People with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome May Have an “Exhausted” Immune System
Myalgic encephalomyelitis / Chronic Fatigue Syndrome (ME / CFS) is a debilitating multisystem disorder from which adults are rarely recovered. The researchers had trouble finding changes in the body underlying the disease, which often appears after an infection, in part because it can occur in different forms. Now, scientists from the National Institutes of Health (NIH) may have completed the most complete study of Me / CFS to date by examining a group of carefully selected participants. In the study, which was published today in Nature communicationsResearchers have observed changes that reveal how the disease disrupts immune and nervous systems.
In addition to having overwhelming fatigue, people with Me / CFS experience a range of other symptoms such as brain fog, hypersensitivity to light and short -term memory loss. Health professionals have historically rejected condition as a psychosomatic disorder by implying that the disease has no physiological basis.
These disdainful opinions have retained research on me / CFS, and scientists have made little progress towards the development of diagnoses and therapies and to understand the mechanism behind the condition. In recent years, some progress has been made to accept the Ego / CFS as a real physiological condition, partly due to the emergence of the long coide (a condition which, according to some studies, is qualified for a diagnosis Me / CFS about half of the time). But doubt about his legitimacy persists. Alison Sbrana, a person with me / CFS who participated in the new study, says that she would be shocked to meet someone with me / CFS who did not have their concerns dismissed at some point.
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Avindra Nath, a neurologist at NIH, decided to disentangle the internal functioning of the condition. First, his team had to carefully select a cohort of participants in Me / CFS for the study because the condition has many forms that may not share the same physiological manifestations. The researchers focused on a subset of people with me / CFS who had developed the condition after an infection (before the cocovio pandemic). They dressed in this group by continuing a rigorous selection process, and they only inclined participants that a panel of five clinicians agreed unanimously met the criteria. Only 17 ME / CFS participants stayed after the selection process, alongside 21 healthy volunteers. With its carefully selected cohort, Nath’s team used a series of tests to study several bodily systems.
The researchers saw signs that the immune system had become “exhausted” among the participants in Me / CFS. In the blood of this group, they found that the tute cells, which normally target infected cells for destruction, had a reduction in the levels of a protein called CD226 which would otherwise increase their proliferation and activity. In the cerebrospinal fluid, the killer cells had high levels of programmed cell death protein 1 (PD1). This protein is considered to be a “exhaustion” marker, and its presence may indicate that an over -waved cell has stopped. “The immune system is exhausted, becomes exhausted and can no longer respond to infectious triggers,” explains Katharine Seton, an immunologist who does research on Me / CFS at the Quadram Institute, who was not involved in this study.
Nath speculates that such exhaustion could occur if leftovers of an infection persist for a long time after its end and continue to stimulate immune cells in the long term, but other evidence is necessary to confirm it. Seton hypothesizes that a “fleeing intestine” could be another trigger. If inflammatory microbes that live in the intestine decrease in the blood circulation, they could perpetually perpetuate immune cells, leading to exhaustion, she says.
But all the defenses of the immune system do not decrease in me / CFS. Previous studies have also indicated a overactive Immune response: a condition called autoimmunity, by which other immune cells wrongly attack healthy tissues, often by producing autoantibodies that target body proteins. Nath’s team has found low autoantibodies in one person with me / CFS. But the researchers may not have identified more because they excluded participants who had underlying autoimmune conditions. Maureen Hanson, biologist of cells and molecular at Cornell University who works on Me / CFS but has not been involved in this study, adds that “it is very difficult to examine all possible antibodies”, which makes it difficult to exclude the presence of other autoantibodies.
Nath found indirect evidence of autoimmunity. His team observed hyperactive B cell genes in female participants ME / CFS. B cells are the source of autoantibodies, so it is possible that this change predisposed women to self-permeator, he suggests. This and other sex differences that have arisen show that “there are potentially two different mechanisms that occur in men and women,” says Seton, who could partly explain why Me / CFS is three times more common in women.
Beyond the immune system, Nath’s team has looked for changes in the brain. When the participants were invited to grasp an object, those with Me / CFS had decreased activity in their right time-buttal junction, a region of the brain involved in self-agency, by which the brain predicts an action before it is aware. Although other brain differences in people with me / CFS have been known for some time, “this particular discovery of this particular region is new,” explains Hanson. Nath hypothesizes that this decrease in activity suggests that the brain warns people with me / CF against exercising it for force during the handle test, which, according to him, makes sense because the symptoms of me / CFS often intensify if people with the condition of overwork themselves. However, the discovery is preliminary and other experiences are necessary to corroborate it.
The study was “one of the first of its kind,” said Seton, but it had some limits. Given the small number of participants, the researchers may have lacked subtle differences between people with me / CFS and healthy controls, she says. Nath explains that the pandemic blocked recruitment. “We hoped to recruit at least 10 if not 20 others [people with the condition]”, He said. [ME/CFS] research.”
The next Nath plans to study a long time. “I think that is how I can benefit patients with me / CFS much faster than I could otherwise,” he says. It is easier to recruit a more important cohort given the climbing of the number of people with a long cocoan and because their condition started after the same viral trigger, which could help standardize the analysis, says Nath. It has already started clinical trials of intravenous immunoglobulin, current treatment for disorders or autoimmune infections, in people with very coated. “I think if it shows an advantage, it will benefit [other ME/CFS] Patients too. »»
In the meantime, Sbrana hopes that this study will raise awareness of his illness. Before the study, many people – even health professionals – did not think that his condition was real. “I was on the left on the left and right each time I was trying to receive care,” she says. “Once my return from the NIH, my experience of care in my local community has radically changed.” No one called into question their condition once the NIH put it in writing. “But we were only 17 of us [took part]And I hope that all the patients with me / CFS can be taken seriously in the way I was, ”she says.
