Thorax 1993;48:5-9 5 Cohabiting with domestic mites Thorax: first published as 10.1136/thx.48.1.5 on 1 January 1993. Downloaded from As lorng ago as 1662 it was realised that the inhalation of Arachnida. Their ecology is relatively well described.'""8 dust particles in the air could lead to symptoms now At least 50 species have been found in domestic house dust, recognised as typical of an allergic reaction. John Baptista and in temperate climates the most important, both clin- van Helmont, a Flemish physician, wrote of one of his ically and numerically, are the mites Dermatophagoides patients (a monk): pteronyssinus and D farinae (and its sibling species ". .. as oft as any place is swept or the wind doth otherwise microceras) of the family Pyroglyphidae. In the last few stir up the dust, he presently falls down, being almost years it has been suggested that another species, Eurogly- choked." phus maynei, may be clinically important.920 Storage mites, Not until the 1960s, however, did Voorhorst et al' and such as Acarus spp, Tyrophagus spp, and Glycophagus spp, Miyamoto et al2 independently establish that the house may be relevant to occupational asthma. In tropical and dust mite was a major source of allergen in house dust. subtropical regions mites from the genus Blomia have been Miyamoto subsequently showed experimentally that inhal- shown to be clinically important.2'"23 In view of the ing mite extracts could induce asthmatic symptoms. Iden- widening range ofmites believed to have important clinical tification of domestic mites as the major source ofallergens effects, the term "domestic" mites has been proposed.'8 has prompted research to isolate and characterise the allergens concerned, to identify the mechanisms and the LIFE CYCLE AND PHYSIOLOGY timing of sensitisation, and to evaluate measures for mite Mites are small and invisible to the naked eye. Identifying avoidance. species and determining viability may be difficult, but the main morphological characteristics are well described.'4 Mites and asthma Mites hatch from eggs and proceed through larval, pro- Studies in different populations have shown that up to 85% tonymphal, and tritonymphal stages before reaching of people with atopic asthma but only 5-30% of the non- adulthood, when they are about 400 gum in length. The asthmatic population are skinprick sensitive to mites.' A average life cycle is three months, during which the female causal relation between asthma and sensitivity to mites is may lay up to 300 eggs. Up to 100 000 mites may live in one unproved, but there is considerable evidence to suggest it. square metre of carpet. Mites feed on desquamated human Inhalational challenge with mite extracts causes both early skin and fungi that grow on the skin scales. Some species of and late asthmatic responses, with an accompanying mites (Cheylitidae spp) feed on other mite species,24 but this increase in non-specific bronchial reactivity. The introduc- appears to be of little consequence with respect to control- tion of Western style bedding, with high concentrations of ling mite numbers. Mites have a well developed gastro- mites, in populations previously free of asthma has been intestinal tract with digestion and food absorption

associated with a dramatic increase in the incidence of primarily in the midgut and water resorption in the http://thorax.bmj.com/ asthma and in mite sensitivity, found in as many as 91 %. A hindgut.'42526 In the posterior midgut the food is enveloped longitudinal study of a cohort of children in England has by a fluid that solidifies to form a peritrophic membrane27 shown a strong correlation between levels ofmite exposure and the resulting food balls later coalesce to be excreted as and the subsequent development of bronchial hyperreac- faecal pellets. These vary in size from 10 to 40 gum and each tivity and asthma.8 This is supported by a study ofpatients mite will produce about 20 pellets a day. In contrast to the with newly diagnosed asthma, showing that they were gastrointestinal system, mites have no specialised res- exposed to higher concentrations of mites in their homes piratory structure and oxygen is obtained by passive in New Zealand the assess- diffusion across their cuticle. As a result of this relatively than were controls.9 Similarly, on October 4, 2021 by guest. Protected copyright. ment of risk factors for the development of asthma has hard but pervious layer they are very sensitive to water loss shown that an atopic response to mites represents an and are essentially in equilibrium with the atmosphere, the independent risk variable.'0 Point prevalence correlations