Chronic fatigue syndrome/Myalgic encephalomyelitis and parallels with autoimmune disorders
Date of this Version
Autoimmune disorders are known to affect a substantial number of people worldwide and in some cases may be fatal. They occur in the presence of unregulated inflammatory responses including failure in self-tolerance. Some unexplained disorders with immune compromises may demonstrate certain characteristics that suggest an autoimmune disorder
including Chronic Fatigue syndrome/Myalgic Encephalomyelitis (CFS/ME). CFS/ME remains an unsolved disorder with multiple symptoms and no single causative factor. These
symptoms may include but are not limited to incapacitating fatigue, weakened short term memory or attentiveness, sore throat, tender cervical or axillary lymph nodes, muscle pain, severe headaches, impaired sleep and postexertional malaise. To date succinct and concise mechanisms that underlie this disorder have not yet being identified although, many hypotheses have been put forward. CFS/ME often occurs as a consequence of a post-infectious
episode accompanied by compromises in the immune, endocrine and nervous systems. The consequences of these events have not being clearly identified. Importantly, immune deterioration in CFS/ME is related to heightened or suppressed cell function, differential gene expression, equivocal levels of immune cell numbers and protein secretion promoting adverse
inflammatory activation. Both innate and adaptive immune system perturbations persist in CFS/ME. These characteristics are in many respects similar to mechanisms of disease in autoimmune disorders suggesting that the changes in immune response may develop from
cellular and molecular changes in immune cells and proteins. We propose here that as the mechanism of CFS/ME may involve certain immunological factors that have been shown to be compromised in other autoimmune diseases, CFS/ME may in some cases have an autoimties of neutrophils in MS include heightened levels of IL-8, TLR2, degranulation, impediment in apoptosis (Naegele et al., 2012).
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