ArticleNeuroImmune pharmacology and therapeutics2026
Selective inhibition of TLR2 stimulates the maturation of oligodendroglial progenitor cells to oligodendrocytes.
Article in NeuroImmune pharmacology and therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
It is important to describe new technologies for overcoming the barrier and promoting remyelination because many axons remain demyelinated in the CNS of multiple sclerosis (MS) patients. Recent studies indicate that LR2 is a negative regulator of maturation of oligodendroglial progenitor cells (OPCs) to oligodendrocytes (OLs) and that TLR2 is present in human MS chronic lesions. However, until recently, there was no specific inhibitor of TLR2. Therefore, we have engineered a peptide corresponding to the TLR2-interacting domain of MyD88 (TIDM) that specifically inhibits TLR2, but not other TLRs. This study underscores the importance of wild type TIDM (wtTIDM) peptide in promoting the maturation of OPCs to oligodendrocytes. The expression of different maturation markers including PLP, MBP and MOG increased in cultured OPCs in response to wtTIDM, but not mTIDM. While investigating mechanisms, we found that wtTIDM peptide increased the maturation of OPCs isolated from TLR4
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