Multiple sclerosis (MS) represents a T-cell-mediated autoimmune demyelinati
ng disease of the central nervous system associated with altered immunoregu
lation. Interleukin (IL)-6 is a cytokine that has several effects on the ne
uroimmune system. Specific IL-6 receptors have been found in human lymphocy
tes and neuroglial cells. The aim of the present study was to assay IL-6 bi
nding on peripheral blood T lymphocytes in MS patients. We found that T cel
ls from MS patients had significantly more IL-6 receptors [B-max: 279 +/- 7
vs. 246 +/- 8 (mean +/- SEM) receptors/cell, in patients and controls, res
pectively], whereas K-d values were similar to those of healthy subjects [2
6.8 +/- 0.7 vs. 25.4 +/- 0.6 (mean +/- SEM) pM, in patients and controls, r
espectively]. Significant (P < 0.05) differences in IL-6 binding values wer
e observed between stable patients and those relapsing (272 +/- 9 vs. 300 /- 12 (mean +/- SEM) receptors/cell, respectively). We found significantly
(P < 0.001) higher amounts of IL-6 receptors on CD4+ T cells from MS patien
ts than on CD4+ lymphocytes from controls (434 +/- 11 vs. 363 +/- 9 (mean /- SEM) receptors/cell, respectively); CD8+ T cells showed very few IL-6 re
ceptors in both patients and controls. These data are discussed in terms of
MS immune pathogenesis and pathophysiology, because T-cell activation seem
s to be linked to increased IL-6 binding. The upregulated IL-6 system might
be involved in antibody-mediated demyelinating pathways, because IL-6 is w
ell known to enhance humoral immune response.