ambient humidity determining their water content. between exposure, sensitivity and asthma have been found in many studies in Europe, North and South America, NATURAL FACTORS INFLUENCING DISTRIBUTION AND China, India, Korea, Australia, New Zealand, Brunei, and ABUNDANCE New Guinea.3 D pteronyssinus and Dfarinae appear to thrive best at 80% If continued exposure to mites exacerbates asthma a relative humidity and 250C.'4 As the humidity falls, how- reduction in the level of exposure might be expected to ever, they stop reproducing and become immobile, and produce a reduction in the expression of symptoms and below 50% relative humidity they are likely to die. bronchial reactivity. Sending patients to Alpine sanatoria Although eggs and protonymphs survive at lower relative has long been recognised as a means of reducing asthmatic humidity the water content of the air still appears to be a symptoms, and more recently concentrations of mite factor in the distribution and abundance of mites in the allergen have been found to be very low at these altitudes." home, and this is reflected in the seasonality associated with Subsequently several studies have confirmed that clinical mites in some parts of the world. Modern energy efficient improvement occurs when asthmatic patients are moved to housing with air conditioning, reduced ventilation, and such sites.'2 Similarly, avoidance of allergen associated heating may also be influencing the abundance, distribu- with admission to hospital has been shown to be related to tion, and seasonality of mite populations. As well as being an improvement in asthma.'3 Whether the use of acaricidal humidity dependent, mites are photophobic, and these two agents to reduce concentrations of mites in the home is factors influence their choice of habitat-namely, at the beneficial remains controversial, but some studies have base ofcarpets; inside mattresses; and in bedding, soft toys, shown benefit (see below). and soft furnishings. 4 1618 Ecology and biology of mites Mite allergens SPECIES ALLERGEN IDENTIFICATION AND NOMENCLATURE With spiders, scorpions, etc, mites belong to the class Patients who are allergic to house dust mites produce 6 Feather, Warner, Holgate, Thompson, Stewart

specific IgE antibodies against various mite allergens. If residues and has a molecular weight of about 14 000 more than 90% of a population allergic to mites produce daltons.38 5455 Der p II and Der f II have both been cloned IgE antibodies to a specific allergen then it is regarded as a and sequenced, but so far no biological activity has been major allergen.28 Although as many as 30 mite allergens ascribed to Der p II, though its physicochemical properties

have been identified only five or six appear to predomin- strongly suggest it may be lysozyme.56 Currently only B cell Thorax: first published as 10.1136/thx.48.1.5 on 1 January 1993. Downloaded from ate.29131 Most mite allergens are proteins that are soluble in epitopes have been described.495758 Although group II water and are found in the faecal pellets of mites."6173233 allergens are thought to be associated with mite bodies Immunological, physicochemical, and molecular biological there is evidence that they can be found in faecal particles techniques have been used to isolate, characterise, and they have also been detected in the atmosphere after sequence, and clone specific allergens.'6 17 3 35 This has now disturbance of dust.5960 been done for several allergens, and with libraries of mite complementary DNA available detailed knowledge of Group III further allergens may be expected. The group III allergens, only recently been described, Initially, there was no standard procedure for naming have molecular weights of about 30 000 daltons.3942 Bio- allergens and confusion has occurred as different research chemically they are trypsins and partial amino acid sequen- groups isolated similar allergens. The International Union ces have been reported. Der p III appears to be a major of Immunological Societies has issued guidelines for allergen and reacts with the serum of every person allergic allergen nomenclature and these have been adopted for to mites.39 Mite extracts have been shown to contain several mite allergens.36 The recommended nomenclature uses the proteases,6164 including a chymotrypsin and an elastase like first three letters ofthe genus (for example, Der) followed by enzyme. Chymotrypsin is allergenic but whether the others the first letter of the species (for example, p) followed by are is not yet known. Immunoblotting studies, however, sequential numbering ofthe allergens in the order in which indicate that