An immunological and transcriptomics approach on differential modulation of NK cells in multiple sclerosis patients under interferon-β1 and fingolimod therapy.

This study aims to compare NK cells obtained from multiple sclerosis (MS) patients receiving interferon-β1 and fingolimod therapies. Fingolimod reduced the CD56 NK cell subset. The remaining CD56 NK cells displayed NKG2D, NKp46, CD107a, and IFN-γ levels similar to those from the patients under interferon-β1 therapy.

Promotion of experimental autoimmune encephalomyelitis upon neutrophil granulocytes' stimulation with formyl-methionyl-leucyl-phenylalanine (fMLP) peptide.

It has been acknowledged that neutrophil granulocytes, the common mediators of immune responses against extracellular bacteria, can also intercede autoimmune reactions such as experimental autoimmune encephalomyelitis (EAE). Formyl-methionyl-leucyl-phenylalanine (fMLP) is a microbial peptide that can be well-tolerated when intravenously administered and can directly lead to activation and accumulation of neutrophils into the blood circulation. Here, this antigenic peptide was injected to the mice at the induction of EAE, and the immunological and pathological outcomes were assessed.

Evaluation of Th17-related cytokines and receptors in multiple sclerosis patients under interferon β-1 therapy.

Th17-related cytokines (IL-17, IL-23, and IL-26) and receptors (IL-17R and IL-23R) were evaluated in MS patients under immunomodulatory IFN-β1 therapy during a 2year follow-up. Before the initiation of treatment, no significant difference was found in cytokine or receptor expression between controls and MS patients. Of the three cytokines evaluated, IL-26 was the highest in the patients' sera.

Lack of association of the CD14/C -- 159T polymorphism with susceptibility and progression parameters in Turkish multiple sclerosis patients.

Soluble (s) CD14, being a receptor for lipopolysaccharides (LPSs) may inhibit LPS-triggered apoptosis and T lymphocyte proliferation. C to T exchange at position -159 in the promoter region of the CD14 gene might lead to higher sCD14 levels. Limited number of groups have studied whether these polymorphisms might influence the development of organ specific autoimmunity and whether higher CD14 levels are associated with increased levels of cytokines trigerring inflammatory processes.