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Atopy and Its Inheritance Genetics Is Building a Bridge Between the Immediate and Delayed Components Ofatopy

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Atopy and Its Inheritance Genetics Is Building a Bridge Between the Immediate and Delayed Components Ofatopy France (38 2), Japan (37-8), and Germany before unification of the bottom 10% of the population fell by 14%, and their (482).8 share of the national income was halved. The proportion of Given these figures, it is unsurprising that the implications people living in households with an income below half the of an aging population for spending on welfare are not average income in 1979 was 9%; by 1990-1 it had increased to dramatic. It has been estimated that if Britain spent the same 24%."3 Without the welfare state the situation would be far BMJ: first published as 10.1136/bmj.307.6911.1019 on 23 October 1993. Downloaded from as it does now on welfare for each person of a given age, but worse. Welfare services are arguably the only bulwark against had the age structure that will exist in 2041, the total spending increasing poverty and ill health, social misery, and perhaps on welfare would rise by just over 11%, equivalent to about social instability. The question is not whether we can afford to 2.5% of the gross domestic product.9 Another estimate have a properly funded welfare state; it is whether we can confined to health and social services concludes that aging will afford not to have one. add only 10% to per capita spending on these services by JUUIAN LE GRAND 2026.10 Professorial fellow Moreover, the assumption that we shall continue to spend King's Fund Institute, the same amount per person on the care and support ofelderly London W2 4HT people as we do now may be unjustified. This is particularly true with respect to health care. It is a matter of controversy 1 Daruvalla A. Dutch welfare state cut by government. BMJ 1993;307:152. whether elderly people at any given age are getting more or 2 Dorozynski A. France's health service will cost more. BMJ 1993;306:1362. 3 Dorozynski A. France struggles to save Fr3Obn. BMJ 1993;307:86. less healthy.'1 But an increased awareness of the different cost 4 Karcher H. German workers fight loss ofsickness pay to fund reforms. BMJ 1993;307:87. of for at different 5 Department ofSocial Security. The growth ofsocialsecurity. London: HMSO, 1993. effectiveness treatment people ages, coupled 6 HM Treasury. The government's expenditure plans 1993-4 to 1995-6: Department of Health. London: with pressures to allow people to "die with dignity," may lead HMSO, 1993. (Cm 2212.) 7 Hills J, Glennerster H, Ie Grand J. Investigating welfare. London: London School of Economics, to a shift ofspending towards younger age groups.'2 1992. (Welfare State Programme discussion paper 92.) In fact, it could be argued that the real British crisis is 8 Willetts D. The age ofentitlement. London: Social Market Foundation, 1993. 9 Hills J. Thefutaure ofwelfare. York: Joseph Rowntree Foundation (in press). quite the reverse of that commonly portrayed. A social 10 ErnischJ. Fewer babies, longerlives. York: Joseph Rowntree Foundation, 1990. phenomenon whose importance is difficult to exaggerate is the 11 Robine JM, Blancher M, Dard JE. Health expectancy. London: HMSO, 1992. (OPCS studies on medical and population subjects No 59.) growth in inequality and poverty over the past decade. The 12 National Confidential Enquiry into Perioperative Deaths. Report of the national confidential enquiry intoperioperative deaths 1991/2. London: NCEPOD, 1993. personal disposable income of the average household after 13 Departmnent of Social Security. Households below average income: a statistical analysis 1979-1990/1. housing costs rose by 35% between 1979 and 1990-1; but that London: HMSO, 1993. Atopy and its inheritance Genetics is building a bridge between the immediate and delayed components ofatopy It took a philologist to invent the word "atopy." Coca and linkage in the families of either those with atopic eczema I or Cooke launched it in 1923,1 but they had been supplied with those with respiratory allergy 6 though the reasons for this are http://www.bmj.com/ the word, custom built, by Professor Perry of Colombia still not clear.910 Atopy is a complex condition: genetic University. Since then atopy has more than lived up to its heterogeneity and differences in definition, selection, and linguistic derivation as a "strange" disease: it has been race may all have played some part. slippery to handle, and establishing its mode of inheritance Nevertheless, such contradictions are familiar to those who has sometimes seemed almost impossible. Nevertheless, a followed the earlier wave of clinically based inheritance strong genetic component was obvious from the start. But so studies. Atopic eczema, for example, with a reported con- too was a contribution from