several allergens have similar molecular they were identified. With Dermatophagoides pteronyssinus, weights, and this raises the possibility that each is aller- for example, the allergens that have been identified and genic.35 Recent studies have shown that trypsin activity can characterised are referred to as Der p I, Der p II, Der p III, also be found in E maynei extracts. and Derp IV. The known Dfarinae equivalents are DerfI, Der f II, and Der f III, and similar allergens from other Group IV mite species are put in the same groups (I-IV). There are Der p IV is a single chain protein and has a molecular amino acid sequence homologies of 81% between the weight of about 60 000 daltons.65 It is an amylase like group I allergens Der p I and Derf I, of 88% between the enzyme and is recognised by up to 46% of individuals group II allergens Der p II and Der f II, and of 75% allergic to mites. This enzyme is also found in both D between the group III allergens Derp III and DerfIII.3-39 farinae and E maynei extracts.66 Although other allergens have been partially characterised, they do not as yet fit into this categorisation.' BIOCHEMISTRY OF ALLERGENS Monoclonal and polyclonal antibodies to mite allergens Interestingly, Der p I is a cysteine protease, Der p III have been prepared by several research groups and mono- trypsin, and Der p IV amylase. Although this reflects the http://thorax.bmj.com/ clonal antibodies to group I, II, and III allergens are source of the allergens-namely, the gut-it also raises the available.4 42 These antibodies have proved extremely possibility that the enzymatic activity of these allergens useful not ony for isolating allergens but also for quantify- facilitates their interaction with the host's immune system. ing allergen exposure in the environment. This is supported by the observation that enzymatically active Der p I increases the permeability of respiratory STRUCTURE AND ACTIVITY OF KNOWN ALLERGENS epithelium and is able to hydrolise IgG and activate the Group I kallikrein-kinin system. 63 67 68 Der p I is a chain 222 amino single protein containing acid on October 4, 2021 by guest. Protected copyright. residues and has a molecular weight of about 25 000 SENSITISATION TO MITE ALLERGENS daltons.4344 This and the equivalent allergens from D Domestic mites are found in most inhabited areas. Not farinae and E maynei24 3245 have been cloned and found to be everyone in contact with them becomes sensitised, cysteine proteases with substantial homology with papain, however, and not everyone who is sensitised experiences actinidin, and cathepsin B and H.'47 Cysteine proteases symptoms of allergic disease. The reasons for this are not have a cysteine residue in the catalytic site that is analogous clear. The atopic predisposition has a strong genetic to the serine residue found in serine proteases such as component, however: ifone parent is allergic the child has a trypsin and chymotrypsin. The homology shown by the 50% chance of developing an allergic disease, and if both allergen has been sufficient for a three dimensional struc- parents are allergic the proportion rises to 80%.69 Recently ture to be assigned to it, based on the structures ofactinidin the gene putatively responsible for atopy has been reported and papain. Such three dimensional modelling is helping to to be resident on chromosome 11 and to be transmitted in facilitate the localisation of likely T and B cell epitopes, an autosomal dominant fashion.70 Irrespective of the which are currently being mapped with the help ofpeptides inheritance ofatopy, however, disease ofspecific organs and produced by both chemical and molecular biological tech- expression of symptoms remain highly variable and are niques.4>50 The group I allergens appear to be associated likely to depend on a multiplicity of environmental factors, with faecal particles,5 38 39 51 52 which become airborne with the most important of which is likely to be the level of domestic activity.53 Because of their size, faecal pellets do exposure to the sensitising allergen. not stay airborne for long, and measurable quantities in the Evidence is accumulating that exposure to potential air disappear within minutes. Once such particles have allergens early in life is important. More specifically, the landed on a moist surface, such as a mucosal membrane, nature of the first allergens encountered, their concentra- Der p I and other allergens are leached out within 30 tions, and the timing of the exposure seem fundamental. seconds.2829 Sporik et al have shown that the risk of sensitisation relates not only to the intensity of the exposure but also