Expression of Toll-like receptor 2 on human Schwann cells: a mechanism of nerve damage in leprosy

Rosane B Oliveira, Maria T Ochoa, Peter A Sieling, Thomas H Rea, Anura Rambukkana, Euzenir N Sarno, Robert L Modlin

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

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.
Original languageEnglish
Pages (from-to)1427-33
Number of pages7
JournalInfection and Immunity
Issue number3
Publication statusPublished - Mar 2003

Keywords / Materials (for Non-textual outputs)

  • cell, cultured
  • DNA Damage
  • Drosophila Proteins
  • Humans
  • Immunity, Innate
  • leprosy
  • Lipoproteins
  • Membrane Glycoproteins
  • Receptors, Cell Surface
  • Schwann Cells
  • Toll-Like Receptor 2
  • Toll-Like Receptor


Dive into the research topics of 'Expression of Toll-like receptor 2 on human Schwann cells: a mechanism of nerve damage in leprosy'. Together they form a unique fingerprint.

Cite this