Seasonal immunity: Activity of thousands of genes differs from winter to summer

[melihtas]

Seasonal immunity: Activity of thousands of genes differs from winter to summer

Our immune systems vary with the seasons, according to a study led by the University of Cambridge that could help explain why certain conditions such as heart disease and rheumatoid arthritis are aggravated in winter whilst people tend to be healthier in the summer.

The study, published today in the journal Nature Communications, 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 adipose tissue (fat).

Scientists have known for some time that various diseases, including cardiovascular disease, autoimmune diseases such as type 1 diabetes and multiple sclerosis, and psychiatric disorders, display seasonal variation, as does vitamin D metabolism. However, this is the first time that researchers have shown that this may be down to seasonal changes in how our immune systems function.

“This is a really surprising – and serendipitous – discovery as it relates to how we identify and characterise the effects of the susceptibility genes for type 1 diabetes,” says Professor John Todd, Director of the JDRF/Wellcome Trust Diabetes and Inflammation Laboratory. “In some ways, it’s obvious – it helps explain why so many diseases, from heart disease to mental illness, are much worse in the winter months – but no one had appreciated the extent to which this actually occurred. The implications for how we treat disease like type 1 diabetes, and even how we plan our research studies, could be profound.”

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Widespread seasonal gene expression reveals annual differences in human immunity and physiology

Abstract
Seasonal variations are rarely considered a contributing component to human tissue function or health, although many diseases and physiological process display annual periodicities. Here we find more than 4,000 protein-coding mRNAs in white blood cells and adipose tissue to have seasonal expression profiles, with inverted patterns observed between Europe and Oceania. We also find the cellular composition of blood to vary by season, and these changes, which differ between the United Kingdom and The Gambia, could explain the gene expression periodicity. With regards to tissue function, the immune system has a profound pro-inflammatory transcriptomic profile during European winter, with increased levels of soluble IL-6 receptor and C-reactive protein, risk biomarkers for cardiovascular, psychiatric and autoimmune diseases that have peak incidences in winter. Circannual rhythms thus require further exploration as contributors to various aspects of human physiology and disease.

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[Mark]

Wow this is massive, thanks melihtas!

I posted here a year or two ago about this I think, and always thought this seemed likely to be crucial given the confusing picture of the research and non reproducability of results...and some researchers finding the opposite of what others found. This seems especially true in me/CFS work on this subject. Perhaps from a UK perspective, the Aussies have always had it exactly wrong!

Lipkin was careful to control for this factor, taking control samples at the same time as patients I think, so that study is secure, and now surely the task is on to re-appraise the entire evidence base. Conceivably that exercise could provide the killer evidence and scientific clue that we need, maybe? And future studies can be expected to give us multiple data points through the year, as well as latitude of subjects - latitude will be key because clearly (surely) the process going on here is triggered by light, no?

I think this is incredibly exciting - now that we understand what's going on with the variability, this area can hopefully yield consistent results at last.

 

[JaimeS]

...just had a conversation elsewhere about always being more ill in summer!

-J

 

[Valentijn]

Huh, we've been trying to figure out why my fiance's blood glucose levels and apparent reaction to insulin jump all over the place for no apparent reason. Maybe there is a seasonal link - he's generally needing a lot less insulin (sometimes none at all) during vacations, which are during the summer ...

 

[JaimeS]

@Valentijn - could be that he needs less because of seasonal variation. Insulin needs are also directly related to stress response. Perhaps he's more relaxed on vacation.

Life is full of variables!

-J

 

[daisybell]

I'm currently in the UK on holiday from NZ, and am experiencing the most significant improvement in symptoms that I've ever had. I feel incredibly much better, and the improvement has been ongoing over the past three weeks.... Could the rapid switch of seasons be the reason??

 

[adreno]

So summer/warm climate is better for us than winter/cold climate?

 

[user9876]

Wow this is massive, thanks melihtas!

I posted here a year or two ago about this I think, and always thought this seemed likely to be crucial given the confusing picture of the research and non reproducability of results...and some researchers finding the opposite of what others found. This seems especially true in me/CFS work on this subject. Perhaps from a UK perspective, the Aussies have always had it exactly wrong!

Lipkin was careful to control for this factor, taking control samples at the same time as patients I think, so that study is secure, and now surely the task is on to re-appraise the entire evidence base. Conceivably that exercise could provide the killer evidence and scientific clue that we need, maybe? And future studies can be expected to give us multiple data points through the year, as well as latitude of subjects - latitude will be key because clearly (surely) the process going on here is triggered by light, no?

I think this is incredibly exciting - now that we understand what's going on with the variability, this area can hopefully yield consistent results at last.

Its one of the reasons why it would be good to have a shared database of individual results with data about how they are obtained (time, location, patient profile, activity profile for a few days/weeks prior to sample etc) then researchers could go back through data and look for patterns that might confirm different readings.

 

[Mark]

Its one of the reasons why it would be good to have a shared database of individual results with data about how they are obtained (time, location, patient profile, activity profile for a few days/weeks prior to sample etc) then researchers could go back through data and look for patterns that might confirm different readings.

Absolutely: it's a very strong argument for Open Data and for keeping archived details of all research. Also it highlights that collection of location information re: sample collection could become important in the future for reasons that aren't now clear. Any studies of these matters from the past that have failed to preserve the key data about location and date/time of sample collection will now effectively have to be thrown away, because their findings have become uninterpretable given what we now know. This must be a massive quantity of research; not just ME/CFS studies, we may be in the position of throwing away billions of dollars worth of past research now because the key data is not available...

 

[user9876]

Absolutely: it's a very strong argument for Open Data and for keeping archived details of all research. Also it highlights that collection of location information re: sample collection could become important in the future for reasons that aren't now clear. Any studies of these matters from the past that have failed to preserve the key data about location and date/time of sample collection will now effectively have to be thrown away, because their findings have become uninterpretable given what we now know. This must be a massive quantity of research; not just ME/CFS studies, we may be in the position of throwing away billions of dollars worth of past research now because the key data is not available...

I know this article is talking about seasons (and I assume that means weather driven) but I wonder if with ME one of the reasons for differing results is the state of exertion at the time blood was taken. Stuff like how far parking is from the clinic or whether someone had to get public transport. Any measures that could vary in the short term based on exertion would be suspect without care. Such values would also need to be kept for proper interpretation. Which comes to the point that until we understand what may affect variation then we run the risk of misinterpreting results or finding inconsistencies. So storing as much contextual data would seem to make sense.