to the timing, the degree of sensitisation at 11 years of age Group II correlating best with the exposure levels documented at 1 Der p II is a single chain protein containing 129 amino acid year of age.8 Other studies have suggested that the critical Editorials 7 timing might be even earlier. For example, individuals avoidance measures. Intervention studies focusing on born just before or during the birch pollen season in using bedding materials less conducive to mite colonisa- Scandinavia have a 28% greater chance of developing an tion, or using barrier methods to separate the mites from allergy to birch pollen than those born after the season, who the sleeper, have tended to show some benefit, either in are therefore not exposed until they are about 9 months reduced mite allergen concentrations or in the symptoms Thorax: first published as 10.1136/thx.48.1.5 on 1 January 1993. Downloaded from old.7' This suggests a vulnerable period in the first three to assessed. The use of liquid nitrogen on bedding has been six months of life. shown to reduce the numbers of mites substantially, and a Minimum concentrations of mite allergens causing sen- modest decrease has also been achieved by the use of sitisation and promoting disease have been proposed. electric blankets to reduce the humidity in the bedding Initial sensitisation has been proposed to occur in a materials.7677 In contrast, simple cleaning and vacuuming susceptible individual if the concentration of Der p I is alone have been shown to be of negligible benefit. The above 2 pg/g ofhouse dust.372 A concentration of10 jg/g of benefit of removing carpets and soft furnishings as an house dust has been proposed as a concentration that isolated measure is unproved, but should be considered as triggers episodes of asthma but this has been based on data complementary to the use of alternative bedding materials. on concentrations from the homes of patients attending An alternative approach is to alter the overall interior of emergency departments.73 As such these values do not the home to make it less conducive to colonisation by mites. signify discrete threshold values, but rather may be useful This can be achieved by modification of temperature and in identifying populations "at risk" and serving as goals for humidity. Unfortunately, the environment created by a mite eradication programmes. More recently it has been modern energy efficient home, with central heating and questioned whether concentrations ofallergen measured in limited ventilation to reduce energy costs, is ideal for the settled dust are representative of the concentrations to growth and reproduction of mites. To make the environ- which people are exposed, and it has been suggested that ment less suitable for mites the indoor humidity would concentrations of airborne allergen are more likely to need to be substantially reduced. In cooler climates, such as correlate with the degree of allergic lung disease. This has that of the United Kingdom, this could be achieved with been supported by data showing that in a group of increased ventilation; but this would be associated with an asthmatic children living in Greater London 80% of mite increase in energy requirements to maintain indoor tem- sensitive individuals had detectable quantities of airborne perature, which is not environmentally attractive. Heat Der p I in their homes, whereas in the carpets only 37% had exchange ventilation systems may offer an alternative. concentrations greater than 2 4ug/g of dust.74 It seems Older dwellings affected by ground moisture would also sensible therefore to exercise caution when the use of these need modification. thresholds in avoidance studies is being advocated as they The use ofacaricidal agents is currently under investiga- may be inappropriate-and, despite the enormous effort tion and in some instances safety and efficacy have yet to be required, reducing concentrations to these levels may not demonstrated. A wider range of products is becoming be sufficient to prevent sensitisation. It is also obvious that available and a particular advantage of these is that, in the types of furnishings, the amount of ventilation, and the addition to killing mites, some contain agents such as tannic degree of human activity within the home may all exert an acid that minimise the allergenicity of the offending http://thorax.bmj.com/ influence on the amounts of allergen to which people are proteins, providing an almost immediate reduction in exposed. allergen exposure.78 Once achieved, however, a lower level Despite the inherent problems of preventing sensitisa- of exposure would need to be maintained indefinitely, as tion, investigation of new techniques for reducing allergen any benefit to the sensitised individual would rapidly should in the first instance prove useful in the treatment of reverse when he was re-exposed. Studies with acaracides sensitised patients. have either shown a reduction in numbers ofmites without assessing patients' symptoms or simply failed to reduce

