New research from The Australian National University (ANU) has uncovered a surprising connection between a protein in our immune system and the severity of certain autoimmune diseases, such as irritable bowel disease (IBS), type 1 diabetes, and eczema.
This protein, known as DECTIN-1, was originally thought to protect the body from fungal infections but has now been found to contribute to the worsening of autoimmune conditions.
This discovery opens the door to developing more effective drugs with fewer side effects than current treatments.
In addition to potentially helping individuals with severe autoimmune disorders, this breakthrough could also have implications for cancer treatment. The study’s findings have been published in Science Advances.
The researchers have unveiled a previously unknown function of DECTIN-1, particularly when it mutates. In its mutated state, this protein reduces the production of T regulatory cells, often called ‘guardian’ cells in the immune system.
These guardian cells are vital for preventing autoimmune diseases because they help regulate an overactive immune system, which can be harmful when not properly controlled.
The immune system is naturally designed to protect the body from infections. Still, in severe cases, it becomes overactive and mistakenly targets healthy cells, leading to the onset of autoimmune diseases.
Dr. Cynthia Turnbull, the study’s lead author, explained, “Although the DECTIN-1 protein helps combat fungal infections, in its mutated form, it also exacerbates severe autoimmune diseases.”
Understanding how this mutated protein contributes to autoimmunity brings us closer to developing more effective treatments. It offers hope to the over one million Australians who suffer from various autoimmune diseases.
The researchers believe they can influence the immune system by manipulating the DECTIN-1 protein, effectively turning it on and off like a light switch.
Turning it on would reduce the intensity of the immune system’s defensive response, which could be beneficial for treating autoimmune diseases. Conversely, turning it off might boost the immune system, enhancing its ability to combat different diseases.
What makes these findings particularly exciting is the rarity of modifier proteins like DECTIN-1, which can alter the immune system’s behavior to the extent of causing or preventing diseases.
Moreover, DECTIN-1’s potential extends to cancer treatment. Cancer cells often evade the immune system by releasing certain proteins and chemicals that make them invisible to natural defenses.
Dr. Turnbull noted, “By using drugs to deactivate the DECTIN-1 protein, in combination with existing therapies, we can activate the immune system to identify and target cancerous cells.”
Unlike current treatments for autoimmune diseases, which can have limited effectiveness and harmful side effects because they suppress the entire immune system, targeting DECTIN-1 could provide a more precise approach.
To further support their findings, the researchers examined the DNA of a Spanish family and found that a DECTIN-1 mutation exacerbated a chronic autoimmune disease in their only child.
Interestingly, the family also carried a mutated version of another immune system protein called CTLA-4, known to cause severe autoimmune disease in a significant portion of those who inherit it.
The combination of DECTIN-1 and CTLA-4 mutations helped explain why the family’s child developed severe autoimmunity, while his parents, who each had only one mutation, did not.
This discovery sheds light on why some individuals with gene mutations from their family members develop severe autoimmune diseases while others do not.
The research was a collaborative effort between ANU, the University of Queensland, and the Francis Crick Institute, offering hope for a better understanding of autoimmune diseases and developing more targeted treatments.
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The research findings can be found in Science Advances.
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