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.
This was surprising as both TLR3 and IL-10 play protective roles in animal models of MS. Interestingly, combination of TLR3 triggering with the other TLRs, enhanced IL-10 through the modulation of its transcription, via interferon (IFN)-β, but independently of IL-27.
Here, we evaluated whether targeted delivery of MSCs with triple PSGL1/SLeX/IL-10 engineering improves therapeutic outcomes in mouse experimental autoimmune encephalomyelitis (EAE), a murine model for human MS. We found PSGL-1/SLeX mRNA transfection significantly enhanced MSC homing to the inflamed spinal cord.
This mAb exerted immunosuppressive activity on MS-derived T cell lines through induction and release of high amounts of interleukin-10 and decreased levels of interleukin-12 from activated monocytes providing the biological basis for a potential new treatment for MS and other immune-mediated neurological disorders.
TLR4 and CD40 co-stimulation synergistically increased the frequency of IL-10-producing but not pro-inflammatory cytokine-producing B cells at MS relapse.
In human settings, we show that MGL expression is increased in active MS lesions and on alternatively activated microglia and macrophages which, in turn, induces the secretion of the immunoregulatory cytokine IL-10, underscoring the clinical relevance of this lectin.
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).
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.
Ligation of the complement regulatory protein CD46 facilitates the differentiation of T helper 1 (T<sub>H</sub>1) effector cells into interleukin-10 (IL-10)-secreting type 1 regulatory T cells (Tr1 cells), and this pathway is defective in MS patients.
The levels of TNF-a and IL-10 in the serum and CSF at the relieving stage of MS patients were higher than those of healthy individuals, suggest that at relieving stage, MS may be still developing.
MP treatment induced significant amplification in the transcript levels of iNOS and TNF-α (M1-related markers) in the corpus callosum of the MS mice, whereas no change detected in the expression of IL-10 (M2-related marker) between the groups.
Decreased interleukin-10 and increased interleukin-12p40 mRNA are associated with disease activity and characterize different disease stages in multiple sclerosis.
Fingolimod therapy modulates circulating B cell composition, increases B regulatory subsets and production of IL-10 and TGFβ in patients with Multiple Sclerosis.
The concentration of sCD27 was higher in the NMO group than in the MS (p = 0.082) and CTL (p = 0.002) groups, and there was a positive correlation with CSF IL-6 (p = 0.000) and a negative correlation with IL-10 (p = 0.073).
Increasing evidence indicates that IL-10 plays an important role in both the onset and development of auto-immune diseases, such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), Sjogren's syndrome (SS), multiple sclerosis (MS), Crohn's disease (CD), and psoriasis.
Results showed that: 1) CD19+/TNFα+, CD19+/IL-12+ and CD19+/IFNγ+ lymphocytes are significantly increased in primary progressive (PP) compared to secondary progressive (SP), relapsing-remitting (RR), benign (BE) MS and HC; 2) CD19+/IL-6+ lymphocytes are significantly increased in PP, SP and RR compared to BEMS and HC; and 3) CD19+/IL-13+, CD19+/IL-10+, and CD19+/IL-10+/TGFβ+ (Bregs) B lymphocytes are reduced overall in MS patients compared to HC.
Besides, the levels of anti-inflammatory cytokines include IL-4 and IL-10 was significantly higher in MS patients infected with HP when compared with MS patients seronegative for HP infection.