Tag: Multiple sclerosis

Interferon-beta drugs inhibit albumin binding to the red blood cells, thereby reducing its ability to deliver ligands such as C-peptide and zinc ions to the cell and normalizing the basal hypermetabolic state. The authors noted that based on their data, a daily, less concentrated dose prior to insulin/C-peptide release from pancreatic beta cells would be more appropriate for MS patients rather than subcutaneous injections that are weeks apart.

Pasithea Therapeutics announced encouraging preclinical results that support the efficacy of a tolerizing, inverse DNA vaccine for multiple sclerosis (MS). Based on experiments conducted on the EAE mouse model, Pasithea reported that intramuscular injections of the candidate vaccine (PAS002) delayed the onset of paralysis and reduced severity of peak disease. Prophylactic administration also reduced the incidence and severity of relapse in the mouse model.

A new study has analyzed molecular signatures of circulating immune cell types in identical, monozygotic twins where both siblings carry the same genetic and early-life environmental risks, but only one sibling is affected by MS. The researchers use a combination of mass cytometry, genetics, and machine learning to identify characteristic proteins in the immune cells of the sick twin and decode the genes that are switched on in abnormally activated T cells that infiltrate into the CNS.

Increase in the levels of NETs—neutrophil extracellular traps, web like structures made of DNA and histones that trap pathogens—have been linked to autoimmune diseases. In a new study, scientists show NETs, through their histones, activate T cells and enhance Th17 cell differentiation. The innate stimulation of a specific adaptive immune cell subset provides a mechanistic link among neutrophils, T cells and autoimmunity which can be targeted to develop therapeutics against autoimmune diseases.

Scientists at the University of Geneva (UNIGE) showed that colder temperatures provoke a trade-off of energy resources between autoimmunity and thermogenesis in mice. Cold decreases the antigen-presenting protein—major histocompatibility complex class II (MHCII)—on monocytes at steady state and in various inflammatory conditions including in a mouse model of multiple sclerosis. In addition, cold suppresses T-cell priming and pathogenicity against the body’s own antigens through the modulation of monocytes, thereby reducing neuroinflammation in mouse models of multiple sclerosis.