-associated susceptibility haplotype in c-ALL and supports an infectious aetiology.

Summary Epidemiological studies suggest that childhood common acute lymphoblastic leukaemia (c-ALL) may be the rare outcome of early post-natal infection with a common infectious agent. One of the factors that may determine whether a child succumbs to c-ALL is how it responds to the candidate infection. Since immune responses to infection are under the partial control of (human leucocyte antigen) HLA genes, an association between an HLA allele and c-ALL could provide support for an infectious aetiology. To Gly26, His30, Val57, encoding motifs in c-ALL compared with controls. Since these amino acids are not restricted to DQBI*0501, our results suggest that, as with DPBI, the increased risk of c-ALL associated with DQBI is determined by specific amino acid encoding motifs rather than by an individual allele. These results also suggest that HLAassociated susceptibility to c-ALL may not be restricted to the region bounded by DPBI and DQBI.

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Previous serological studies documenting an association between acute lymphoblastic leukaemia (ALL) and HLA‐Cw antigens suggested that the HLA‐C locus might influence susceptibility to ALL. However, associations with more than one Cw antigen suggest that polymorphic variants shared by more than Cw allele could be involved. Recent studies have shown that the HLA‐C locus encodes two ligands (NK1 and NK2) recognized by receptors on natural killer (NK) cells. HLA‐Cw alleles encoding these ligands are dimorphic, dependent on whether they encode one or other NK ligand. To determine whether susceptibility to the common (CD10+) form of childhood ALL (c‐ALL) is associated with NK1 or NK2, we carried out a molecular analysis of 94 childhood c‐ALL patients and 136 infant controls. We found no difference in the frequency of NK1 and NK2 alleles, phenotypes or genotypes between the patients and controls, suggesting that this does not explain the role of the HLA‐C locus in susceptibility to childhood c‐ALL.