Tuesday 24 October 2017

Scientists find welcome relief for eczema sufferers

Nicola Anderson

Nicola Anderson

A NEW groundbreaking study into the causes of eczema shows that the breakdown of the skin barrier can be a reason for the condition, rather than a result.

Irish scientists have helped pinpoint a new genetic mutation that helps to explain the development of the chronic skin inflammation.

A major international research project led by Trinity College Dublin and the University of Dundee in Scotland found a new gene mutation that leads to atopic dermatitis – an itchy rash which is the most common form of eczema – in mice.

They took the work further to show a variant of the gene in humans.

They found a mutation in the gene Matt/Tmem79 led to the development of spontaneous dermatitis in mice.

The gene makes the protein 'mattrin' malfunction, leading to skin problems.

After identifying the relationship between the mutation and eczema, scientists screened large cohorts of patients suffering from the skin condition, compared with those who did not.

They discovered similar findings in human genes.

Professor Irwin McLean, Scientific Director of the Centre for Dermatology and Genetic Medicine at the University of Dundee, jointly led research between scientists in Ireland, the UK, the USA, Germany and Singapore.


He said that the study shows that disruption of the barrier function of the skin is a "key driving force" in the development of eczema.

"Without an intact skin barrier, foreign substances can enter the body and trigger inflammation and allergy," he explained.

Professor Padraic Fallon, Chair of Translational Immunology in the School of Medicine at Trinity, also led the project and said that the study highlights the value of research in which genetic patterns in animals can provide a starting point for the investigation of some human diseases.

He said the approach will ultimately help in the understanding of factors leading to inflammatory diseases and assist in developing new treatments.

Irish Independent

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