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Y M Lucisano

Publications and source records attributed to Y M Lucisano.

5 recordsLinked to original sources
PubMed1998

Precipitated immune complexes of IgM induce the generation of reactive oxygen species by rabbit polymorphonuclear leucocytes.

We report that immune complexes of IgM (ICIgM) antibodies and ovalbumin in the form of a precipitate from the equivalence zone induce the generation of reactive oxygen species by rabbit blood polymorphonuclear leucocytes (PMN), as measured by the chemiluminescence (CL) production in the presence of luminol. The kinetics of CL generation induced by ICIgM is quite different from that induced by precipitated immune complexes of IgG (ICIgG): the maximum rate of CL production for ICIgM occurs around 14 min, whereas for ICIgG it occurs about 5 min after incubation with the cells. Also the triggering of the process requires a higher concentration of ICIgM than of ICIgG. Evidence is presented that these effects are not mediated by interaction of the antigen (ovalbumin) with the cell, since immune precipitates of ovalbumin and the F(ab')2 fragment had no effect. Our observations that precipitated ICIgM can also be an effective stimulus for CL generation and thus for O2- production reveal a new functional capability of PMN. These results may have implications for the understanding of the participation of ICIgM (as well as of ICIgG) in inflammatory reactions mediated by PMN in immune complex diseases, and in the mechanisms of defense against microbes and other non-self agents.

Animals↗
PubMed1992

Precipitated immune complexes of IgM as well as of IgG can bind to rabbit polymorphonuclear leucocytes but only the immune complexes of IgG are readily phagocytosed.

We have shown by in vitro experiments, using immunofluorescence techniques, that precipitated immune complexes of IgM antibodies and ovalbumin (ICIgM) are able to bind to rabbit blood polymorphonuclear leucocytes (PMN), as well as immune complexes of IgG antibodies (ICIgG). This binding capacity for both classes of immune complexes is exhibited by more than 80% of the PMN cell population and is independent of Ca2+ in the medium. For ICIgG the binding to PMN can be completely inhibited by preincubation of the cells with soluble IgG used at physiological concentrations (competition for the Fc gamma receptors) while for ICIgM there is no such inhibition by fluid-phase IgM. After binding to the leucocytes there was a striking difference in the fate of ICIgM and ICIgG: whereas the ICIgG was readily phagocytosed (endocytosed), the ICIgM remained mostly on the cell surface, being only poorly endocytosed after 1 hr incubation at 37 degrees. This was demonstrated by a quantitative fluorimetric method developed to assay phagocytosis of immune complexes, and was confirmed by a qualitative fluorescence quenching technique. These results may have implications for understanding the fate of these classes of immune complexes formed in circulation or deposited in tissues, and the participation of PMN in inflammatory reactions and tissue injury in immune complex diseases.

Animals↗
PubMed1988

The role of complement in the stimulation of lysosomal enzyme release by polymorphonuclear leucocytes induced by immune complexes of IgG and of IgM.

The effect of complement components incorporated into precipitated immune complexes (IC) of IgG or of IgM on their capacity for stimulating lysosomal enzyme release from rabbit polymorphonuclear leucocytes was studied in vitro. We have found that: (i) complement causes an amplification in the stimulatory capacity of both classes of IC, the effect being dependent on the concentration of the IC, and higher for the IgM class; (ii) dose-effect experiments of competition by fluid-phase immunoglobulins have shown that IgG (in physiological or smaller concentrations) can inhibit greatly the stimulation by this class of immune complex; this inhibition can be prevented, however, by the presence of complement in the IC (a situation expected to occur in vivo); for IgM immune complexes there was no such competitive inhibition, so complement would not be necessary; (iii) the relevant complement factors must be located in the range C1-C3. These results help us to understand the importance of complement (besides the well-known generation of chemotactic factors) in the mechanisms of tissue injury produced by neutrophils in immune complex diseases.

Animals↗
PubMed1984

Lysosomal enzyme release from polymorphonuclear leukocytes induced by immune complexes of IgM and of IgG.

Lysosomal enzyme release by rabbit polymorphonuclear leukocytes induced by immune complexes of IgM or IgG antibodies and ovalbumin was studied by in vitro experiments. It was shown that IgM immune complexes in the form of precipitates were able to stimulate the release of the lysosomal enzymes beta-glucuronidase and alkaline and acid phosphatases, in contrast to heat-aggregated IgM, which had only a small effect. This stimulation was dependent on the presence of Ca2+ in the extracellular medium; Mg2+ showed a slight effect as a substitute for Ca2+. IgG precipitated immune complexes prepared from different regions of the precipitation curve were tested. It was shown that immune precipitates from the equivalence region were the most effective; those at antibody excess have a smaller but comparable capacity, whereas the precipitated immune complexes at antigen excess were the least effective. Soluble immune complexes of IgG with an excess of antigen concentration in the range of 2.5 to 5 times that of equivalence were also able to stimulate the enzyme release, but that capacity decreased rapidly with the increase in antigen concentration. The enzyme release induced by IgM immune complexes was not inhibited by competition with free immunoglobulin in the medium, either IgM or IgG in approximate physiologic concentrations; contrarily, with IgG immune complexes, free monomeric IgG (but not IgM) can completely block the process. The possible implications of these findings in the immune complex diseases are discussed.

Animals↗