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Mycobacterium leprae-specific, HLA class II-restricted killing of human Schwann cells by CD4+ Th1 cells: a novel immunopathogenic mechanism of nerve damage in leprosy.
J Immunol. 2001 May 15; 166(10):5883-8.JI

Abstract

Peripheral nerve damage is a major complication of reversal (or type-1) reactions in leprosy. The pathogenesis of nerve damage remains largely unresolved, but detailed in situ analyses suggest that type-1 T cells play an important role. Mycobacterium leprae is known to have a remarkable tropism for Schwann cells of the peripheral nerve. 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 Ags of M. leprae to Ag-specific, inflammatory type-1 T cells and that these T cells subsequently damage and lyse infected Schwann cells. Thus far it has been difficult to study this directly because of the inability to grow large numbers of human Schwann cells. We now have established long-term human Schwann cell cultures from sural nerves and show that human Schwann cells express MHC class I and II, ICAM-1, and CD80 surface molecules involved in Ag presentation. Human Schwann cells process and present M. leprae, as well as recombinant proteins and peptides to MHC class II-restricted CD4(+) T cells, and are efficiently killed by these activated T cells. These findings elucidate a novel mechanism that is likely involved in the immunopathogenesis of nerve damage in leprosy.

Authors+Show Affiliations

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

Pub Type(s)

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

Language

eng

PubMed ID

11342602

Citation

Spierings, E, et al. "Mycobacterium Leprae-specific, HLA Class II-restricted Killing of Human Schwann Cells By CD4+ Th1 Cells: a Novel Immunopathogenic Mechanism of Nerve Damage in Leprosy." Journal of Immunology (Baltimore, Md. : 1950), vol. 166, no. 10, 2001, pp. 5883-8.
Spierings E, de Boer T, Wieles B, et al. Mycobacterium leprae-specific, HLA class II-restricted killing of human Schwann cells by CD4+ Th1 cells: a novel immunopathogenic mechanism of nerve damage in leprosy. J Immunol. 2001;166(10):5883-8.
Spierings, E., de Boer, T., Wieles, B., Adams, L. B., Marani, E., & Ottenhoff, T. H. (2001). Mycobacterium leprae-specific, HLA class II-restricted killing of human Schwann cells by CD4+ Th1 cells: a novel immunopathogenic mechanism of nerve damage in leprosy. Journal of Immunology (Baltimore, Md. : 1950), 166(10), 5883-8.
Spierings E, et al. Mycobacterium Leprae-specific, HLA Class II-restricted Killing of Human Schwann Cells By CD4+ Th1 Cells: a Novel Immunopathogenic Mechanism of Nerve Damage in Leprosy. J Immunol. 2001 May 15;166(10):5883-8. PubMed PMID: 11342602.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mycobacterium leprae-specific, HLA class II-restricted killing of human Schwann cells by CD4+ Th1 cells: a novel immunopathogenic mechanism of nerve damage in leprosy. AU - Spierings,E, AU - de Boer,T, AU - Wieles,B, AU - Adams,L B, AU - Marani,E, AU - Ottenhoff,T H, PY - 2001/5/9/pubmed PY - 2001/8/10/medline PY - 2001/5/9/entrez SP - 5883 EP - 8 JF - Journal of immunology (Baltimore, Md. : 1950) JO - J Immunol VL - 166 IS - 10 N2 - Peripheral nerve damage is a major complication of reversal (or type-1) reactions in leprosy. The pathogenesis of nerve damage remains largely unresolved, but detailed in situ analyses suggest that type-1 T cells play an important role. Mycobacterium leprae is known to have a remarkable tropism for Schwann cells of the peripheral nerve. 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 Ags of M. leprae to Ag-specific, inflammatory type-1 T cells and that these T cells subsequently damage and lyse infected Schwann cells. Thus far it has been difficult to study this directly because of the inability to grow large numbers of human Schwann cells. We now have established long-term human Schwann cell cultures from sural nerves and show that human Schwann cells express MHC class I and II, ICAM-1, and CD80 surface molecules involved in Ag presentation. Human Schwann cells process and present M. leprae, as well as recombinant proteins and peptides to MHC class II-restricted CD4(+) T cells, and are efficiently killed by these activated T cells. These findings elucidate a novel mechanism that is likely involved in the immunopathogenesis of nerve damage in leprosy. SN - 0022-1767 UR - https://www.unboundmedicine.com/medline/citation/11342602/Mycobacterium_leprae_specific_HLA_class_II_restricted_killing_of_human_Schwann_cells_by_CD4+_Th1_cells:_a_novel_immunopathogenic_mechanism_of_nerve_damage_in_leprosy_ L2 - http://www.jimmunol.org/cgi/pmidlookup?view=long&pmid=11342602 DB - PRIME DP - Unbound Medicine ER -