Transcriptome profiling of peripheral blood immune cell populations in multiple sclerosis patients before and during treatment with a sphingosine-1-phosphate receptor modulator.

Aims: Fingolimod is a sphingosine-1-phosphate (S1P) receptor modulator approved for the treatment of the relapsing form of multiple sclerosis (MS). It prevents the egress of lymphocyte subpopulations from lymphoid tissues into the circulation. Here, we explored the broad effects of fingolimod on gene expression in different immune cell subsets.

Fingolimod alters the transcriptome profile of circulating CD4+ cells in multiple sclerosis.

Multiple sclerosis is a demyelinating disease affecting the central nervous system. T cells are known to contribute to this immune-mediated condition. Fingolimod modulates sphingosine-1-phosphate receptors, thereby preventing the egress of lymphocytes, especially CCR7-expressing CD8+ and CD4+ T cells, from lymphoid tissues.

High-Resolution Expression Profiling of Peripheral Blood CD8 Cells in Patients with Multiple Sclerosis Displays Fingolimod-Induced Immune Cell Redistribution.

Fingolimod, a sphingosine-1-phosphate (S1P) receptor modulator, is an oral drug approved for the treatment of active relapsing-remitting multiple sclerosis (RRMS). It selectively inhibits the egress of lymphocytes from lymph nodes. We studied the changes in the transcriptome of peripheral blood CD8 cells to unravel the effects at the molecular level during fingolimod therapy.

MicroRNA expression changes during interferon-beta treatment in the peripheral blood of multiple sclerosis patients.

MicroRNAs (miRNAs) are small non-coding RNA molecules acting as post-transcriptional regulators of gene expression. They are involved in many biological processes, and their dysregulation is implicated in various diseases, including multiple sclerosis (MS). Interferon-beta (IFN-beta) is widely used as a first-line immunomodulatory treatment of MS patients.