The discovery could pave the way for new and more effective drugs, without the nasty side effects of existing treatments. In addition to helping to manage severe autoimmune conditions, the breakthrough could also help treat all types of cancer.

The scientists have discovered a previously unknown function of the protein, known as DECTIN-1, which in its mutated state limits the production of T regulatory cells or so-called ‘guardian’ cells in the immune system.

These guardian cells are crucial to preventing autoimmune disease because they suppress the effects of a hyperactive immune system, which can be extremely dangerous if not properly regulated.

The immune system is designed to protect the body from infection, but in severe cases it becomes overactivated and turns the body’s natural defences against itself.

“When this happens, the immune system wrongly perceives healthy cells as a threat, causing it to attack the body and promote the onset of autoimmune disease,” lead author Dr Cynthia Turnbull, from ANU, said.

“Although the DECTIN-1 protein helps to fight fungal infections, in its mutated state it’s also responsible for exacerbating severe autoimmune disease.

“Understanding how and why the mutated version of this protein causes autoimmunity in patients brings us a step closer to developing more effective drugs and offers new hope to more than one million Australians who suffer from some form of autoimmune disease.”

The scientists believe they can control the immune system by turning the DECTIN-1 protein on and off, like a light switch.

“Turning on the protein would lower the intensity of the immune system’s defensive response which would help to treat conditions such as autoimmune disease,” Professor Carola Vinuesa, from the Francis Crick Institute, said.

“On the other hand, turning off the protein could give the immune system a boost, sending its defensive mechanisms into overdrive and allowing the body to treat an entirely different set of diseases.

“The findings are exciting because there haven’t been many discoveries of so-called modifier proteins such as DECTIN-1, which can change the way the immune system behaves to the extent it can either cause a disease or prevent it.”

According to Dr Turnbull, this means DECTIN-1 could play a key role in treating cancer.

“Cancer cells can disguise themselves by releasing certain proteins and chemicals into the body that essentially render them invisible from the immune system’s natural defences,” she said.

“We think that by using drugs to turn off the DECTIN-1 protein, in combination with existing therapies, we can activate the immune system and help it identify and attack the cancerous cells.”

Current treatments for autoimmune?disease aren’t very effective and have a lot of damaging side effects. This is because the majority of existing treatments suppress the entire immune system rather than targeting a specific area.

“That means it might not fix the exact problem behind the patient’s disease and could inadvertently make them vulnerable to infections. Many people on these kinds of treatments also get bacterial, fungal and viral infections which can make their autoimmunity worse,” Professor Vinuesa said.

By examining the DNA of a Spanish family, the researchers discovered the DECTIN-1 mutation was responsible for exacerbating the severity of a chronic autoimmune disease suffered by the family’s only child.

“We found the family was also carrying a mutated version of another immune system protein known as CTLA-4. The CTLA-4 mutation prevents guardian cells from working properly and is known to cause severe autoimmune disease in about 60 to 70 per cent of people who carry it in their DNA,” Dr Pablo Canete, from the University of Queensland, said.

“Strangely, the remaining 30 to 40 per cent of the population who carry this mutated protein don’t develop disease.

“We discovered?the family’s only child had both the DECTIN-1 mutation and the CTLA4 mutation, while his parents had only one of each. This helped us identify why the child, who is now in his twenties, was the only person in the family to develop severe autoimmunity, ending a 20-year-long mystery behind the cause of his disease.

“By discovering the existence of mutated versions of modifier proteins such as DECTIN-1, we finally have an explanation for why some people develop severe autoimmune diseases while others don’t, even if they inherit gene mutations passed down from family members.”

However, there may be hope for some tropical reefs in the form of feathered friends.

A new study led by researchers at Lancaster University has found that the presence of seabirds on islands adjacent to tropical coral reefs can boost coral growth rates on those reefs by more than double.

And as a result of this faster growth, coral reefs near seabird colonies can bounce-back much quicker from bleaching events — which often cause mass die off of corals when seas become too hot — the international team of researchers also discovered.

The study, published today in Science Advances, focused on Acropora, an important type of coral that provides complex structures supporting fish populations and reef growth, and which is also important for protecting coastal areas from waves and storms. The researchers found that Acropora around islands with seabirds recovered from bleaching events by around 10 months faster (approx. three years eight months) compared to reefs located away from seabird colonies (four years six months).

Researchers say these shorter recovery times could prove the difference between continuing to bounce back for some reefs in the face of a warming planet where damaging bleaching events now occur much more frequently than in earlier decades.

