ME/CFS Evidence Browser — Classified Studies on Myalgic Encephalomyelitis

821–840 of 1,186 studies

E3 PreliminaryMechanismPEM not requiredMechanistic

MicroRNAs hsa-miR-99b, hsa-miR-330, hsa-miR-126 and hsa-miR-30c: Potential Diagnostic Biomarkers in Natural Killer (NK) Cells of Patients with Chronic Fatigue Syndrome (CFS)/ Myalgic Encephalomyelitis (ME).

Petty, Robert D, McCarthy, Neil E, Le Dieu, Rifca et al.·PloS one·2016

This study examined tiny molecules called microRNAs in immune cells from ME/CFS patients and healthy people. Researchers found that four specific microRNAs were abnormally high in patients' blood, particularly in natural killer (NK) immune cells. When they tested these microRNAs in the lab, they found they affected how NK cells work, suggesting this might contribute to ME/CFS symptoms.

BiomarkersImmune System

E3 PreliminaryMechanismPEM unclearMechanistic

Serum BAFF and APRIL Levels, T-Lymphocyte Subsets, and Immunoglobulins after B-Cell Depletion Using the Monoclonal Anti-CD20 Antibody Rituximab in Myalgic Encephalopathy/Chronic Fatigue Syndrome.

Lunde, Sigrid, Kristoffersen, Einar K, Sapkota, Dipak et al.·PloS one·2016

Researchers tested whether a drug called rituximab, which removes B cells (a type of immune cell) from the blood, helps ME/CFS patients by examining immune system changes. They found that some ME/CFS patients had higher levels of a substance called BAFF that activates B cells, but this didn't predict who would improve with treatment. While some patients did get better with rituximab in earlier trials, the immune cell changes measured in this study didn't fully explain why.

Immune System

E3 PreliminaryReviewPEM unclearReview-Narrative

The Deleterious Effects of Oxidative and Nitrosative Stress on Palmitoylation, Membrane Lipid Rafts and Lipid-Based Cellular Signalling: New Drug Targets in Neuroimmune Disorders.

Morris, Gerwyn, Walder, Ken, Puri, Basant K et al.·Molecular neurobiology·2016

This review discusses how oxidative and nitrosative stress—a form of cellular damage—may be associated with changes in how cells communicate via lipid-based signalling pathways. The authors propose that these changes could contribute to neuroimmune disorders including ME/CFS, and suggest that omega-3 fatty acid supplementation might help restore normal cell signalling. However, this is a narrative review synthesising existing literature rather than new experimental evidence, so the specific relevance to ME/CFS patients remains preliminary.

Energy MetabolismImmune SystemNeuroinflammation

E3 PreliminaryCommentaryPEM not requiredEditorial

Autoantibody pain.

Goebel, Andreas·Autoimmunity reviews·2016

Your immune system sometimes makes proteins called autoantibodies that attack your own body's tissues and nerves. This review explores how these autoantibodies might cause pain directly by interfering with nerve signals, rather than just causing inflammation. Interestingly, ME/CFS appears to involve this type of autoantibody-related pain mechanism, which could open doors to new treatments for conditions that currently don't respond well to standard pain medications.

Immune System

E3 PreliminaryReviewPEM unclearReview-Narrative

Herpesviruses dUTPases: A New Family of Pathogen-Associated Molecular Pattern (PAMP) Proteins with Implications for Human Disease.

Williams, Marshall V, Cox, Brandon, Ariza, Maria Eugenia·Pathogens (Basel, Switzerland)·2016

This review examines how herpesvirus proteins called dUTPases may trigger harmful immune responses in ME/CFS and other diseases. Most adults carry dormant herpesviruses (like Epstein-Barr virus) that can reactivate throughout life. The researchers suggest that proteins released during reactivation may overstimulate the immune system, potentially worsening ME/CFS symptoms and inflammation.

Immune System

E3 PreliminaryReviewPEM unclearReview-Narrative

Fecal Microbiota Transplantation and Its Usage in Neuropsychiatric Disorders.

Evrensel, Alper, Ceylan, Mehmet Emin·Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology·2016

This review examines fecal microbiota transplantation (FMT)—a treatment where healthy gut bacteria from a donor are transferred to a patient—and its potential use in treating brain and mental health conditions. While FMT is already proven effective for certain gut infections and inflammatory bowel diseases, researchers are exploring whether it might help with conditions like ME/CFS, autism, and Parkinson's disease. Early results are promising, but much more research is needed to understand if it's safe and effective long-term.

