PubMed · 4592712
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D Zucker-Franklin. 1974. Eosinophil function and disorders.. https://pubmed.ncbi.nlm.nih.gov/4592712/
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We investigated the interaction of immune complexes (IC) isolated from hepatitis C virus (HCV)-infected individuals with several cell lines that differentially express Fc receptors, and analyzed viral infection by the presence of HCV RNA sequences. Monocytic (U937 and Monomac-6) and lymphocytic (MOLT-4 and Jurkat) cell lines were incubated with interferon- plus phorbol myristate acetate to stimulate the expression of Fc receptors before addition of IC. Cell interaction with IC was monitored by flow cytometry. Positive cell fluorescence was detected in U937 and Monomac-6 cells [mean fluorescence intensity (MFI) 10.56+/-0.8 and 11.60+/-0.8, respectively]. Incubation of cells with monoclonal antibodies against Fc receptors for IgG before addition of IC decreased MFI in both cell lines (U937 2.1+/-0.5, Monomac-6 4.4+/-0.8, P<0.001), indicating that cell-IC interaction through these receptors was inhibited. In particular, the blockage of FcgammaRII was responsible for this effect. No binding of IC with either MOLT-4 or Jurkat cell lines was detected, which correlated with a very low Fc receptor expression. HCV RNA sequences were identified in the cells up to 120 h of post incubation with IC. These results suggest that IC can mediate entry of HCV to both U-937 and Monomac-6 cell lines mainly through the FcgammaRII.
A significant fraction of IL-8 in lung fluids from patients with the acute lung injury (ALI) is associated with anti-IL-8 autoantibodies (anti-IL-8:IL-8 complexes), and lung fluid concentrations of these complexes correlate with development and outcome of ALI. In this study, we examined whether anti-IL-8:IL-8 complexes exhibit proinflammatory activity in vitro. These complexes were purified from pulmonary edema fluid samples obtained from patients with ALI. First, we found that IL-8 bound to the autoantibody retained its ability to trigger chemotaxis of neutrophils, whereas control antibody did not have significant chemotactic activity. Next, we examined the ability of anti-IL-8:IL-8 complexes to induce neutrophil activation, i.e., neutrophil respiratory burst and degranulation. Anti-IL-8:IL-8 complexes triggered superoxide and myeloperoxidase release from human neutrophils, and in contrast, the control antibody had no effect. We also demonstrated that IgG receptor, FcgammaRIIa, is the receptor involved in cellular activation mediated by these complexes. Blockade of FcgammaRIIa completely reverses activity of the complexes with the exception of chemotaxis. Both FcgammaRIIa and IL-8 receptors mediate chemotactic activity of anti-IL-8:IL-8 complexes, with FcgammaRIIa being, however, a predominant receptor. Furthermore, activity of the complexes is partially dependent on the activation of the mitogen-activated protein kinases, i.e., ERK and p38, important components of the FcgammaRIIa signaling cascade. Anti-IL-8:IL-8 complexes may therefore be involved in the pathogenesis of lung inflammation in clinical acute lung injury.
OBJECTIVES: To investigate the possible relationship between oxidized low-density lipoprotein (ox-LDL) and LDL immune complexes (IC). METHODS: Both LDL-IC and ox-LDL were detected by sandwich ELISA. The levels were also studied in 60 patients with coronary heart disease (CHD) and 50 control subjects. RESULTS: Compared to controls, both the plasma ox-LDL concentrations (595.5 +/- 194.8 vs. 440.3 +/- 175.0 microg/l, P < 0.001) and LDL-IC levels (2.74 +/- 0.73 vs. 1.38 +/- 0.78 AU, P < 0.001) in the patients with CHD were significantly increased. The relationships between LDL-IC, ox-LDL levels, and other lipid parameters in all the studied subjects (n = 100) were analyzed. LDL-IC levels were positively correlated with TC, TG, LDL-C, lipoprotein(a) [Lp(a)], and apolipoprotein B (apoB) concentration, while negatively correlated with apoA1 concentration, respectively. Similarly, ox-LDL levels were also found positively correlated with TC, LDL-C, and apoB concentrations, respectively. Furthermore, a significantly positive correlation between ox-LDL and LDL-IC levels was found (r = 0.313, P < 0.005). CONCLUSION: In vivo oxidized LDL positively correlates with circulating levels of LDL immune complexes.