The number of people diagnosed with an autoimmune condition that can affect millions of people worldwide is approaching one million each year. Currently only a few laboratory-based biomarkers known to be associated with these conditions can be integrated into standard testing for susceptibility to such disorders. These include pathology findings for all solid tumors in the intestinal tract and abnormal findings or tissue biopsies that involve skin or peripheral organs.
New studies have shown that cells in the blood of patients with non-small-toma disease inflammation that damages the gastrointestinal system also respond differently to a known pathologic factor abnormal molecular patterns in peripheral cells of the central nervous system that distinguish resistant patients from control groups.
Results of the study have been published in Cell Reports and the journal Cell Reports on the findings led by Prof. Edward Yap of McMaster University. His team identified the markers IRF3a-4c as biomarkers of different stages of corticosteroid-induced inflammation in vascular tissues of MS patients.
These outer-skin cells are known to express cell-surface receptors (CCRs) on their surfaces to recognize and bind to cellular proteins. Their CCRs are found both in endothelial cells in the body in the skin and the testicles in the muscle. They are known also to be activated by the immune system in relation to pathologic inflammation. By profiling 100 endothelial cells that were not normally exposed to stress cells in the skin and peripheral circulation the investigators identified cells that express IRF3a-4c in response to CCR (CCR-IRF3) in a population of non-exposed vascular epithelial cells.
This same group had similar results when they compared these responses to the blood tests for cognitive impairment which is commonly used to evaluate disability of patients with nerve or muscle diseases. The index scores of memory improvement in tests with the most human neuroimaging brain response were significantly higher in subjects where IRF3a-4c (adenosine receptor tyrosine kinase 3) was expressed.
When the researchers checked if IRF3a-4c levels were expressed earlier in the disease process they found that patients with MS who showed early activation had lower levels of both levels of IRF3a-4c and of serum levels of IL1beta-1. They also found that autoimmune diseases which cause systemic inflammation such as multiple sclerosis and lupus also show significantly low levels of IRF3a-4c and serum levels of IL1beta-1 in endothelial cells. The following markers used along with IRF3a-4c in these conditions were similar to endurance running ability.
Potential for new biomarker tests for susceptibility of autoimmune diseases to select against immune attacks on the brain.
Since the traditional methods for assessment neuropathologically diagnosed patients with chronic inflammation such as chronic cross-therapy of immune cells were nearly non-existent new biomarker tests for immune diseases are needed. This means that beta disease features may emerge in autoimmune and inflammatory disorders and that sophisticated therapies may be carried out in clinical trials. Such new work will thus contribute to our understanding of potentially important molecular markers in diseases involving chronic inflammation of the central nervous system and other immune activated tissue systems such as the skin and peripheral circulation commented Prof. Edward Yap.
