About 3 million people worldwide Multiple sclerosis (MS) is an autoimmune disease by which the immune system mistakenly attacks the brain and central nervous system.
Although MS treatments have improved over time, there continues to be no cure. This is essentially because researchers still don't fully understand what goes improper with the immune system that causes MS. But our latest research has revealed recent insights into the behavior of certain immune cells in individuals with MS. The discovery brings us closer to understanding why some people get MS – and it might be a vital step towards higher treatments and even a cure.
Although the causes of MS will not be fully understood, we do know. Genetics, lifestyle and environmental factors All can affect the chance of MS. But the largest risk for developing MS appears to be a typical virus called Epstein-Barr virus (EBV).
EBV normally infects people without symptoms in childhood – so most early infections go unnoticed. But if the infection occurs during adolescence, it could cause glandular fever (infectious mononucleosis), which, although debilitating within the short term, normally No long term effects.
Most viral infections are cleared quickly by the body's immune system, but EBV is smarter than most viruses. Although the immune system controls the infection, it’s unable to completely eliminate the virus since it hides throughout the virus itself. Immune cell type called B cells (which normally produce antibodies that attach to and destroy invading viruses or bacteria). Once you're infected with EBV, you carry it for all times – although for most individuals it doesn't cause any problems.
About 95% of individuals are infected with EBV by maturity, but only in individuals with MS almost 100% are affected. Large epidemiologic studies have shown that EBV infection increases the chance of developing MS by greater than 30-fold. The risk is even higher for individuals who have glandular fever. Research has also shown that in individuals with MS, EBV infection It happens before Early stages of the disease.
Many researchers now imagine that exposure to EBV is greater than a risk think about MS – it’s important.
But how does EBV cause MS – and why does a typical virus cause MS in just a number of people? Multiple theories Investigations are currently being conducted.
One theory is that immune cells activated by EBV in some people mistakenly attack parts of the brain and central nervous system. This process, called molecular mimicry, also occurs in other autoimmune diseases, e.g Guillain-Barre syndrome. This may explain why drugs are shown to dam immune cells from entering the brain. Dramatically improve MS symptoms.
Meltius Veras/Shutterstock
Research into EBV molecular mimicry in MS has focused totally on the viral protein EBNA1. Without EBNA1, EBV cannot survive in B cells, and MS patients have high levels of antibodies. EBNA 1.
But EBV makes greater than 80 different proteins during its life cycle. In our latest work we investigated the immune response to those other viral proteins in individuals with MS.
Altered immunity
We Compare the immune response 31 individuals with MS, 33 healthy people and 11 individuals who had recently recovered from glandular fever. We desired to see if each group responded otherwise to EBV infections.
We found that antibodies targeting EBNA1 and one other viral protein called VCA were higher in individuals with MS than in other groups. People with MS are also more more likely to have antibodies that concentrate on several other viral proteins. This suggests that EBV antibodies change more in MS than previously thought – but it surely is just not certain whether these antibodies are fighting infection or have a job in MS disease.
Antibodies will not be the entire story. Previous research has suggested that one other form of immune cell, called a T cell, may play a vital role since it High number of MS brain lesions. Thus, we wanted to know whether the T cells that fight EBV were different in individuals with MS.
By analyzing blood samples we found that, although EBV T cell numbers were similar in MS and healthy people, these cells behaved otherwise in individuals with MS. T cells from individuals with MS produced barely higher amounts of an inflammatory substance called interleukin-2. The body normally produces this substance in response to injury or infection, but an excessive amount of interleukin-2 May cause chronic disease.
We also checked out molecular simulations, wondering if EBVT cells mistakenly goal brain proteins as a substitute of fighting the virus.
Intriguingly, we found that in each MS and healthy individuals, their EBV T cells responded to a variety of proteins present in the brain. Specifically, most individuals had EBV T cells that targeted a protein called myelin oligodendrocyte glycoprotein, or Mog, which surrounds nerves.
Looking in additional detail in an individual with MS, we found individual T cells that directly recognized each EBNA1 and Mog. This signifies that, as a substitute of just fighting the infection, some EBV T cells may goal nerve cells within the brain.
This widespread misdirection between EBV T cells and the brain explains how infection with this common virus can result in MS. But its presence in healthy people is somewhat ambiguous. One possible explanation could also be that EBV T cells in individuals with MS are capable of cross the blood-brain barrier (a powerful lining of cells that protect the brain). This idea is something we would really like to explore in future research.
Although we still don't know much about these misdirected EBV T cells within the brain, our latest findings provide fresh evidence for researchers and can hopefully result in the event of latest, targeted therapies for MS. will