Researchers from the University of Birmingham have devised an approach to prevent the body's immune system from recognizing its own proteins, thus preventing an attack on healthy cells in autoimmune disorders.
In their study, the authors analyzed the mechanism of T-cells, which controlled the body's immune function and discovered that they could be manipulated to prevent its attack on its own cells.
For example, with multiple sclerosis, an autoimmune disease involving the brain and spinal cord, the new technique discovered would hinder the body from attacking the Myelin Basic Protection (MBP) by fooling the immune system to perceive the protein as a part of itself.
According to Professor David Wraith, an author of the study from the Institute of Immunology and Immunotherapy, the team's findings have vital connotations for millions of patients suffering from autoimmune conditions that physicians currently find difficult to treat.
Additionally, his co-author, Professor Peter Cockerill from the Institute of Cancer and Genomic Sciences, says that the study has led to further understanding about the underlying foundation of immunotherapies, which numbs the immune system.
The findings of the study supported by the Medical Research Council were published in the journal Cell Reports on June 9, 2020.
The Pathophysiology of Multiple Sclerosis
Autoimmune diseases are caused by the immune system losing its standard focus when fighting infections or illnesses within the body. It is caused by the attack of healthy cells within the body.
In multiple sclerosis (MS), the body attacks proteins in the myelin sheath, which is the fatty insulation-like tissue enclosing the nerves. In patients with MS, nerves lose control over muscles.
A 2017 study on the disease says it commonly involves sensory disturbance, cognitive deficits, bladder dysfunction, unilateral painless loss of vision, limb weakness, double vision, ataxia, fatigue, and bowel problems.
Although MS is linked with a change in a patient's average life expectancy, it is not considered a fatal condition. Furthermore, its clinical course, which appears highly changeable, is unpredictable for the individual patient.
The disease usually starts with the sudden onset of neurological deficits. In most cases, it shows a purely relapsing-remitting course with the absence of symptoms, apart from the relapses. Moreover, the recurrent periods are followed by remission periods after complete or partial recovery.
Role of Myelin Basic Protein in Autoimmune Diseases
According to another study conducted in 2016, the breakdown of myelin sheaths is a pathological symbol of various nervous system autoimmune diseases.
In the first stage of the new research led by Professor Wraith, the researchers displayed that the immune system can be tricked into recognizing MBP by presenting it with repeated doses of a soluble fragment of the protein in which white blood cells react to.
The method, which is similar to a technique previously used to desensitize people against allergies, showed that the white blood cells that acknowledge MBP converted from attacking the proteins to becoming protective of the body.
In the second stage led by Professor Cockerill, the scientists probed deep within the white blood cells that responded to MBP. It demonstrated how genes were rewired in response to the form of immunotherapy to permanently reprogram the immune system.
The reiterated exposure to the same protein fragment caused a response that turned on genes that stifled the immune system instead of switching it on. The cells then had traces of this exposure to MBP implanted in the genes to stop them from starting an immune response. When T-cells are made receptive, other genes that aim to activate the immune system continue becoming silent.
According to the authors of the study, long term clinical trials would be needed to verify if antigen-specific immunotherapies could deliver long-lasting benefits. If proved to be successful, the study will be the first of its kind in defining the existing mechanisms of how T-cells can be made tolerant to the body's own proteins. The scientists are confident that their findings could lead to further advances in the battle to beat autoimmunity.