New study paves the way for better diagnosis and treatment of these types of diseases.
Autoimmune diseases are believed to be the result of mistaken identities. The “guard” immune cells, ready to defend the body against pathogens, mistake normal human cells for infected cells and point their weapons at their own healthy tissue. In most cases, however, it has been difficult for scientists to find the source of the confusion – the small fragment of normal human protein that looks dangerously like a protein from a pathogen. This missing piece of the puzzle has hampered efforts to develop effective diagnoses and specific therapies for many autoimmune conditions.
This situation could finally change. A team of researchers from Washington University School of Medicine in St. Louis, Stanford University School of Medicine and the University of Oxford has developed a way to pinpoint the crucial protein fragments that drive autoimmunity and the immune cells that respond to them. The findings, published Dec. 7 in Nature, open up a promising avenue for the diagnosis and treatment of autoimmune diseases.
“Of all of them, the HLA genes exhibit the greatest amount of variation in the human population. There are tons of autoimmune diseases associated with specific HLA gene variants, and in most cases we don’t know why,” said co-author Wayne M. Yokoyama, MD, Sam J. Levin and Audrey Loew Levin Professor of Arthritis Research at the Washington University. “This paper outlines a strategy for understanding why certain HLA variants are linked to certain diseases. Furthermore, it provides strong evidence that cross-reactivity between human and microbial proteins drives autoimmunity in at least two diseases and possibly many more. Now that we understand what the underlying factors are, we can start focusing on the approaches that are most likely to produce benefits for patients.”
- Autoimmunity-associated T cell receptors recognize HLA-B*27-bound peptides (nature.com)
