A protein within the immune system that’s programmed to guard the body from fungal infections can increase the severity of certain autoimmune diseases corresponding to irritable bowel syndrome (IBS), type 1 diabetes, eczema and other chronic disorders. can be responsible, in accordance with recent research from The Australian National. University (ANU) has found
The discovery could pave the way in which for brand new and more practical drugs, without the nasty unwanted side effects of current treatments. In addition to helping manage severe autoimmune conditions, the breakthrough could help treat every kind of cancer.
Scientists have discovered a previously unknown function of the protein, called DECTIN-1, which in its mutated state limits the production of T regulatory cells, or so-called 'guardian' cells, within the immune system.
These guardian cells are critical to stopping autoimmune disease because they suppress the consequences of a hyperactive immune system, which might be extremely dangerous if not properly regulated.
The immune system is designed to guard the body from infection, but in severe cases it becomes overactive and turns the body's natural defenses against itself.
“When this happens, the immune system mistakenly perceives healthy cells as a threat, causing it to attack the body and promote the onset of autoimmune disease,” from the ANU. Renowned creator Dr Cynthia Turnbull said.
“Although the DECTIN-1 protein helps fight fungal infections, in its mutated state it’s also answerable for exacerbating severe autoimmune disease.
“Understanding how and why a mutated version of this protein causes autoimmunity in patients brings us one step closer to developing more effective drugs and offers new hope to more than one million Australians. who are suffering from some type of autoimmune disease.”
Scientists imagine they will control the immune system by turning the DECTIN-1 protein on and off like a light-weight switch.
“Activating the protein will reduce the intensity of the immune system's defensive response which will help treat conditions such as autoimmune disease,” said Professor Carola Vanessa from the Francis Crick Institute.
“On the opposite hand, blocking the protein can boost the immune system, sending its defense mechanisms into overdrive and allowing the body to treat a complete different set of diseases.
“The findings are interesting because there have not been many discoveries of so-called modifier proteins, such as DECTIN-1, which can alter the behavior of the immune system to the extent that it can cause or prevent disease.”
According to Dr Turnbull, this implies DECTIN-1 may play a key role in cancer treatment.
“Cancer cells can disguise themselves by releasing certain proteins and chemicals into the body that essentially make them invisible to the immune system's natural defenses,” he said.
“We think that by using drugs to block the DECTIN-1 protein, in combination with existing treatments, we can activate the immune system and help it identify and attack cancer cells. are.”
Current treatments for autoimmune disease aren’t very effective and have many harmful unwanted side effects. This is because the vast majority of current treatments suppress your entire immune system quite than targeting a particular area.
“This means it may not address the real problem behind the patient's illness and may inadvertently leave them vulnerable to infections. Many people also develop bacterial, fungal and viral infections on this type of treatment. which can impair their auto-immunity,” said Professor Venosa.
By examining the DNA of a Spanish family, researchers discovered that a DECTIN-1 mutation was answerable for increasing the severity of a chronic autoimmune disease within the family's only child.
“We found that this family also has a mutated version of another immune system protein called CTLA-4. CTLA-4 mutations prevent the host cells from working properly and about 60 to 70 percent It is known to cause severe autoimmune disease in people who carry it in their DNA,” said Dr Pablo Canet of the University of Queensland.
“The strange thing is that the remaining 30 to 40 percent of the population who carry this mutated protein don’t develop the disease.
“We discovered that the one child within the family had each a DECTIN-1 mutation and a CTLA4 mutation, while his parents had only certainly one of each. This helped us discover that the kid, who Now in his twenties, why was he the one person to develop severe autoimmunity, ending the 20-year-long mystery behind his illness?
“By discovering the existence of altered versions of modifier proteins such as Dectin-1, we finally have an explanation for why some people develop severe autoimmune diseases while others do not.” Whether they inherit the gene variation from members of the family.”