The Immune System in Patients with Chronic Fatigue Syndrome

Abstract

Several hypotheses have been proposed to explain the disabling fatigue with normal routine tests of inflammation, endocrinopathy and organ dysfunction that characterises chronic fatigue syndrome (CFS). It is quite possible that it represents the phenotypic endpoint of one or more pathogenic agents possibly acting on a background of stress, mood disturbance and disordered sleep to produce impaired immune function. Conflicting and inconsistent early reports regarding cytokine abnormalities and disturbance of CD4 and CD8 T cells has now given way to a new appreciation of the subtleties of the immune impairment in this condition. Thus impaired T cell homing and altered NK cell function combined with dysregulated B cell maturation are likely. The clinical benefits of anti-B cell monoclonal antibody therapy in particular has encouraged a more detailed analysis of these cells in CFS as it has in many systemic connective disorders. The notion of inefficient elimination of autoreactive B cells leading to a non-inflammatory quiet autoimmunity affecting the central nervous system and the immune system itself is proposed. This may explain the diverse range of symptoms evident in this enigmatic condition and even the incoherent immune reports that have hindered its understanding.