Innate immune mechanisms in the pathogenesis of systemic lupus erythematosus (SLE)

Immunol Lett. 2001 Jul 2;77(3):175-80. doi: 10.1016/s0165-2478(01)00220-6.

Abstract

Immune imbalance in SLE increases the susceptibility to infectious diseases. The aim of this study was to analyze several mechanisms related to non-specific immunity in this autoimmune disorder. We studied in vivo CD11b expression, phagocytosis, and chemotaxis in polymorphonuclear cells (PMN) from SLE patients. All tests were also performed under hrIL-8 stimulating conditions and analyzed by flow cytometry. Intracellular leucocyte (monocytes and PMN) enzyme activity was evaluated using specific substrates for cathepsin B and D, collagenase, and oxidative burst by flow cytoenzymology. An exaggerated in vivo CD11b expression was observed on PMN from SLE patients without noticeably in vitro effect upon hrIL-8. Similarly both, phagocytosis and chemotaxis were diminished and showed no response to hrIL-8 stimulation. The opposite was found in PMN from controls. Intracellular enzyme activity was comparable between groups as far as cathepsin B and D are concerned. A tendency of decreased oxidative-burst induction was noted in monocytes and PMN from SLE patients, whereas collagenase activity was found clearly increased in both leucocyte subpopulations. Our results may represent a deficient ability of the innate immune mechanisms for the clearance of infectious agents, immune complexes, satisfactory resolution of inflammatory processes and tissue repair in SLE.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Cathepsin B / metabolism
  • Cathepsin D / metabolism
  • Chemotaxis, Leukocyte
  • Collagenases / metabolism
  • Female
  • Flow Cytometry
  • Humans
  • Immunity, Innate
  • Interleukin-8 / pharmacology
  • Lupus Erythematosus, Systemic / enzymology
  • Lupus Erythematosus, Systemic / immunology*
  • Macrophage-1 Antigen / analysis
  • Male
  • Middle Aged
  • Monocytes / enzymology
  • Monocytes / immunology*
  • Monocytes / metabolism
  • Neutrophils / enzymology
  • Neutrophils / immunology*
  • Neutrophils / metabolism
  • Phagocytosis
  • Recombinant Proteins / pharmacology
  • Respiratory Burst

Substances

  • Interleukin-8
  • Macrophage-1 Antigen
  • Recombinant Proteins
  • Cathepsin B
  • Cathepsin D
  • Collagenases