“Possible class II MHC deficiency in patients with Myalgic Encephalomyelitis or Chronic Fatigue Syndrome (ME/CFS)”
Principal Investigator: Bruno Paiva (PhD)
University of Navarra, Spain
“Possible class II MHC deficiency in patients with Myalgic Encephalomyelitis or Chronic Fatigue Syndrome (ME/CFS)”
Principal Investigator: Bruno Paiva (PhD)
University of Navarra, Spain
Collaborators: Manuel Ruiz Pablos, Rosario Montero Mateo (MD), Aintzane Zabaleta Azpiroz (PhD), Diego Alignani (PhD), Idoya Rodriguez Serrano, Sonia Garate Luzuriaga
Bruno Paiva (University of Navarra) is an expert researcher in immunology and diseases of the blood. Working with six co-Investigators, Dr. Paiva will investigate if inherent defects in class II molecules of the major histocompatibility (MHC) – a specific immune system pathway foundational to your body’s defense – is driving ME/CFS symptoms for a subgroup of patients. Decreased expression of these molecules would be consistent with previous reports of altered populations of immune cells in people with ME/CFS and could account for recurrent infections experienced by many patients.
– Manuel Ruiz Pablos, Medical Student
(Left to right) Bruno Paiva and collaborators Sonia Garate Luzuriaga, Aintzane Zabaleta Azpiroz, Idoya Rodriguez Serrano, Diego Alignani, Manuel Ruiz Pablos, and Rosario Montero Mateo
Read the research study abstract below:
Chronic Fatigue Syndrome or Myalgic Encephalomyelitis (CFS/ME) is a disease of unknown origin, which appears suddenly in a previously active individuals and whose onset could be related to an acute infection in most cases. Of particular note are Epstein-Barr virus (EBV), cytomegalovirus (CMV), herpes simplex 6 (HHV-6), enterovirus, and murine leukemia virus (XMRV). Among these viruses, the one that is being most investigated in CFS/ME is the Epstein Barr virus, which after generating infectious mononucleosis increases the probability of producing CFS/ME in these patients. It is believed that this could be due to some genetic predisposition.
It is more frequent in women than in men. These patients present hormonal alterations, digestive, generalized pains, muscular problems, dizziness, fever or temperatures of 35ºC when the disease is more advanced, inflamed cervical ganglia, increased respiratory allergies, insomnia … But the predominant symptom is the presence of fatigue (both physically and mentally), which does not improve with rest and can become incapacitating, preventing the normal activities of daily life.
Currently, this disease is diagnosed through symptoms, hence the need to find biomarkers to help make more accurate diagnoses, so that these patients can access treatments that currently cannot.
Several investigations have shown inadequate immune function and signs of autoimmunity as well as alterations in NK cells, cytokine profiles and in the functionality of T cells. There are several intracellular pathogens that reduce the expression of MHC class II molecules as a mechanism for evasion of the immune system, among which we highlight the Epstein Barr virus, the cytomegalovirus and the varicella zoster virus.
For all these reasons, there is an unmet need to study the possibility of an immunodeficiency due to MHC class II deficit in these patients. Patients with Chronic Fatigue Syndrome could have an alteration in the activation of T cells caused by a decrease in the HLA-II antigenic presentation due to intracellular pathogens.
If we confirm there is a class II MHC deficiency immunodeficiency in CFS/ME patients, it would allow a diagnostic protocol using immunological markers. This would help to link the infection of intracellular pathogens with this type of immunodeficiency. In addition, CFS/ME patients with this new diagnosis could access immunotherapy treatments that currently are not indicated and, therefore, develop new treatment strategies.
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