Abstract:
: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-Barré 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.
journal_name
J Neuroimmunoljournal_title
Journal of neuroimmunologyauthors
Dahle C,Vrethem M,Ernerudh Jdoi
10.1016/0165-5728(94)90032-9subject
Has Abstractpub_date
1994-09-01 00:00:00pages
219-25issue
2eissn
0165-5728issn
1872-8421pii
0165-5728(94)90032-9journal_volume
53pub_type
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