Immune SystemGut Microbiome

E3 PreliminaryReviewPEM not requiredReview-Narrative

The Many Neuroprogressive Actions of Tryptophan Catabolites (TRYCATs) that may be Associated with the Pathophysiology of Neuro-Immune Disorders.

Morris, Gerwyn, Carvalho, André F, Anderson, George et al.·Current pharmaceutical design·2016

When the body has chronic inflammation and immune activation, it breaks down an amino acid called tryptophan differently than usual, creating byproducts called TRYCATs. Some of these byproducts can damage nerve cells and mitochondria (the energy factories in cells), while others may protect the brain but at the cost of causing brain fog and emotional problems. This review examines how this abnormal tryptophan breakdown might contribute to ME/CFS and other neurological conditions.

Energy MetabolismImmune SystemNeuroinflammation

E3 PreliminaryCohortPEM unclearCross-Sectional

Killer Cell Immunoglobulin-like Receptor Genotype and Haplotype Investigation of Natural Killer Cells from an Australian Population of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis Patients.

Huth, T K, Brenu, E W, Staines, D R et al.·Gene regulation and systems biology·2016

This study looked at special immune cells called Natural Killer cells and the genes that control them in people with ME/CFS compared to healthy people. Researchers examined specific genetic variations in 20 ME/CFS patients and 20 healthy controls. They found that people with ME/CFS had a lower frequency of a particular genetic pattern related to immune cell control, which may help explain why some ME/CFS patients have weaker immune responses.

Immune System

E3 PreliminaryCommentaryPEM unclearEditorial

[Chronic fatigue syndrome: A new disorder?].

de Korwin, J-D, Chiche, L, Banovic, I et al.·La Revue de medecine interne·2016

This article reviews what we know about ME/CFS more than 30 years after it was first recognized as a distinct condition. The authors explain that ME/CFS likely results from multiple causes working together—such as infections that trigger the illness and ongoing problems with the immune system, inflammation, and energy production in muscle cells. They discuss a newer framework called Systemic Exertion Intolerance Disease that may help doctors diagnose and treat the condition more effectively.

Immune System

E3 PreliminaryReviewPEM not requiredReview-Narrative

The Role of Microbiota and Intestinal Permeability in the Pathophysiology of Autoimmune and Neuroimmune Processes with an Emphasis on Inflammatory Bowel Disease Type 1 Diabetes and Chronic Fatigue Syndrome.

Morris, Gerwyn, Berk, Michael, Carvalho, André F et al.·Current pharmaceutical design·2016

This review explores how problems with the gut barrier and changes in gut bacteria may trigger widespread immune activation and brain inflammation in ME/CFS and other autoimmune diseases. When the intestinal lining becomes more permeable (leaky), bacteria and their products can enter the bloodstream, potentially causing the fatigue, brain fog, and other symptoms characteristic of ME/CFS.

Immune SystemNeuroinflammation

E3 PreliminaryMechanismPEM requiredCross-Sectional

Dysregulation of Protein Kinase Gene Expression in NK Cells from Chronic Fatigue Syndrome/Myalgic Encephalomyelitis Patients.

Chacko, Anu, Staines, Donald R, Johnston, Samantha C et al.·Gene regulation and systems biology·2016

This study looked at immune cells called NK cells in people with ME/CFS to understand why they don't work properly. Researchers examined the activity of hundreds of genes that control how these immune cells function and found that many genes were turned on or off abnormally in severely ill patients compared to healthy people. This suggests that problems with how these genes are regulated may explain why NK cells cannot fight infections effectively in ME/CFS.

Immune System

E3 PreliminaryReviewPEM unclearReview-Narrative

The Neuro-Immune Pathophysiology of Central and Peripheral Fatigue in Systemic Immune-Inflammatory and Neuro-Immune Diseases.

Morris, Gerwyn, Berk, Michael, Galecki, Piotr et al.·Molecular neurobiology·2016

This review examines why people with ME/CFS and similar immune-based illnesses experience severe, disabling fatigue. The authors identify multiple biological pathways that may contribute to this fatigue, including excessive inflammation, problems with how cells produce energy, and chemical imbalances in the brain and muscles. The fatigue appears to result from a complex interaction between the immune system, energy production, and brain function rather than a single cause.

