Molecular mimicry in autoimmune neurological disease after viral infection.
Viral infections have been associated with the development of several neurological and neuroendocrine autoimmune diseases. Structural similarities between environmental proteins and self-proteins have long been proposed to be targets for immune cross reactivity associated with initiation of autoimmune diseases. This mechanism called molecular mimicry has also been put forward for immune mediated neurological diseases associated with viral infection. Although many potential candidates for cross reactivity have been put forward, only few have been substantiated on the molecular level. For the definition of cellular immune cross-reactivity, it proved critical to appreciate that recognition patterns of T-cells are not linear. Subsequent microarray studies unequivocally demonstrated functional mimicry of seemingly disparate amino acid sequences. This review summarises the present evidence for molecular mimicry in neurological autoimmune diseases and virus
Roep
Bart O
BO
Department Immunoheamtology & Blood Transfusion, Leiden University Medical Center, Leiden, The Netherlands. boroep@lumc.nl
D000595:Amino Acid Sequence; D001327:Autoimmune Diseases / Q000276:immunology / Q000821:virology*; D006801:Humans; D008954:Models, Biological; D018716:Molecular Mimicry; D008969:Molecular Sequence Data; D009422:Nervous System Diseases / Q000276:immunology*; D014777:Virus Diseases / Q000276:immunology*