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Allergic asthma and hay fever may be passed from mother to child, according to an Anglo-Japanese research team. It has identified a gene which, when inherited from the maternal line, seems to sensitise immune cells in the nose and lungs to common allergens such as grass pollen.

For several years, geneticists in Oxford, led by Julian Hopkin of the Churchill Hospital, have been studying DNA from a large number of families to see how the allergic tendency, known as atopy, is passed down. Two years ago, working with researchers from Tokyo, they homed in on chromosome 11. Now they have singled out a gene on the chromosome.

The team found that 10 out of 60 families susceptible to atopy carry a particular variant of the gene. In these 10, all children with the variant have atopy. In contrast, the tendency was found in only 2 out of 12 children who did not have the variant. ‘It’s a very strong association,’ says Bill Cookson at the John Radcliffe Hospital in Oxford, a senior member of the team.

Tying down other disorders, such as Alzheimer’s disease and schizophrenia, to particular genes has proved very difficult. But Cookson is confident that the team has the correct gene: he says that two other research groups have confirmed the link. He also reckons that a single gene cannot account for all atopy. ‘There are obviously more,’ he says, ‘probably four or five.’

In all 10 families with the rogue gene, the variant was always inherited from the mother. This, say the researchers, could be because of some influence of women’s imm-une systems on the development of their children before or around birth, or it could be because of some residual effect of the father’s DNA. The precise nature of these parental influences is still obscure, however.

In last week’s edition of Nature Genetics, the reseachers say that further studies are needed to see if the same variant causes atopy if it is passed down by fathers. Differences in the ability of a particular gene to influence a child’s development depending on who it was inherited from, have been seen in a number of disorders, including Huntington’s disease and fragile-X syndrome (‘Why genes have a gender’, New Å®ÉúСÊÓƵ, 22 May 1993).

The gene on chromosome 11 is responsible for producing a ‘receptor’ on the surface of mast cells, immune cells that guard the nose and lungs. The receptor attaches to a form of antibody known as immunoglobulin E or IgE. And this, in turn, binds to allergens such as pollen. When IgE binds to its target, the mast cell disintegrates, releasing chemicals that cause the swelling and irritation of allergic reactions.

The molecule produced from the genetic variant differs from the usual by only a single amino acid. But this is enough to change the way mast cells respond to allergens. ‘We think people who have this variant have a more sensitive trigger,’ says Cookson. Stopping IgE from attaching to mast cells by blocking the receptor could dampen down this sensitivity, says Cookson. But, he stresses, ‘any treatment is many years away’.