Immune SystemNeuroinflammation

E3 PreliminaryMechanismPEM unclearMechanistic

Novel identification and characterisation of Transient receptor potential melastatin 3 ion channels on Natural Killer cells and B lymphocytes: effects on cell signalling in Chronic fatigue syndrome/Myalgic encephalomyelitis patients.

Nguyen, T, Staines, D, Nilius, B et al.·Biological research·2016

This study looked at special channels called TRPM3 on immune cells (natural killer cells and B cells) that help control calcium flow inside cells. Researchers found that people with ME/CFS have fewer of these channels on certain immune cells and problems with calcium movement compared to healthy people. This suggests that broken calcium control in immune cells might play a role in ME/CFS, though much more research is needed to understand what this means for the illness.

Immune System

E3 PreliminaryReviewPEM unclearReview-Narrative

Aluminum adjuvants of vaccines injected into the muscle: Normal fate, pathology and associated disease.

Gherardi, R K, Aouizerate, J, Cadusseau, J et al.·Morphologie : bulletin de l'Association des anatomistes·2016

This study reviews how aluminum compounds used in vaccines are processed by the body and whether they might cause long-term health problems. The researchers found that aluminum can persist in the body for extended periods, accumulate in organs, and in some cases may be associated with muscle pain, fatigue, and cognitive difficulties—a condition called macrophagic myofasciitis. The authors suggest that the long-term safety of aluminum-containing vaccines needs more careful examination.

Immune System

E3 PreliminaryReviewPEM unclearReview-Narrative

Efficacy of rintatolimod in the treatment of chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME).

Mitchell, William M·Expert review of clinical pharmacology·2016

This review examines rintatolimod, a potential ME/CFS treatment that works by activating the immune system's antiviral defenses. The drug has shown promising results in clinical trials, with patients experiencing meaningful improvements in their symptoms and few serious side effects. This is important because ME/CFS currently has no approved medications, and rintatolimod represents one of the most advanced treatment options in development.

Immune System

E3 PreliminaryCohortPEM unclearCase-Control

Coxiella burnetii dormancy in a fatal ten-year multisystem dysfunctional illness: case report.

Sukocheva, Olga A, Manavis, Jim, Kok, Tuck-Weng et al.·BMC infectious diseases·2016

This case report describes a young woman who developed severe, long-lasting illness after a Q fever infection and died 10 years later. After her death, researchers examined her tissues and found pieces of the bacteria (Coxiella burnetii) and its DNA still present in multiple organs, including her brain, heart, lungs, and spleen. This suggests that Q fever bacteria can persist in the body in a dormant or inactive form, potentially triggering ongoing illness.

Immune System

E3 PreliminaryMechanismPEM not requiredMechanistic

Effects of Chronic Diurnal Disruption and Acute Inflammatory Challenge on Mice with Latent Murine Gammaherpesvirus Infection.

Trammell, Rita A, Toth, Linda A·Comparative medicine·2016

This study examined how disrupted sleep-wake cycles (like those from shift work) affect mice infected with a dormant virus, especially when their immune systems are weakened. Researchers found that mice exposed to disrupted schedules who then experienced inflammation had higher levels of reactivated virus in their lungs. This suggests that combining poor sleep patterns with immune challenges might trigger symptom flare-ups similar to those seen in ME/CFS.

Immune System

E3 PreliminaryMechanismPEM not requiredMechanistic

Activation of the NLRP3 inflammasome in lipopolysaccharide-induced mouse fatigue and its relevance to chronic fatigue syndrome.

Zhang, Zi-Teng, Du, Xiu-Ming, Ma, Xiu-Juan et al.·Journal of neuroinflammation·2016

Researchers created a mouse model of fatigue by exposing mice to immune stress (a bacterial compound) combined with physical stress. They found that a specific immune protein called NLRP3 becomes active in the brain during fatigue, and that blocking this protein reduced fatigue symptoms. This suggests that controlling this immune pathway might help treat fatigue in conditions like ME/CFS.

Immune SystemNeuroinflammation

E3 PreliminaryCohortPEM not requiredCase-Control

Reversal of Refractory Ulcerative Colitis and Severe Chronic Fatigue Syndrome Symptoms Arising from Immune Disturbance in an HLA-DR/DQ Genetically Susceptible Individual with Multiple Biotoxin Exposures.

