CDR3 spectratyping analysis of the T cell receptor repertoire in Guillain-Barré and Fisher syndromes.

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.