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DC-SIGN association with the Th2 environment of lepromatous lesions: cause or effect?

E J Soilleux1, E N Sarno, M O Hernandez

  • 1Department of Histopathology, Papworth Hospital, Papworth Everard, Cambridge CB3 8RE, and Nuffield Department of Clinical Laboratory Sciences, University of Oxford, UK. E.J.Soilleux.91@cantab.net

The Journal of Pathology
|April 4, 2006
PubMed

Insights

Leprosy

Area of Science:

  • Immunology
  • Microbiology
  • Dermatology

Background:

  • Leprosy's clinical spectrum correlates with immune responses.
  • Non-responsiveness to Mycobacterium leprae (ML) is linked to Th2 profiles.
  • The cause of polarized immune responses in leprosy is unknown.

Purpose of the Study:

  • Investigate the role of DC-SIGN in leprosy.
  • Determine if DC-SIGN mediates ML entry into host cells.

Main Methods:

  • Assessed DC-SIGN expression in leprosy patient tissues (HIV-positive and negative).
  • Examined the interaction between ML and DC-SIGN.
  • Investigated ML entry via DC-SIGN using lipoarabinomannan.

Main Results:

  • Abundant DC-SIGN expression observed in lepromatous leprosy, but not borderline tuberculoid leprosy.
  • DC-SIGN acts as an entry receptor for ML, similar to M. tuberculosis.
  • DC-SIGN is present on ML-infected cells, supporting its receptor role.

Conclusions:

  • DC-SIGN is upregulated in lepromatous leprosy.
  • DC-SIGN may facilitate ML entry into macrophages, contributing to disease pathogenesis.

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