Gunn, Shelly R, Gunn, G Gibson, Mueller, Francis W·The American journal of case reports·2016

This case report describes one 25-year-old man who had both severe inflammatory bowel disease and chronic fatigue syndrome that improved dramatically after identifying and removing mold exposure from his home, receiving a hormone replacement therapy (VIP), and doing stress-reduction exercises. The patient's genetic makeup made him more susceptible to problems when exposed to toxic mold, and treating the underlying immune disturbance resolved his symptoms without medication.

Immune System

E3 PreliminaryCohortPEM requiredCase-Control

A Pair of Identical Twins Discordant for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Differ in Physiological Parameters and Gut Microbiome Composition.

Giloteaux, Ludovic, Hanson, Maureen R, Keller, Betsy A·The American journal of case reports·2016

This study compared two identical twins—one with ME/CFS and one without—to understand what causes the illness. The affected twin showed reduced exercise capacity, abnormal responses to physical exertion, and differences in immune markers and gut bacteria compared to the healthy twin. These findings suggest that ME/CFS involves problems with how the body responds to exercise and changes in the gut bacteria that may trigger inflammation.

Immune SystemGut MicrobiomePost-Exertional Malaise

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MicroRNAs hsa-miR-99b, hsa-miR-330, hsa-miR-126 and hsa-miR-30c: Potential Diagnostic Biomarkers in Natural Killer (NK) Cells of Patients with Chronic Fatigue Syndrome (CFS)/ Myalgic Encephalomyelitis (ME).

Serum BAFF and APRIL Levels, T-Lymphocyte Subsets, and Immunoglobulins after B-Cell Depletion Using the Monoclonal Anti-CD20 Antibody Rituximab in Myalgic Encephalopathy/Chronic Fatigue Syndrome.

The Deleterious Effects of Oxidative and Nitrosative Stress on Palmitoylation, Membrane Lipid Rafts and Lipid-Based Cellular Signalling: New Drug Targets in Neuroimmune Disorders.

Autoantibody pain.

Herpesviruses dUTPases: A New Family of Pathogen-Associated Molecular Pattern (PAMP) Proteins with Implications for Human Disease.

Fecal Microbiota Transplantation and Its Usage in Neuropsychiatric Disorders.

The Many Neuroprogressive Actions of Tryptophan Catabolites (TRYCATs) that may be Associated with the Pathophysiology of Neuro-Immune Disorders.

Killer Cell Immunoglobulin-like Receptor Genotype and Haplotype Investigation of Natural Killer Cells from an Australian Population of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis Patients.

[Chronic fatigue syndrome: A new disorder?].

The Role of Microbiota and Intestinal Permeability in the Pathophysiology of Autoimmune and Neuroimmune Processes with an Emphasis on Inflammatory Bowel Disease Type 1 Diabetes and Chronic Fatigue Syndrome.

Dysregulation of Protein Kinase Gene Expression in NK Cells from Chronic Fatigue Syndrome/Myalgic Encephalomyelitis Patients.

The Neuro-Immune Pathophysiology of Central and Peripheral Fatigue in Systemic Immune-Inflammatory and Neuro-Immune Diseases.

Novel identification and characterisation of Transient receptor potential melastatin 3 ion channels on Natural Killer cells and B lymphocytes: effects on cell signalling in Chronic fatigue syndrome/Myalgic encephalomyelitis patients.

Aluminum adjuvants of vaccines injected into the muscle: Normal fate, pathology and associated disease.

Efficacy of rintatolimod in the treatment of chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME).

Coxiella burnetii dormancy in a fatal ten-year multisystem dysfunctional illness: case report.

Effects of Chronic Diurnal Disruption and Acute Inflammatory Challenge on Mice with Latent Murine Gammaherpesvirus Infection.

Activation of the NLRP3 inflammasome in lipopolysaccharide-induced mouse fatigue and its relevance to chronic fatigue syndrome.

Reversal of Refractory Ulcerative Colitis and Severe Chronic Fatigue Syndrome Symptoms Arising from Immune Disturbance in an HLA-DR/DQ Genetically Susceptible Individual with Multiple Biotoxin Exposures.

A Pair of Identical Twins Discordant for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Differ in Physiological Parameters and Gut Microbiome Composition.

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