Our immune systems vary with the seasons, according to a study led by the University of Cambridge that could help explain why conditions such as type 1 diabetes are more frequently diagnosed during the winter months.
The study, funded by JDRF, the Wellcome Trust and the NIHR Cambridge Biomedical Research Centre was published today in the journal Nature Communications. The study shows that the activity of almost a quarter of our genes (5,136 out of 22,822 genes tested) differs according to the time of year, with some more active in winter and others more active in summer. This seasonality also affects our immune cells and the composition of our blood and fat tissue.
Scientists have known for some time that various diseases, including autoimmune diseases such as type 1 diabetes and multiple sclerosis, display seasonal variation. However, this is the first time that researchers have shown that this may be down to seasonal changes in how our immune systems function.
An international team, led by researchers from the JDRF/Wellcome Trust Diabetes and Inflammation Laboratory at the Cambridge Institute for Medical Research, examined samples from over 16,000 people living in both the northern and southern hemispheres, in countries including Australia, the UK, USA, Iceland and The Gambia. These samples included a mixture of blood samples and fat tissue.
The researchers used a variety of techniques to study the samples, including looking at the cell types found in the blood and measuring the level of expression, or activity, of the individuals’ genes. They found that thousands of genes were expressed differently in blood and fat tissue depending on what time of year the samples were taken. Similarly, they identified seasonal differences in the types of cells found in the blood.
One gene of particular interest was ARNTL, which was more active in the summer and less active in the winter. Previous studies have shown that ARNTL suppresses inflammation in mice, and if it has similar activity in humans, may explain why some diseases are more prevalent in winter. In the case of type 1 diabetes, low expression of ARNTL in winter may increase the likelihood of an inflammatory autoimmune process being triggered, leading to destruction of insulin-producing islets.
“As we approach winter here in Australia, we expect to see an uptick in the number of children and adults diagnosed with type 1 diabetes” said Mike Wilson, CEO of JDRF Australia. “This is consistent with the rest of the world where diagnosis levels of type 1 diabetes are higher in winter. Given that Australia has the 6th highest prevalence of type 1 diabetes in the world, we welcome the new insights this study reports – that the activity of almost a quarter of our genes differs according to the time of year. It shows us how seasonality affects our immune cells and why the body may be more prone to the autoimmune attack seen in type 1 diabetes in colder months.”
It is not clear yet what mechanism maintains the seasonal variation seen in the immune system, though it may be due to environmental cues such as daylight and ambient temperature. Our internal body clock – known as our circadian rhythm – is in part coordinated by changes in daylight, which explains why people in jobs that do not fit with the daily cycle, such as factory shift workers or crews on long haul flights, can be affected by poorer health. The insight provided by this study opens new avenues of research that could help untangle the complex web of genetic and environmental factors behind the development of autoimmune conditions like type 1 diabetes.
To read the journal article, click here.