02152nas a2200373 4500000000100000008004100001260001300042653001400055653002000069653001500089653002400104653001100128653002100139653001200160653001700172653002700189653002800216653001800244653002500262653002400287100001500311700001300326700001500339700001000354700001700364700001200381700001400393245010300407856006900510300001200579490000700591520116600598022001401764 2003 d c2003 Mar10aApoptosis10aCells, Cultured10aDNA Damage10aDrosophila Proteins10aHumans10aImmunity, Innate10aleprosy10aLipoproteins10aMembrane Glycoproteins10aReceptors, Cell Surface10aSchwann Cells10aToll-Like Receptor 210aToll-Like Receptors1 aOliveira R1 aOchoa MT1 aSieling PA1 aRea T1 aRambukkana A1 aSarno E1 aModlin RL00aExpression of Toll-like receptor 2 on human Schwann cells: a mechanism of nerve damage in leprosy. uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC148832/pdf/1045.pdf a1427-330 v713 a
Nerve damage is a clinical hallmark of leprosy and a major source of patient morbidity. We investigated the possibility that human Schwann cells are susceptible to cell death through the activation of Toll-like receptor 2 (TLR2), a pattern recognition receptor of the innate immune system. TLR2 was detected on the surface of human Schwann cell line ST88-14 and on cultured primary human Schwann cells. Activation of the human Schwann cell line and primary human Schwann cell cultures with a TLR2 agonist, a synthetic lipopeptide comprising the N-terminal portion of the putative Mycobacterium leprae 19-kDa lipoprotein, triggered an increase in the number of apoptotic cells. The lipopeptide-induced apoptosis of Schwann cells could be blocked by an anti-TLR2 monoclonal antibody. Schwann cells in skin lesions from leprosy patients were found to express TLR2. It was possible to identify in the lesions Schwann cells that had undergone apoptosis in vivo. The ability of M. leprae ligands to induce the apoptosis of Schwann cells through TLR2 provides a mechanism by which activation of the innate immune response contributes to nerve injury in leprosy.
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