Premium
Correlation of immunological studies and disease progression in chronic progressive multiple sclerosis
Author(s) -
Trotter John L.,
Clifford David B.,
McLnnis Jane E.,
Griffeth Rogers C.,
Bruns Kathy A.,
Perlmutter Monica S.,
Anderson Charles B.,
Collins Kelly G.,
Banks Geneva,
Hicks Byron C.
Publication year - 1989
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.410250211
Subject(s) - concanavalin a , multiple sclerosis , medicine , peripheral blood mononuclear cell , stimulation , cd8 , interleukin 2 , immunology , correlation , peripheral , central nervous system disease , endocrinology , gastroenterology , immune system , cytokine , biology , biochemistry , geometry , mathematics , in vitro
Abstract Thirty untreated patients with clinically definite chronic progressive multiple sclerosis were matched with 10 patients with clinically stable definite multiple sclerosis and 16 patients with other neurological diseases. A group of 12 normal control (NC) volunteers was matched to these groups. All patients with chronic progressive multiple sclerosis and normal control subjects were analyzed for the concanavalin A suppressor assay, mitogen stimulation, and phenotyping of peripheral blood mononuclear cells. In addition, serum was analyzed for interleukin‐2 levels. Results of mitogen stimulation studies did not distinguish the groups. Concanavalin A–induced suppression was significantly decreased in the patients with chronic progressive multiple sclerosis ( p < 0.01). Phenotyping of fresh cells showed an elevated CD4 : CD8 ratio in the patients with chronic progressive multiple sclerosis. Neither phenotyping nor concanavalin A–induced suppression correlated with or predicted the degree of disability, but the serum levels of interleukin‐2 correlated inversely with disability ( p < 0.01) and directly with a poor prognosis after 18 months of observation ( p < 0.05). Serum levels of interleukin‐2 decreased as the disease progressed.