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Notes: Twenty-five atopic children under 11 years of age were studied, using skin and RAST tests, for their specific IgE response to four species of pyroglyphid house dust mites, Dermatophagoides pteronyssinus, D. farinae, D. microceras and Euroglyphus maynei. All of the children were sensitive to D. pteronyssinus, 20 (80%) of these children were also sensitive to D. farinae and D. microceras, and 16 of the latter (64%) were also sensitive to E. maynei. Dust samples from various sites in the homes of the children revealed D. pteronyssinus in all homes studied but no D. farinae or D. microceras. E. maynei, although identified, was not present in significant numbers in any site. A control group of 20 atopic children of similar age who were not sensitive to house dust mite allergens had a similar exposure to the four mite species. These results suggest that factors in addition to mite exposure are important in the development of specific IgE responses to house dust mites.

Notes: Antibodies were measured in the sera of fifteen patients with untreated coeliac disease and twenty-eight patients with inflammatory bowel disease. Increased levels of specific IgG, IgG1, IgG2, and IgG4 antibody to wheat gluten fraction B, measured by an enzyme-linked immunosorbent assay, were shown in the coeliac disease group, but not in the inflammatory bowel disease group. No specific IgE antibody to fraction B was detected but 33% of the patients with coeliac disease had specific short-term sensitizing (anaphylactic) IgG antibody activity (IgG S-TS) to fraction B. There was no correlation between the IgG2 or IgG4 specific antibody and the presence of IgG S-TS activity.

Notes: Twenty-three patients with extrinsic allergic alveolitis due to an allergy to inhaled budgerigar serum protein (budgerigar fancier's lung disease) were typed for HLA-A, B, C and HLA-DR antigens. Antigen frequencies were compared with those found in 154 healthy control subjects. No statistically significant variation in the frequency of any HLA antigen was detected. Exclusion of two patients who had concurrent coeliac disease, and subdivision of the population into those with acute and chronic disease, failed to reveal any significant association with an HLA specificity. A non-significant increase in B8-DR3 amongst the patients with acute disease was noted. Possible reasons for the apparent HLA associations previously reported by others for extrinsic allergic alveolitis are discussed.

Notes: The results of testing for linkage between atopy and the chromosome 11 marker D11S97 is shown for all the 723 subjects genotyped by us up to January 1992. Lod score estimations were confounded by the high population prevalence of atopy, maternal inheritance of atopy at the 11q locus, genetic heterogeneity, and excess of atopy in families not ascertained through a single proband. Affected sib-pair analysis shows evidence for linkage which is not dependent on the definition of atopy or model specification. We suggest that presentation of sib-pair data will be suitable for meta-analysis of the different studies of genetic linkage and atopy.

Notes: Precipitins against budgerigar serum proteins were not found in subjects without budgerigars or in healthy budgerigar fanciers. In budgerigar fanciers with respiratory disease, precipitins were found in sixteen out of nineteen suffering from allergic alveolitis, in four out of fourteen with asthma and two others in whom other respiratory diseases had been diagnosed. Specific IgE to budgerigar serum proteins was present in the atopic subjects with asthma due to budgerigar allergen but not in the nonatopic subjects with allergic alveolitis. Haemagglutination tests corresponded with the precipitin tests. Radio-immunoelectrophoretic tests showed that the precipitins belonged in the IgG, IgM and IgA classes. The presence of precipitins in budgerigar fanciers was closely associated with the presence of respiratory disease.

Notes: We have undertaken a double blind placebo controlled study of the effect of nasal beclomethasone on the tendency to wheeze in 20 unselected hay fever sufferers, half with a history of previous seasonal wheezing. We found no difference between either bronchial hyperresponsiveness, as measured by methacholine challenge, home-monitored PEFR, nor recorded wheeze nor cough between treated and placebo groups although the numbers were small. All were allowed the antihistamine cetirizine hydrochloride 10 mg daily. Eighteen out of the 19 patients had either bronchial hyper-responsiveness (PD20 methacholine 〈 8 μmol or a 〉 2 doubling dose change in their PD20 during the pollen season). We have shown a significant positive correlation between a hay fever score (HFS) (created by taking the sum of the home scored; nasal discharge, nasal blockage, eye irritation, sneeze and antihistamine use) and peak seasonal specific IgE to mixed grass pollen (Spearman correlation coefficient 0.5 P〈0.02). There was also a positive correlation between the rise in specific IgE from pre to peak season and the HFS, correlation coefficient 0.6 P =0.03).

