[Chronic fatigue syndrome: a review]. / La sindrome da stanchezza cronica.

Chronic fatigue sindrome is a relatively unknown and underdiagnosed entity in Italy where its epidemiology remains uncertain, as well as its etiology, although it causes important disability in those affected. Classification criteria by Fukuda are available to diagnose the syndrome. Its epidemiology indicates that it is probably more frequent in Northern countries and it is described in Gulf War veterans. Etiological hypotheses include infectious diseases, immunology and neurology. Among these hypotheses sickness behavior mimes certain aspects of this syndrome and is characterized by a cytokine imbalance in the central nervous system and in the periphery. There are no valid therapies available at the moment. In the laboratory of Immunogenetics, we are constituting a biological bank of the syndrome to study the immunogenetic aspects of the disease in the hope of delucidating some of the obscure areas of its etiopathogenesis.

Excess of activating killer cell immunoglobulin­like receptors and lack of HLA-Bw4 ligands: a two­edged weapon in chronic fatigue syndrome.

Chronic fatigue syndrome (CFS) is an inflammatory disease of unknown aetiology. Researchers have proposed infectious, neurological and immunological causes of this syndrome. Recently, the xenotropic murine leukemia virus-related virus was detected in 67% of patients with CFS in a US study. This observation is in agreement with one ascertained aspect of the disease: a decreased efficiency in NK cell lytic activity in CFS patients. Here, we analyzed the genomic polymorphism of killer cell immunoglobulin-like receptors (KIRs) and their HLA class I cognate ligands in patients with certified CFS. An excess of KIR3DS1 was found in CFS patients with respect to controls, as well as an increased frequency of the genotype missing KIR2DS5. Forty-four CFS patients and 50 controls also underwent genomic typing for the HLA-ligands. In the patients, a great proportion of KIR3DL1 and KIR3DS1 receptors were found to be missing their HLA-Bw4Ile80 binding motif. We hypothesize that an excess of KIR3DS1, combined with an excess of ligand-free KIR3DL1 and KIR3DS1 receptors, may hamper the clearance of a pathogen via NK cells, thus favouring the chronicity of the infection.