Clusterin deficiency is associated with a lack of response to teriflunomide in multiple sclerosis.

A study has found that clusterin deficiency may be a biomarker for a lack of response to teriflunomide, an oral therapy for multiple sclerosis (MS). The study used RNA sequencing to identify genes that showed differential expression in responders and non-responders to teriflunomide treatment, and clusterin was the only gene that was validated and found to be downregulated in non-responders. Further analysis revealed that clusterin expression was primarily reduced in certain T cells from non-responders. Another study investigated the effects of teriflunomide treatment on T-cell metabolism, apoptosis, and proliferation in MS patients. It found that teriflunomide treatment reduced the respiratory and glycolytic capacities of T-cells, but there were no significant differences in the metabolic profile between responders and non-responders. Non-responders had a higher resistance to apoptosis and a reduced proliferative response in memory T-cell populations compared to responders. These findings suggest that teriflunomide non-responders may have abnormal persistence of pathogenic T-cells in the blood. Further research is needed to validate these findings and their implications for identifying non-responders to teriflunomide treatment. [Extracted from the article]