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Defective immunoreguktion in multiple sclerosis
Author(s) -
Goust Jean M.,
Hoffman Paul M.,
Pryjma Juliusz,
Hogan Edward L,
Hugh Fudenberg H.
Publication year - 1980
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410080510
Subject(s) - multiple sclerosis , medicine , medline , neuroscience , psychology , biology , psychiatry , biochemistry
Imbalances in T cell subpopulations have been reported in multiple sclerosis (MS). In the present study of 31 MS patients, the percentage of T cells with Fc receptors for IgG (T G ) was found to be increased in patients with chronic progressive diseare, and another T cell subset binding to the Raji B lymphoid cell line was decreased. An inverse correlation ( r = −0.675; >95% confidence limit) was found between these two subsets, suggesting that they vary inversely in MS. The mitogenic responses of MS mononuclear cells, isolated T cells, and recombined T and non‐T cells to the lectins phytohemagglutimn and pokeweed mitogen (PWM) did not differ from those of normal cells. However, more immunoglobulin (Ig)‐producing cells were generated in a PWM‐driven system with cells from MS patients than with cells from age‐matched controls ( p < 0.05). Autologous recombination of separated T and non‐T cells did not significantly modify these results. T cells from MS patients added to B cells from normal controls exerted an effect that was related to their percentage of T G cells; that is, values above 15% were associated with a suppression of Ig production, whereas for T G values below 12%, a helper effect or no modification was observed. These results suggest that changes in T cell subsets in MS are related to changes in functional ability to modulate Ig production by normal B cells. However, MS B cells partly escape regulation by their own T cells, suggesting an associated B cell hyperactivity.