Guillain-Barre syndrome (GBS) is an inflammatory disease that affects the nerves. It is thought to be an autoimmune disorder, and while the cause is not fully understood, it often arises after a person has experienced a viral or bacterial infection. Many people have been affected by a flu-like illness or gastrointestinal disturbance about two weeks before the onset of GBS, and GBS has also been linked to Zika virus outbreaks.
There are about one or two cases of GBS for every 100,000 individuals in the US and Europe, making GBS a relatively rare disease. It can impact anyone, and while GBS affects people differently, it can be very serious. The disease tends to start with tingling or weakness in the legs, and then spreads to the upper body. Movement may become difficult, and in severe cases patients might experience paralysis of their breathing muscles.
There are some treatments that can reduce the severity of the disease and may shorten recovery time. But patients often have to be hospitalized, and there is no cure for GBS. Around 20 percent of GBS patients are severely disabled or may die from the disease.
A study has now offered new insights into the cause of GBS. The findings have been reported in Nature.
T lymphocytes are a crucial part of the immune system. They help find threats like pathogens or aberrant cells, and work to remove them. But in rare cases, these T cells go rogue and attack the body's own cells, which can lead to autoimmune disease. This study showed that there are abnormal T lymphocytes in GBS patients. These dysfunctional T cells attack nerve tissue, and the insulating sheath called myelin that covers nerves and helps them propagate signals quickly.
Aberrant T lymphocytes were found in GBS patients that have a particular type of the disease in which myelin is lost, noted corresponding study author Daniela Latorre, an SNSF PRIMA group leader at the Institute of Microbiology at ETH Zurich.
In samples from other GBS patients who had gotten GBS after a viral infection, the investigators found cells that were reacting to antigens on the myelin of peripheral nerves, as well as viral antigens. This provides evidence that the disease can be triggered by a viral infection.
The investigators are hopeful that this latest data will provide new drug targets that could treat GBS in a more specific way than current approaches, which have broad effects.
Sources: ETH Zurich, Nature