the environment, creating an cordance rate of 0-86 in monozygotic and 0-21 in dizygotic awkward tangle that has taken 70 years and the full might of twins," has in its time been said to follow autosomal on 26 September 2021 by guest. Protected copyright. the new genetics to unravel even to the present limited extent. dominant, recessive, and polygenic modes of inheritance. Atopy is a state in which an exuberant production of IgE This confusion remains, but recent studies, using more occurs as a response to common environmental allergens, and precise clinical definitions, have shown two interesting atopic subjects may or may not develop one or more of the phenomena. atopic diseases such as asthma, hay fever, and eczema. Firstly, atopic diseases tend to run true to type within each Investigators into the genetics of atopy therefore have two family: in some families most of the affected members will options: to look at IgE concentrations or to look for the atopic have eczema while in others asthma or hay fever will diseases themselves; and, of course, the two do not always predominate.'21' This constancy has still to be explained. correspond. Up to a third of those with undoubted atopic Secondly, some studies confirm that atopic diseases, whether eczema, for example, have normal IgE concentrations. respiratory or eczematous,"'5 are inherited more often from In 1988 a multidisciplinary group in Oxford interested in the mother than from the father, and this, of course, echoes respiratory allergy defined atopy on the basis not of clinical the findings ofthe Oxford group and the locus on chromosome disease but of positive response to a prick test, a positive 1lql3. specific IgE titre, a high total concentration of IgE, or any The Oxford group have now put forward a candidate gene combination of these.2 It proposed an autosomal dominant which looks all the more plausible because of the group's IgE mode ofinheritance and mapped a gene important in atopy to based definition of atopy.'6 The high affinity receptor for IgE chromosome 1 1q13.' Inheritance via this locus was found to is composed ofot, ,3, and X subunits. The (3 subunit gene lies on occur only through the female line.4 Atopy can, of course, chromosome 11q13 and is closely linked to the suspected gene be inherited paternally, and the authors thought that the for atopy. The high affinity IgE receptor is found both on proportion attributable to the locus on chromosome 11 was mast cells, which are important in immediate hypersensitivity, only about 60%. and on Langerhans cells, which are important as antigen Several other groups have since failed to confirm the presenting cells in the skin. The Langerhans cells are the only BMJ VOLUME 307 23 OCTOBER 1993 1019 cells in the epidermis to express the high affinity IgE 4 Cookson WOCM, Young RP, Sandford AJ, Moffatt MF, Shirakawa T, Sharp PA, et al Maternal inheritance ofatopic IgE responsiveness on chromosome 1 lq. Lancet 1992;340:381-4. receptor'7 and do so especially in atopic eczema,18 in which 5 Coleman R, Trembath RC, Harper 1I. Chromosome 1 1q13 and atopy underlying atopic eczema. IgE may play a part in antigen presentation.'9 Lancet 1993;341:1 121-2. 6 Hizawa N, Yamaguchi E, Ohe M, Itoh KA, Furuya K, Ohnuma N, et al. Lack of linkage between These strands of information still have to be woven into a atopy and locus 1 lql 3. Clin ExpAlergy 1992;22:1065-9. 7 Amelung PJ, Panhuysen CIM, Postma DS, Levitts RC, Koeter GH, Francomano CA, et al. Atopic coherent theory, and it remains likely that many genes and BMJ: first published as 10.1136/bmj.307.6911.1019 on 23 October 1993. Downloaded from and bronchial hyperresponsiveness: exclusion oflinkage to markers on chromosomes 1 lq and 6p. environmental factors play a part in the pathogenesis ofatopic CGn ExpAiergy 1992;22:1077-84. 8 Lympany P, Welsh Kl, Cochrmne GM, Kemeny DM, Lee TH. Genetic analysis of the linkage diseases. Nevertheless, at last a bridge is being built between between chromosome 1 lq and atopy. Clin ExpAlergy 1992;222:1085-92. the immediate hypersensitivity components of atopy, such as 9 Moffatt MF, Sharp PA, Faux JA, Young RP, Cookson WOCM, Hopkin JM. Factors confounding genetic linkage between atopy and chromosome 1 lq. ClinExpAery 1992;22:1046-51. asthma and hay fever, and the delayed ones, such as eczema. 10 MortonNE. Major locifor atopy? ClnExpAlergy 1992;22:1041-3. We must wait for the next instalment of this still shadowy 11 Schultz Larsen FS, Holm NV, Henningsen K. Atopic dermatitis. J Am Acad Dermawol 1986;15:487-94. but important story. Meanwhile, the prevalence of atopy 12 Diepgen TL, Fartasch M. Recent epidemiological and genetic studies in atopic dermatitis. Acta continues to rise. Derm Venereol 1993;suppl 176:13-8. 13 Dold S, Wjst M, Von Mutius E, Reitmeir P, Stiepel E. Genetic risk for asthma, allergic rhinitis and J A SAVIN atopic dermatitis.
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