title: CDR3 spectratyping analysis of the T cell receptor repertoire in Guillain-Barré and Fisher syndromes.
abstract: Several autoimmune and infectious disorders show oligoclonal expansion of particular T cell phenotypes. The extent of T cell involvement in the pathogenesis of Guillain-Barré syndrome (GBS), a post-infectious autoimmune neuropathy, however, is not clear. To identify the pathogenic T cell phenotypes in GBS and Fisher syndrome (FS), variations in T cell receptor use of the V beta 1-24 and V delta 1-5 chain genes were analyzed at complementarity-determining region 3 level in 119 patients with GBS or FS. Overall, V beta and V delta spectratypes were expanded more frequently in patients with GBS (V beta in 77%, V delta in 53%) or FS (V beta in 75%, V delta in 65%) than in the healthy controls (V beta in 59%, V delta in 38%). No particular spectratype was significantly associated with GBS or FS. Subgrouping the patients by Campylobacter jejuni serology and anti-ganglioside IgG antibodies also failed to detect particular spectratype gene use. The frequency of V beta 5.2 expansion tended to be higher in patients with positive Haemophilus influenzae serology (50%) than in the controls (7%), but the difference was not significant. Our findings show that oligoclonal expansion of T cells bearing particular type T cell receptor V beta and V delta genes frequently occurs in GBS and FS, suggestive that T cells mediate the development of these neuropathies. The predominant phenotypes vary, even within subgroups of patients with a syndrome of single etiological origin or those with uniform serological features.
authors.affiliation: Department of Neurology, Dokkyo University School of Medicine, Tochigi, Japan.
authors.forename: Michiaki
authors.initials: M
authors.lastname: Koga
authors.forename: Nobuhiro
authors.initials: N
authors.lastname: Yuki
authors.forename: Yukiko
authors.initials: Y
authors.lastname: Tsukada
authors.forename: Koichi
authors.initials: K
authors.lastname: Hirata
authors.forename: Yoh
authors.initials: Y
authors.lastname: Matsumoto
mesh_terms: D000208:Acute Disease; D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000888:Antibodies, Anti-Idiotypic / Q000032:analysis; D000907:Antibodies, Bacterial / Q000097:blood; D016123:Campylobacter jejuni / Q000276:immunology; D002648:Child; D022801:Complementarity Determining Regions / Q000032:analysis* / Q000235:genetics; D005260:Female; D005732:Gangliosides / Q000276:immunology; D020275:Guillain-Barre Syndrome / Q000276:immunology* / Q000382:microbiology; D006193:Haemophilus influenzae / Q000276:immunology; D006801:Humans; D016130:Immunophenotyping / Q000379:methods; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D019846:Miller Fisher Syndrome / Q000276:immunology* / Q000382:microbiology; D011948:Receptors, Antigen, T-Cell / Q000032:analysis* / Q000096:biosynthesis / Q000235:genetics; D016176:T-Lymphocyte Subsets / Q000737:chemistry / Q000378:metabolism
chemical_list: D000888:Antibodies, Anti-Idiotypic; D000907:Antibodies, Bacterial; D022801:Complementarity Determining Regions; D005732:Gangliosides; D011948:Receptors, Antigen, T-Cell