A common IL-1 complex haplotype is associated with an increased risk of atopy.

The interleukin (IL)-1 gene cluster within chromosome 2 contains genes coding for both antiand proinflammatory cytokines, including IL-1alpha, IL-1beta, IL-1Ra, and several novel cytokines designated IL-1F5 IL-1F10. Proinflammatory cytokines IL-1alpha and beta are involved in the enhancement of inflammation and host defence. Antiinflammatory IL-1Ra counteracts the function of IL-1alpha and IL-1beta. These cytokines are produced by a variety of cell types, for example, monocytes, magrophages, and keratinocytes. All IL-1 family genes are polymorphic and several of these polymorphisms have been shown to be associated with either susceptibility to or severity of inflammatory conditions and diseases. Atopy is a familial syndrome underlying atopic eczema, allergic rhinoconjuctivitis, and bronchial asthma. The skin prick test (SPT) is used to examine specific IgE mediated allergic responses and the results are generally in line with anamnestic data on atopy. Both IL-1alpha and beta have been shown to play a role in the regulation of allergen induced early and late reactions. 5 IL-1alpha has also been found to accelerate cutaneous inflammation, whereas IL-1beta is involved in the regulation of contact sensitisation. In asthmatic bronchial epithelium, the expression of both IL-1beta and IL-1Ra is increased. Cytokines function as a network and thus the net effect on allergic inflammation may be dependent on allele combinations of individual cytokine genes. Recently in our population based case control study, we showed that IL1A (SNP +4845) genotype influences the SPT results. The carriers of the rarer allele 2 had a significantly lower SPT positive rate than that of non-carriers. Now we have expanded the study by analysing two additional SNPs (IL1B SNP +3954 C>T and IL1RN VNTR in intron 2) in the IL-1 gene cluster from the same cohort.