T lymphocyte activation antigens in Guillain-Barré syndrome and chronic idiopathic demyelinating polyradiculoneuropathy
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1Neurology Department, United Medical, School of Guy's Hospital, London, U.K.
Activated circulating T lymphocytes were measured in ten patients with Guillain-Barré syndrome (GBS) and in ten with chronic idiopathic demyelinating polyradiculoneuropathy (CIDP), each paired with an age- and sex-matched healthy control. Activated T cells were identified by double labelling with phycoerythrin-conjugated anti-CD3 antibody and biotinylated antibodies to activation antigens: human leucocyte antigen (HLA)-DR, transferrin receptor (TFR) or interleukin-2 receptor (IL-2R) visualised with an avidin-biotin-fluorescein system. The frequency of activated T cells was increased in the GBS group. The median of the DR-positive T cells in the patients was 3.4% (range 0.5-9.4%), compared with 1.4% (range 0-4.3%) in the controls (P less than 0.01). For TFR the corresponding medians were 3.3% (range 0.5-6.2%) in the patients and 0% (range 0-2.5%) in the controls (P less than 0.01), and for IL-2R 3.7% (range 0-6.0%) in the patients compared with 0% (range 0-2.9%) in the controls (P less than 0.01). In the CIDP group the median percentage of activated T cells was also increased but the differences were less significant: for DR, patients 2.4% (range 0-3.8%), controls 0.5% (range 0-2.0%, P less than 0.05); for TFR, patients 0% (range 0-5.3%), controls 0% (range 0-1.0%, not significant), and for IL-2R, patients 0% (range 0-2.5%), controls 0% (range 0-0.5%, not significant). The activated cells might be directed against microbial antigens encountered during the infection preceding GBS, autoantigens, bacterial antigens encountered during concurrent infection, or a combination of these.
Activated circulating T lymphocytes were measured in ten patients with Guillain-Barré syndrome (GBS) and in ten with chronic idiopathic demyelinating polyradiculoneuropathy (CIDP), each paired with an age- and sex-matched healthy control. Activated T cells were identified by double labelling with phycoerythrin-conjugated anti-CD3 antibody and biotinylated antibodies to activation antigens: human leucocyte antigen (HLA)-DR, transferrin receptor (TFR) or interleukin-2 receptor (IL-2R) visualised with an avidin-biotin-fluorescein system. The frequency of activated T cells was increased in the GBS group. The median of the DR-positive T cells in the patients was 3.4% (range 0.5-9.4%), compared with 1.4% (range 0-4.3%) in the controls (P less than 0.01). For TFR the corresponding medians were 3.3% (range 0.5-6.2%) in the patients and 0% (range 0-2.5%) in the controls (P less than 0.01), and for IL-2R 3.7% (range 0-6.0%) in the patients compared with 0% (range 0-2.9%) in the controls (P less than 0.01). In the CIDP group the median percentage of activated T cells was also increased but the differences were less significant: for DR, patients 2.4% (range 0-3.8%), controls 0.5% (range 0-2.0%, P less than 0.05); for TFR, patients 0% (range 0-5.3%), controls 0% (range 0-1.0%, not significant), and for IL-2R, patients 0% (range 0-2.5%), controls 0% (range 0-0.5%, not significant). The activated cells might be directed against microbial antigens encountered during the infection preceding GBS, autoantigens, bacterial antigens encountered during concurrent infection, or a combination of these.
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