mite numbers or diminish symptoms. Woolcock et al have on October 4, 2021 by guest. Protected copyright. used a commercially available acaricidal agent containing Mite avoidance as a therapeutic option tannic acid to reduced mite numbers and simultaneously Currently treatment of asthma is based on various found a reduction in the allergenicity of the dust.79 More pharmacological agents, ranging from immediate relief of recently studies from the same group have failed to show symptoms with the "bronchodilators" to "anti- benefit in the home80; others, however, have suggested that a inflammatory" or "preventive" treatment with drugs such higher concentration of tannic acid may be beneficial.8' as sodium cromoglycate, nedocromil sodium, and inhaled In this issue of Thorax a further study is reported by and oral corticosteroids. If, however, allergy to domestic Kalra et al,8' where the interventions studied against the mites has a central role in the development of asthma and control group were liquid nitrogen and an acaricidal agent the maintenance of the hyperreactive asthmatic state it and the endpoint was measured levels of Der p I. Although seems prudent to attempt to reduce exposure to mites in both these treatments might be expected to alter numbers those at risk. ofthe live mites authors report little or no effect on allergen Although the benefits of mite avoidance measures have levels at any of the time points. This study used only a yet to be confirmed in a large, well controlled trial (with single application and leaves open the question of whether respect to reducing both the risk of sensitisation in "at risk" repeated applications of either the acaricide or the liquid individuals and expression of symptoms in those already nitrogen would be more efficacious. Even if statistically sensitised), several strategies for reducing allergen significant reductions in Der p I levels were obtained, exposure have been tried. These have concentrated however, clinical endpoints such as reduction of symptoms primarily on reducing the numbers of mites in bedding or would be needed. The distinction between reducing mite altering the overall environment within the home. Few of numbers, reducing allergen levels, and reducing expression these studies have been well controlled, many of them not of symptoms is one of the major difficulties in assessing this including a control group and others comparing changes work. A change in levels of allergen or numbers of mites within groups rather than across the control and interven- must be related to a clinical benefit for these studies to have tion groups.75 any real application. Nevertheless, this study does help us Bedding, soft furnishings and carpets are the areas most to place in some perspective the increasing enthusiasm for heavily colonised by mites, and therefore the main target of these forms of intervention. 8 Feather, Warner, Holgate, Thompson, Stewart

Future perspectives 1 Voorhorst R, Spieksma F, Varekamp H, Leupen M, Lyklema A. The house dust mite (Dermatophagoides pteronyssinus) and the allergens it produces. Despite problems in the past, immunotherapy may yet Identity with the house-dust antigen. J Allergy 1967;39:325-39. prove a useful treatment for allergy to mites. Purification 2 Miyamoto T, Oshima S, Ishizaka T, Sato S. Allergenic identity between the and sequencing of mite related allergens and production of common floor mite (Dermatophagoides farinae Hughes 1961) and house

dust as a causative agent in bronchial asthma. J Allergy 1968;42:14-28. Thorax: first published as 10.1136/thx.48.1.5 on 1 January 1993. Downloaded from recombinant allergens may increase the efficacy of this 3 Platts-Mills TAE, Chapman MD. Dust mites: Immunology, allergic disease mode of treatment. Recently allergen-antibody complex and environmental control. J Allergy Clin Immunol 1987;80:755-75. 