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Allergic asthma (AA) is a multifactorial disease in which the IgE hyperresponsiveness to mite allergens is determinant for its pathogenesis and clinical picture. We have reported previously that IgE responsiveness to mite allergens in AA patients is linked to HLA and possibly controlled by a dominant suppression (Is) gene of that region. The present population study was done to detect alleles involved in the genetic control of mite IgE response that accompanies AA, using polymerase chain reaction and oligonucleotide DNA typing of DP locus. Instead of finding any significant positive association with AA, in this study we found that the allele DPB1*0401 is present mainly in the nonallergic control population and strikingly absent in patients (p less than 0.008), suggesting that this gene could confer resistance to AA and other atopic diseases. Our results add more evidence regarding the existence of Is genes in the HLA region involved in the control of IgE immune response to environmental allergens. Furthermore, they suggest that genes of HLA are important genetic components involved in the etiology of AA.

A monoclonal anti-IgE antibody was obtained that reacted with some IgE myeloma proteins and with all but a few normal sera. Family studies proved that a genetic marker of IgE had been detected. This allotype, called Em(1), segregates in association with certain Gm-Am haplotypes. The available quantitative evidence warrants the conclusion that human IgE has genetic variants, but no subclasses. Samples from various populations of five continents, representative for the respective prevalent Gm-Am haplotypes, were tested for Em(1). Em(1) was absent mainly in haplotypes carrying A2m(2) and G2m(n). These closely linked genes are located in a chromosomal region that comprises the gamma 2-gamma 4-epsilon-alpha 2 CH genes. A hypothesis for the generation of Em(1) is given.