Triggering of respiratory burst by phagocytosis in monocytes of patients with systemic lupus erythematosus

Abstract

SUMMARY The triggering of the respiratory burst by phagocytosis via different receptors in monocytes of patients with systemic lupus erythematosus (SLE) was investigated. The superoxide anion synthesis was assayed by reduction of fcrricytochrome C that was inhibited by superoxide dismutase. The mononuclear cell suspensions were triggered by IgG‐coated latex. C3 complement fragment‐coated and uncoated yeast (Saccharomyces cerevisiae). Superoxide generation induced by phagocytosis via FcγR was decreased in monocytes of patients with SLE. On the other hand. MoAbs against FcγRl, FcγRll and especially CR3 could also induce superoxide anion synthesis. At the same time, superoxide generation induced by anti‐CR3 could be inhibited with C3‐coated yeast.

Phagocyte activity in the peripheral blood of pregnant women with systemic lupus erythematosus and in the cord blood of their newborns

“…It should be noted that the expression of this receptor is quite unstable and is dependent on the activity of the disease. The active phase of the disease leads to an increased expression of CR3 on the cell surface in response to the activation of the complement system . With respect to the low‐affinity receptor for Fc‐fragment of IgG (CD16), its expression was unaffected in SLE women, which is consistent with our observations.…”

Superoxide release in juvenile systemic lupus erythematosus

“…A greater reserve of NADPH in patients with underlying inXammatory conditions may be responsible for the respiratory burst seen in the Wrst time points (5 and 25 min) of our study with stimulated cells. The rapid use of NADPH at the beginning leads to a diminished production of O 2 ¡ toward the end of the study [25]. Furthermore, some authors have reported the existence of serum factors in patients with SLE that can stimulate O 2 ¡ production by stimulated granulocytes [26].…”

Infections in Patients with Systemic Lupus Erythematosus: The Contribution of Primary Immune Defects Versus Treatment-Induced Immunosuppression

“… 2 Production of superoxide following Fcγ receptor-mediated phagocytosis, which is important in the defense against infectious agents, is impaired. 6 This can be further compromised by autoantibodies against the Fcγ receptors. 7 The phagocytic function of macrophages and neutrophils may be influenced by autoantibodies targeting the 3 subclasses of Fcγ receptors (FcγRI, FcγRII, FcγRIII).…”