4 Smith JM, Disney ME, Williams JD, Goels ZA. Clinical significance ofskin inoculations have produced a minor side effect while reactions to mite extracts in children with asthma. BMJ 1969;ii:723-6. producing benefits.83 Immunotherapy has been dis- 5 Burrows B, Martinez FD, Halonen M, Barbec RA, Cline MG. Association of couraged, especially in the United Kingdom, because ofthe asthma with serum IgE levels and skin test reactivity to allergens. N Engl J Med 1989;320:271-7. risks. Allergen modification and the possibility of selective 6 Di Berardino L, Angrisano A, Gorli L, Catlaneo M, Lodi A. Allergy to house presentation to the suppressive component of the immune dust and storage mites in children: epidemiologic observations. Ann Allergy 1987;59:104-6. system, without evoking an acute response, makes this 7 Dowse G, Turner K, Stewart G, Alpers M, Woolcock A. The association form of treatment an interesting and challenging future between Dermatophagoides mites and the increasing prevalence ofasthma prospect. In view of past experiences and the special risks in village communities within the Papua New Guinea highlands. J Allergy Clin Immunol 1985;75:75-83. posed by asthmatic patients, however, this mode of treat- 8 Sporik R, Holgate ST, Platts-Mills TAE, Cogswell JJ. Exposure to house ment is likely to remain in specialist centres and be dust mite allergen (Der p1) and the development of asthma in childhood. to a N Engl J Med 1990;323:502-7. applicable only carefully selected subgroup. 9 Korsgaard J. Mite allergy and residency: a case controlled study on the It is becomingly increasingly clear that the long term impact of exposure to house-dust mites in dwellings. Am Rev Respir Dis goal should be to reduce the level of sensitisation in the 1983;128:231-5. 10 Warner JO, Boner AL. Allergy and childhood asthma. Clin Immunol Allergy population. This seems likely to be achievable by reducing 1988;2:217-29. exposure levels from the time of birth for the population at 11 Spieksma FTM, Zuidema P, Leupen MJ. High altitude and house dust risk. This is not an mites. BMJ 1971;i:82-4. inconsiderable task and will require 12 Charpin D, Kleisbauer JP, Lanteaume A, Razzouk H, Vervloet D, Toumi considerable modifications to lifestyle. If mite avoidance is M, et al. Asthma and allergy to house dust mites in populations living in practised in the community it will take at least a generation high altitudes. Chest 1988;93:758-61. 13 Platts-Mills TAE, Mitchell EB, Nock P, Tovey ER, Moszoro H, Wilkins for these benefits to be realised. Equally important, how- SR. Reduction of bronchial hyperreactivity during prolonged allergen ever, is the reduction of exposure of those already sensi- avoidance. Lancet 1982;ii:675-8. so that and be 14 Wharton GW. House dust mites. J Med Entomol 1976;12:577-621. tised, symptom expression morbidity may 15 Blythe ME. Some aspects ofthe ecological study ofthe house dust mites. BrJ reduced. Dis Chest 1976;70:3-31. The route to this ultimate goal of prevention will 16 Platts MT, Chapman MD. Dust mites: immunology, allergic disease, and environmental control. J Allergy Clin Immunol 1987;80:755-75. necessarily include acceptance of new housekeeping prac- [Published erratum: J Allergy Clin Immunol 1988;82:841.] tices and new interior and structural housing design, as well 17 Platts-Mills TAE, Weck A, eds. International workshop report. Dust mite as the introduction of new for allergens and asthma: a worldwide problem. Bull WHO 1988;66:769-80. technologies bedding, 18 Platts Mills TAE, Thomas WR, Aalberse RC, Vervloet D, Chapman MD. acaricidal agents, and measuring assays for allergen in the Dust mite allergens and asthma: report of a second international work- field. Carefully controlled studies designed to establish shop. J Allergy Clin Immunol 1992;89:1046-60. 19 Colloff MJ. A review of biology and allergenicity of the house-dust mite the efficacy of mite control measures and the optimal time Euroglyphus maynei (Acari: Pyroglyphidae). Exp Appl Acarol 1991;11: for their implementation are still required before major 177-98. http://thorax.bmj.com/ in can be recommended. 20 Blythe ME, Williams JD, Smith JM. Distribution of pyroglyphid mites in changes lifestyle confidently Birmingham with particular reference to Euroglyphus maynei. Clin Allergy 1974;4:25-33. 21 Wraith DG, Cunnington AM, Seymour WM. The role and allergenic importance of storage imtes in house dust and other environments. Clin Conclusions Allergy 1979;9:545-61. 22 Korsgaard J, Dahl R, Hallas T, Iversen M. Storage mites as a cause of A causal relationship between domestic mites and asthma is housing or occupational allergy. Ugeskr Laeger 1984;146:2114-7. strongly suggested but has not been unequivocally proved. 23 van Hage Hamsten M, Machado L, Barros MT, Johansson SG. Immune The close relationships between mite exposure, mite response to Blomia kulagini and Dermatophagoidespteronyssinus in Sweden and Brazil. Int Arch Allergy Appl Immunol 1990;91:186-91. on October 4, 2021 by guest. Protected copyright. sensitivity and asthma make it very likely, however, that 24 Wharton GW, Arlian LG. Predatory behaviour ofthe mite Cheyletus aversor. domestic mites are a major contributor to the development Animal Behaviour 1972;20:719-23. 