“One of the biggest issues facing international sustainability efforts is that smaller, less economically developed countries often don’t have the resources to conduct nuanced, in-depth surveys of local people and the local environment in the threatened area,” says Ana Quiñónez Camarillo, a Ph.D. candidate in environmental conservation at UMass Amherst and the paper’s senior author. “And so environmental organizations often wind up pushing a top-down conservation strategy, which may or may not be acceptable to the local people. If the strategy isn’t acceptable, then it may fail, costing time, money, goodwill and further endangering ecological and social health.”

This is especially true of ecological issues that are widely dispersed, have multiple causes and result in an array of negative effects.

Quiñónez Camarillo and her co-author, UMass Amherst Professor of Environmental Conservation Timothy Randhir, point to Honduras’s Lake Yojoa watershed as an example.

Lake Yojoa is the country’s largest natural lake, and its watershed covers 337 square kilometers of forest and mountains. It is adjacent to two national parks; a major highway runs nearby, and dozens of towns and villages are located within the watershed, some right on the lake’s edge and other tucked up in the mountains. The watershed is rich in biodiversity and has become a popular tourist destination. Aside from tourism, fishing is a major industry, as well as mining and aquaculture.

Many in the region are concerned about water quality, but what water quality looks like depends upon which part of the watershed you are in — and the method of protecting water quality may, on the surface, look like it has nothing to do with water. For instance, in the mountainous highlands, a concern for water quality may mean changing logging or mining practices, since deforestation often leads to silt-filled streams which empty into the lake, which then effect fish and the people who rely upon them for their livelihood. “If you were to tell someone in the mountains, ‘don’t log in this way to protect the fish in the lake,’ it wouldn’t make any sense” says Quiñónez Camarillo.

To help make these connections visible and expedite planning, Quiñónez Camarillo and Randhir adapted a sensitive, flexible and complex framework, called a multiscale ecological framework, to focus on the local perception of threats, consequences and solutions (TCS).

“Academic experts in sustainability all over the world are faced with the challenge of how to use extremely theoretical scientific frameworks to engage the public,” says Randhir, who has been a pioneer in such environmental frameworks. “Our TCS framework makes thinking across multiple scales more approachable for local communities by focusing on the three big areas — threats, consequences and solutions — that are familiar to how people live their daily lives.”

To test the TCS framework, Quiñónez Camarillo and Randhir conducted 224 surveys across 12 communities within the Lake Yojoa watershed, as well as engaging 24 other stakeholders, which ranged from private companies to the National parks and which were selected by the local commonwealth for the Lake Yojoa Watershed, AMUPROLAGO. The surveys were conducted orally in Spanish. The surveys were designed in conjunction with AMUPROLAGO and, in addition to standard demographic questions, focused on threats, consequences and solutions to the loss of forests, wetlands, wildlife, fishing resources, water quality and water quantity.

From the rich data that the researchers collected, they were able to generate a series of detailed tables assessing a wide range of threats, consequences and solutions for the various locales in the Lake Yojoa watershed — grass-roots information which the team hopes will serve as a valuable baseline for conservation and governmental organizations at work in the Lake Yojoa region.

“With the TCS framework,” says Quiñónez Camarillo, we can design better solutions that will be more effective because they are more equitable and acceptable to local people. This framework can help show how big solutions actually affect the things that people really care about at the grass roots.”

This research was supported by the National Institute of Food and Agriculture, the Department of Agriculture, the Massachusetts Agricultural Experiment Station, and the National Science Foundation.

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.”