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

• Published in: Immunology letters Vol. 77; no. 3; pp. 175 - 180
• Main Authors: de la Fuente, Hortensia, Richaud-Patin, Yvonne, Jakez-Ocampo, Juan, González-Amaro, Roberto, Llorente, Luis
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 02.07.2001
• Subjects: Adolescent; Adult; Cathepsin B - metabolism; Cathepsin D - metabolism; CD11b antigen; Chemotaxis; Chemotaxis, Leukocyte; Collagenases - metabolism; Cytoenzymology; 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; SLE; Cytoenzymology; SLE; Chemotaxis; Phagocytosis
• ISSN: 0165-2478; 1879-0542
• DOI: 10.1016/S0165-2478(01)00220-6

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.