The key to how seabirds can help tropical coral reefs to grow and recover more quickly is through their droppings. Seabirds feed on fish in the open ocean far from islands, and then return to islands to roost — depositing nitrogen- and phosphorus-rich nutrients on the island in the form of guano. Some of the guano is washed off the islands by rain and into the surrounding seas where the nutrients fertilise corals, and other marine species.

“Our results clearly show that seabird-derived nutrients are directly driving faster coral growth rates and faster recovery rates in Acropora coral,” said Dr Casey Benkwitt, research fellow in coral reef ecology at Lancaster University and lead author of the study.

“This faster recovery may be critical as the average time between successive bleaching events was 5.9 years in 2016 — a reduction from 27 years in the 1980s. Even small reductions in recovery times during this window may be key to maintaining coral cover over the short-term,” she added.

The researchers’ study focused on a remote archipelago in the Indian Ocean. They compared reefs next to islands with thriving populations of seabirds, such as red-footed boobies, sooty terns and lesser noddies, against reefs next to islands with few seabirds. The islands with few birds have populations of rats, a very damaging invasive species which is devastating to birdlife as they eat eggs and chicks. It is no coincidence that the islands with thriving bird populations are rat-free.

The reefs in the study area suffered extensive coral bleaching and mortality following marine heatwaves in 2015-16, providing an opportunity to observe, and compare, how coral on different reefs recovered. The researchers surveyed the sites from one year before the bleaching event to six years after the bleaching, and modelled the Acropora recovery for the years between surveys.

The research team sampled nitrogen stable isotope values, a reliable tracer of seabird-derived nutrients, and measured growth rates of the Acropora corals for three years.

The results showed that seabird-derived nutrients taken up by corals next to bird islands boosted coral growth rates — with the rate doubling for each unit of seabird nutrient increase.

In contrast, coral near rat-infested islands had similar nutrient values to coral found distant from islands — showing the supply of these nutrients had been virtually cut off by the lack of birds.

The scientists also undertook an experimental approach to find out if the faster growth was directly due to the nutrients, as opposed to other factors such as genetic differences in corals between different islands. They transplanted some Acropora corals between islands with and without rats.

This experiment confirmed that it was the presence of seabirds that caused the nutrient enrichment.

At an island level, coral colonies transplanted to seabird islands grew twice as fast as those transplanted to rat-infested islands. Natural coral colonies were also found to grow faster near to rat-free islands with an estimated 2.4 times faster growth rate compared to coral around rat infested islands.

Dr Benkwitt said: “We’ve been able to show a clear link between the presence of seabirds and faster coral growth. This is really exciting and encouraging that a natural solution is available to help boost the resilience of coral reefs in the face of a warming planet.

“By restoring seabird populations, corals can quickly take-up and benefit from the supply of new nutrients, and our three-year experiment shows that these benefits are not just a short boost — they can be sustained over the long-term.”

The researchers say their findings add further weight to the growing body of evidence that shows the ecological damage across ecosystems on land and sea from invasive rats on tropical islands.

Professor Nick Graham of Lancaster University and Principal Investigator of the study said: “Combined, these results suggest that eradicating rats and restoring seabird populations could play an important role in re-establishing the natural flows of seabird nutrients to the nearshore marine environment, bolstering rapid coral reef recovery which will be critical as we expect to see more frequent climate disturbances.”

Environmental benefits of seabird nutrients go beyond increased rates of coral recovery. “Growth rates of fish on reefs adjacent to islands with large seabird colonies is also faster and overall biomass of fish is 50% greater than on reefs next to islands with rats,” said Dr Shaun Wilson, a co-author of the study from the Australian Institute of Marine Science. “Consequently, rates of grazing and bioerosion by fishes is three times faster on islands with seabirds, which are key processes helping to maintain a healthy reef.”

The results of the study, which was supported by the Bertarelli Foundation as part of the Bertarelli Programme in Marine Science, are outlined in the paper ‘Seabirds boost coral reef resilience’ published by Science Advances.

The authors of the paper are Cassandra Benkwitt, Samuel Healing and Nicholas Graham of Lancaster University; Ruth Dunn of Lancaster University and Heriot-Watt University; Rachel Gunn of Lancaster University and the University of Tubingen; Cecilia D’Angelo, Maria Loreto Mardones and Joerg Wiedenmann of the University of Southampton; Shaun Wilson of the Australian Institute of Marine Science and the University of Western Australia.