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by Marijana Domazet, Wednesday, August 14, 2013 | Categories: Allergies

Researchers have long believed that allergies are the result of a complex interplay between genetics and the environment. Despite significant efforts to unravel these mechanisms, most findings have tended to find ways to alleviate symptoms rather than eradicate them. However, a recently published study has opened a new avenue for research to consider the role of genetics in the development of allergies.

In the study, which was published in Science Translational Medicine, the researchers looked at the occurrence of allergies in a group of 58 children who all had Loeys-Dietz Syndrome (LDS). Within that sample, 31% had food allergies, 45% suffered from asthma and a significant number of them had various types of nasal allergies.

The patient sample was particularly suitable for research into allergies, as the proportion of participants that had one or more allergies was at a significantly higher rate than would generally be found in the population. In addition to that, the participants were particularly suitable for the purpose of the study, as it is commonly known that LDS patients tend to have mutations in specific genes that can result in abnormal TGF-beta signalling. This was paramount to the research, as the role of TGF-beta was one of the key areas of the current study.

After analysing the blood samples, the researchers confirmed that the participants had abnormally high levels of the so-called TGF-beta protein as well as unusually high levels of regulatory T-cells. In addition to that, the researchers noted that the regulatory T-cells were secreting cytokines, which are molecules commonly known for their allergy promoting effects.

As regulatory T-cells have a part in immune cells maturation, which in turn is controlled by TGF-beta, the researchers were keen to see what role TGF-beta played in this situation. Further analysis revealed that the participants had abnormally high levels of a transmitter of TGF-beta signalling called SMAD. This was further corroborated by other research that has indicated that LDS patients treated with a medication that tends to tame TGF-beta signalling had reduced levels of the protein. However, it was not currently known if that sample had a lower level of allergies.

Based on this, the researchers argued that the genetic glitch that leads to the development of illnesses such as LDS also could hold the key for understanding the development of a range of allergies that are common co-morbidities associated with LDS.

Although the tests in the current study were rigorous, we are not yet convinced by the findings. The sample was very limited and had a broad age range between 7 and 20, which means that there could have been several other factors that affected the outcome.

Having said that, there is little doubt that the mechanisms described are plausible and offer an attractive explanation for a complex issue. However, we feel that more research in various populations is needed to replicate and corroborate the findings. A very simple explanation of this study can be found here.

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