Notes: Some 103 patients with asthma and 100 healthy volunteers have been typed for HLA-A, B and C and HLA-DR antigens. The 103 patients consisted of thirty-three with intrinsic asthma, thirty-four with extrinsic asthma, and thirty-six known to have precipitins to Aspergillus fumigatus. No increase in frequency of any of the A, B, C, or DR antigens was found to be significant after correction for the number of comparisons was made. However certain trends comparable to findings in other immunopathic disorders were noted. For example B12 was increased in the allergic asthmatics (46 vs 29% controls) and it is suggested that B12 is associated with the ability to produce the IgE antibodies. A3/B7/DRw2 (which are in linkage disequilibrium) all show a decreased frequency in intrinsic asthma (24, 12 and 9%vs 32, 26 and 24% respectively in controls). Finally B8 and DRw3, which showed a moderate increase in frequency in all three groups of asthmatics, were found in five of seven patients with low atopy but persisting antibodies to A. fumigatus. Further detailed studies of these asthmatic subgroups is warranted.

Notes: Tests of the sera of fifty-eight bird fanciers, comprising eighteen pigeon faticiers, thirty-five budgerigar fanciers and five exposed to other birds, against the sera of the pigeon, budgerigar, hen, turkey, pheasant, canary and finch, showed the presence in the avian sera of antigenically related serum albumin and some β-globulin components. Pigeon serum macro- and γ-globulin components reacted specifically only with the pigeon faticiers'sera, and budgerigar γ-globulin and a β-globulin Bβ2G reacted specifically only with budgerigar fanciers'sera. The pigeon fanciers'sera contained the largest amounts of precipitating and haemagglutinating antibody.Avian serum proteins are present in bird droppings, so that the common antigens may cause reactions in affected subjects on exposure to the droppings dust of different birds. The patients'sera may also be useful for characterization of the avian serum proteins.

Notes: Background Stings from bees and wasps can cause systemic reactions which can be fatal in some individuals. In these venom-sensitive patients, specific IgE to the venom is produced and is considered to participate in the adverse reactions. This immune response requires antigen presentation by human leucocyte antigens (HLA) class II molecules, which includes DR and DP, which are present on antigen presenting cells.Objective To test for associations between HLA class II DRB1 and DPB1 alleles and life- threatening sensitivity to both bee and wasp venoms. To establish further whether any associations are independent of the atopy phenotype.Methods A total of 33 bee- and 44 wasp-venom-sensitive patients was studied. DRB1 genotypes were determined by single stranded oligonucleotide (SSO) probing of PCR products, and DPB1 genotypes by amplified fragment length polymorphism (AFLP) analysis. Total and specific IgE were measured using the Pharmacia Immunocap, FEIA. Patients with specific IgE to the venom antigens only were termed monosensitive and those with additional specific IgE to HDM and/or GP were termed polysensitive.Results Allele frequencies were compared to an unrelated control population. The 33 bee- sensitive patients had a greater prevalence of DRB 1*07 alleles than the control subjects, 26% vs 14%, with an odds ratio (OR) of 2.1 (95%CI, 1.2–3.7, P= 0.015, corrected for multiple comparisons, pc 〉 = ns). This association was confined to the 15 monosensitive bee patients, who had a 43% DRB 1*07 allele frequency when compared with 11% in the 18 polysensitive bee patients, OR 6.1 (95%CI, 1.73–22, P= 0.004, pc= 0.05), and when compared with a control group of non-venom subjects, 43% vs 16%, OR 3.9 (95% CI, 1.72–9.0, P= 0.002, pc= 0.02). The 44 wasp-sensitive patients had an increase in the DRB1*11 allele when compared with the control subjects, 13% vs 6%, with an OR 2.2 (95%CI, 1.0–4.6, P= 0.04, pc= NS), and a decreased prevalence of DRB 1*04 alleles, 10% vs 19%, with an OR 0.33 (95%CI, 0.24–0.99, P= 0.04, pc= NS), but these were not significant when multiple comparisons were taken into account. The DPB1 alleles were not significantly different between the venom sensitive patients and the controls.Conclusion Patients monosensitive to bee venom had a significantly greater prevalence of DRB 1 *07 alleles than the non-venom, control population suggesting that IgE responses in these patients may, in part be controlled by immune response HLA class II genes. These results are also suggestive of wasp-sensitive patients having a higher prevalence of DRB1*11 and a lower prevalence of DRB 1*04 than the control population.