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The functional state of the complement system in leprosy

Gabriela I Gomes1, Edilbert P Nahn, Rose K R G Santos

  • 1Laboratório de Biologia do Reconhecer, Centro de Biociências e Biotecnologia, Universidade Estadual do Norte Fluminense-Darcy Ribeiro, Rio de Janeiro, Brazil.

The American Journal of Tropical Medicine and Hygiene
|April 4, 2008
PubMed

Insights

Leprosy patients with the lepromatous form (LL) show complement system (CS) activation via the classic pathway (CP). This involves reduced C4 levels and higher mannose-binding lectin (MBL) levels, suggesting immune complex involvement.

Area of Science:

  • Immunology
  • Infectious Diseases
  • Dermatology

Background:

  • Leprosy, caused by Mycobacterium leprae, presents diverse clinical forms.
  • The complement system (CS) plays a crucial role in immune responses.
  • Understanding CS activation in different leprosy forms is vital for disease management.

Purpose of the Study:

  • To investigate complement system activation pathways in various clinical forms of leprosy.
  • To identify specific complement components involved in lepromatous leprosy (LL).
  • To explore the role of mannose-binding lectin (MBL) in CS activation in LL.

Main Methods:

  • Assessed total complement system (CS) activity using hemolytic methods.
  • Quantified individual complement components via enzyme-linked immunosorbent assay (ELISA).
  • Analyzed sera from 91 leprosy patients (LL, TL, DL) and 31 healthy donors.

Main Results:

  • Significant CS consumption, specifically via the classic pathway (CP), was observed only in lepromatous leprosy (LL) patients.
  • LL patients exhibited reduced C4 levels but normal factor B (fB) and C3 levels.
  • Elevated serum mannose-binding lectin (MBL) levels were found in LL patients.

Conclusions:

  • The classic pathway (CP) of the complement system is implicated in CS activation in lepromatous leprosy (LL).
  • High serum MBL levels and circulating immune complexes likely initiate CS activation in LL patients.
  • These findings highlight a specific immune mechanism in the LL clinical form of leprosy.

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