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CD2 expression and function in lepromatous leprosy.

L Wong1, P Salgame, V K Torigian

  • 1Section of Dermatology, University of Southern California School of Medicine, Los Angeles 90033.

Infection and Immunity
|September 1, 1989
PubMed
Summary
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In lepromatous leprosy, CD2 expression on T-lymphocytes is normal in skin lesions and peripheral blood. This study found that defective CD2 modulation is not the cause of immune unresponsiveness to Mycobacterium leprae.

Area of Science:

  • Immunology
  • Dermatology
  • Infectious Diseases

Background:

  • Leprosy's clinical spectrum is linked to host immune response.
  • Previous theories proposed M. leprae-specific T-suppressor cells or CD2 modulation cause unresponsiveness in lepromatous leprosy.

Purpose of the Study:

  • To investigate CD2 and CD3 expression on lymphocytes in lepromatous leprosy skin lesions and peripheral blood mononuclear cells (PBMC).
  • To assess the functionality of CD2 expression in T-cell activation in lepromatous leprosy patients.

Main Methods:

  • Immunohistochemistry to analyze CD2 and CD3 expression in skin lesions.
  • Indirect immunofluorescence flow cytometry for peripheral blood lymphocytes.
  • T-cell activation assays using anti-T11(2)/anti-T11(3) or anti-CD3 monoclonal antibodies, measuring 3H-thymidine incorporation and gamma interferon production.

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Main Results:

  • CD2 expression was normal on T-lymphocytes (CD3+) in both lepromatous leprosy skin lesions and peripheral blood.
  • PBMC from lepromatous patients showed normal T-cell activation and gamma interferon production in response to non-specific stimuli.
  • However, lepromatous PBMC did not proliferate or produce gamma interferon when stimulated with M. leprae.

Conclusions:

  • CD2 expression is normal and functional in T-cell activation in lepromatous leprosy.
  • Defective CD2 modulation is unlikely to be the mechanism behind specific immune unresponsiveness to Mycobacterium leprae in lepromatous leprosy.