We used semiquantitative polymerase chain reaction (RT-PCR) to measure mRNA levels for cytokines before and after IFN beta-1b therapy. mRNA was extracted from mononuclear cells of nine healthy controls and 31 patients with MS. Before therapy, IL-10 and leukemia inhibitory factor (LIF) mRNA levels were elevated in stable MS compared to active MS. Twenty four hours after IFN beta-1b treatment, mRNA levels for IL-1, IL-2, IL-4, IL-6, IL-10, IL-12, IL-13, IFN-gamma, TNF-alpha and LIF had not changed.
Our results add to the evidence that IL10 plays a role in multiple sclerosis and suggest that decreased production of this interleukin allows the proliferation of autoreactive T cells at the onset of the disease.
The expression of tumor necrosis factor-alpha, interleukin-10 (IL-10) and IL-12 mRNA in CSF MNC did not differ between MS patients with and without active MRI lesions.
Decreased interleukin-10 and increased interleukin-12p40 mRNA are associated with disease activity and characterize different disease stages in multiple sclerosis.
We analysed this diallelic polymorphism in patients with multiple sclerosis but did not find any association between a certain -1082 IL10 genotype and susceptibility to or severity of multiple sclerosis.
In this study, innate IL-10- and interferon (IFN)-gamma-secreting T cells responsive to TCR peptides were quantified in peripheral blood mononuclear cells of MS patients and healthy controls (HC) using the ELISPOT assay.
The primary progressive MS patients with the low IL-10 expression haplotype showed a trend towards a worse clinical outcome than did patients with medium- or high-expression haplotypes (P = 0.056).
Here, we discuss the role of IL-10 in autoimmune diseases and examine its beneficial effects in cellular-based autoimmune diseases such as multiple sclerosis (MS) or its involvement in humoral-based autoimmune diseases such as systemic lupus erythematosus (SLE).
Our results prove a minor role of IL-10 in the autoimmune diabetes risk, although we found the same association trend with IL-10G(*)12 allele as was previously observed for multiple sclerosis and rheumatoid arthritis.
Although the size of the study group is small, these results indicate that polymorphic variations of two of the major anti-inflammatory cytokines, IL-10 and TGF-beta, may play a role in MS susceptibility.
There were striking defects in the induction of Tr1 cells with CD46 costimulation as measured by IL-10 but not IFN-gamma secretion in patients with MS compared with healthy subjects.