25 Hughes TE. The physiology of the alimentary canal of Tryoglyphusfarinae. and expression of symptoms in atopic asthma. Quarterly Journal ofMicroscopical Science 1950;91:45-61. Asthma is a common disease in our community and the 26 Brody AR, McGrath JC, Wharton GW. Dermatophagoides farinae: the evidence that both its incidence and its are digestive system. New York Entomological Society 1972;80:152-77. suggests severity 27 Wharton GW, Brody AR. The peritrophic membrane ofthe mite, Dermato- increasing. Strategies for dealing with this important cause phagoidesfarinae: Acariformes. J Parasitol 1972;58:801-4. ofmorbidity and mortality must be directed to tackling the 28 Marsh DG. Allergens and genetics of allergy. In: Sele M, ed. The antigens. London: Academic Press, 1975:271-359. environmental cause of the problem. Allergy to dust mites 29 Lind P, Lowenstein H. Identification of allergens in Dermatophagoides is almost certainly one environmental factor that could be pteronyssinus mite body extract by crossed radioimmunoelectrophoresis modified. A concerted research effort is needed not to with two different rabbit antibodypools. ScandJImmunol 1983;17:263-73. only 30 Krilis S, Baldo BA, Basten A. Antigens and allergens from the common ascertain with confidence the part played by domestic mites house dust mite Dermatophagoides pteronyssinus. Part II. Identification of in diseases such as asthma, rhinitis, and eczema but also to the major IgE-binding antigens by crossed radioimmuoelectrophoresis. J Allergy Clin Immunol 1984;74:142-6. continue efforts designed to reduce the levels of the mite 31 Baldo BA, Ford SA, Tovey ER. Towards a definition of the complete allergens to which the population is exposed. This will be spectrum and rank order of importance of the allergens from the house one of the environmental of dust mite, Dermatophagoides pteronyssinus. In: Allergy and molecular greatest challenges preventive biology. Proceedings of the DPC First International Symposium on medicine in the coming decade, but if effective one that is Allergy and Molecular Biology. Adv Biosci 1989;74:13-31. likely to yield great benefits. 32 Tovey ER, Chapman MD, Platts-Mills TA. Mite faeces are a major source of house dust allergens. Nature 1981;289:592-3. I H FEATHER 33 Stewart GA, Lake FR, Thompson PJ. Faecally derived hydrolytic enzymes J A WARNER from Dermatophagoidespteronyssinus: physicochemical characterisation of S T HOLGATE potential allergens. Int Arch Allergy Appl Immunol 1991;95:248-56. Southampton University Faculty of Medicine, 34 Chapman MD. Mite allergens and asthma. Curr Opin Immunol 1989;2: Southampton General Hospital, Southampton 525-30. P J THOMPSON 35 Arlian LG. House-dust-mite allergens: a review. Experimental and Applied Department of Medicine, University of Western Australia, Perth Acarology 1991;10:167-86. G A STEWART 36 Marsh DG, Goodfriend L, King TP, Lowenstein H, Platts Mills TAE. Western Australian Research Institutefor Child Health, Perth, Allergen nomenclature. Bull WHO 1986;64:767-74. Australia 37 Dilworth RJ, Chua KY, Thomas WR. Sequence analysis of cDNA coding for a major house dust mite allergen. Derf I. Clin Exp Allergy 1991;21: Reprint requests to: Dr I H Feather, University of Medicine, Southampton 25-32. General Hospital, Southampton S09 4XY. 38 Trudinger M, Chua KY, Thomas WR. cDNA encoding the major mite Editorials 9

allergen Derf II. Clin Exp Allergy 1991;21:33-7. mite allergens: comparison of group II allergens with group I mite allergen 39 Stewart GA, Ward LD, Simpson RJ, Thompson PJ. The group III allergen and cat-allergen Fel d I. J Allergy Clin Immunol 1991;88:919-26. from the house dust mite Dermatophagoides pteronyssinus is a trypsin-like 60 Sakaguchi M, Inouye S, Yasueda H, Irie T, Yoshizawa S, Shida T. enzyme. Immunology 1992;75:29-35. Measurement of allergens associated with dust mite allergy. II. Concen- 40 Tovey ER, Johnson MC, Roche AL, Cobon GS, Baldo BA. Cloning and trations of airborne mite allergens (Der I and Der II) in the house. Int Arch sequencing of a cDNA expressing a recombinant house dust mite protein Allergy Appl Immunol 1989;90:190-3. that binds human IgE and corresponds to an important low molecular 61 Stewart GA, Thompson PJ, Simpson RJ. Protease antigens from house dust Thorax: first published as 10.1136/thx.48.1.5 on 1 January 1993. 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