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.