T-LYMPHOCYTE SUBSET ABNORMALITIES IN PERIPHERAL-BLOOD FROM PATIENTS WITH THE GUILLAIN-BARRE-SYNDROME

T-lymphocytes are probably of pathogenic importance in many autoimmune diseases. Recently, deviations of circulating T-helper (CD4(+)) subpopulations have been noticed. Blood samples from 12 patients with Guillain-Barre syndrome (GBS) were studied with flow cytometry during their disease course to define circulating T cell populations. The proportion of T-helper cells (CD4(+)) was decreased (mean value 41 +/- 15%, P = 0.01) and the proportion of T cytotoxic/suppressor cells (CD8(+)) was increased (35 +/- 18%, P = 0.0006) as compared to the control group of healthy blood donors (47 +/- 8% and 26 +/- 7% respectively). The CD4(+) population is divided into the helper/inducer (CD4(+)CD29(+)) and suppressor/inducer (CD4(+)CD45RA(+)) subsets, which normally are equally distributed (mean values in our control group were 45 +/- 15% and 44 +/- 15%, respectively). In patients with GBS, the helper/inducer (CD4(+)CD29(+)) subset was increased (54 +/- 10%, P = 0.05) and the suppressor/inducer (CD4(+)CD45RA(+)) subset was decreased (31 +/- 9, P = 0.005) compared to the controls. The proportion of activated HLA-DR-expressing T cells was increased (7 +/- 8%, P = 0.005) as compared to controls (3 +/- 3%). The total proportions of T cells (CD2(+)), B cells (CD19(+)) and natural killer (NK) cells (CD56(+)) were similar in patients and controls. The CD4(+) and CD8(+) populations, as well as the activated HLA-DR(+) T cells, normalized during the disease course. The deviations within the CD4(+) population also tended to normalize, but even at follow up after 6-33 (mean 23) months, some abnormalities remained. In conclusion, we confirm previous reports of T cell activation in peripheral blood from patients with GBS. A new finding is the deviation of T helper subpopulations with an increased helper/inducer (CD4(+)CD29(+)) subset and a decreased suppressor/inducer (CD4(+)CD45RA(+)) subset, which indicates a possible autoimmune character of GBS.