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Novel mechanisms in the immunopathogenesis of leprosy nerve damage: the role of Schwann cells, T cells and Mycobacterium leprae.
Immunol Cell Biol. 2000 Aug; 78(4):349-55.IC

Abstract

The major complication of reversal (or type 1) reactions in leprosy is peripheral nerve damage. The pathogenesis of nerve damage remains largely unresolved. In situ analyses suggest an important role for type 1 T cells. Mycobacterium leprae is known to have a remarkable tropism for Schwann cells that surround peripheral axons. Reversal reactions in leprosy are often accompanied by severe and irreversible nerve destruction and are associated with increased cellular immune reactivity against M. leprae. Thus, a likely immunopathogenic mechanism of Schwann cell and nerve damage in leprosy is that infected Schwann cells process and present antigens of M. Leprae to antigen-specific, inflammatory type 1 T cells and that these T cells subsequently damage and lyse infected Schwann cells. Previous studies using rodent CD8+ T cells and Schwann cells have revealed evidence for the existence of such a mechanism. Recently, a similar role has been suggested for human CD4+ T cells. These cells may be more important in causing leprosy nerve damage in vivo, given the predilection of M. leprae for Schwann cells and the dominant role of CD4+ serine esterase+ Th1 cells in leprosy lesions. Antagonism of molecular interactions between M. leprae, Schwann cells and inflammatory T cells may therefore provide a rational strategy to prevent Schwann cell and nerve damage in leprosy.

Authors+Show Affiliations

Departments of Immunohematology and Blood Transfusion and Infectious Diseases, Leiden University Medical Center, The Netherlands. H.T.Spierings@lumc.nlNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

10947859

Citation

Spierings, E, et al. "Novel Mechanisms in the Immunopathogenesis of Leprosy Nerve Damage: the Role of Schwann Cells, T Cells and Mycobacterium Leprae." Immunology and Cell Biology, vol. 78, no. 4, 2000, pp. 349-55.
Spierings E, De Boer T, Zulianello L, et al. Novel mechanisms in the immunopathogenesis of leprosy nerve damage: the role of Schwann cells, T cells and Mycobacterium leprae. Immunol Cell Biol. 2000;78(4):349-55.
Spierings, E., De Boer, T., Zulianello, L., & Ottenhoff, T. H. (2000). Novel mechanisms in the immunopathogenesis of leprosy nerve damage: the role of Schwann cells, T cells and Mycobacterium leprae. Immunology and Cell Biology, 78(4), 349-55.
Spierings E, et al. Novel Mechanisms in the Immunopathogenesis of Leprosy Nerve Damage: the Role of Schwann Cells, T Cells and Mycobacterium Leprae. Immunol Cell Biol. 2000;78(4):349-55. PubMed PMID: 10947859.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Novel mechanisms in the immunopathogenesis of leprosy nerve damage: the role of Schwann cells, T cells and Mycobacterium leprae. AU - Spierings,E, AU - De Boer,T, AU - Zulianello,L, AU - Ottenhoff,T H, PY - 2000/8/18/pubmed PY - 2000/9/23/medline PY - 2000/8/18/entrez SP - 349 EP - 55 JF - Immunology and cell biology JO - Immunol Cell Biol VL - 78 IS - 4 N2 - The major complication of reversal (or type 1) reactions in leprosy is peripheral nerve damage. The pathogenesis of nerve damage remains largely unresolved. In situ analyses suggest an important role for type 1 T cells. Mycobacterium leprae is known to have a remarkable tropism for Schwann cells that surround peripheral axons. Reversal reactions in leprosy are often accompanied by severe and irreversible nerve destruction and are associated with increased cellular immune reactivity against M. leprae. Thus, a likely immunopathogenic mechanism of Schwann cell and nerve damage in leprosy is that infected Schwann cells process and present antigens of M. Leprae to antigen-specific, inflammatory type 1 T cells and that these T cells subsequently damage and lyse infected Schwann cells. Previous studies using rodent CD8+ T cells and Schwann cells have revealed evidence for the existence of such a mechanism. Recently, a similar role has been suggested for human CD4+ T cells. These cells may be more important in causing leprosy nerve damage in vivo, given the predilection of M. leprae for Schwann cells and the dominant role of CD4+ serine esterase+ Th1 cells in leprosy lesions. Antagonism of molecular interactions between M. leprae, Schwann cells and inflammatory T cells may therefore provide a rational strategy to prevent Schwann cell and nerve damage in leprosy. SN - 0818-9641 UR - https://www.unboundmedicine.com/medline/citation/10947859/Novel_mechanisms_in_the_immunopathogenesis_of_leprosy_nerve_damage:_the_role_of_Schwann_cells_T_cells_and_Mycobacterium_leprae_ L2 - https://doi.org/10.1046/j.1440-1711.2000.00939.x DB - PRIME DP - Unbound Medicine ER -