Requirement of extracellular complement and immunoglobulin for intracellular killing of micro-organisms by human monocytes.

Leijh, P. C. J.; Barselaar, M. T. Van Den; Zwet, T L van; Daha, Mohamed R.; Furth, R. van

doi:10.1172/jci109362

Cited by 134 publications

(73 citation statements)

References 32 publications

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“…Intracellular killing of opsonized-ingested bacteria by monocytes required binding of heterogeneous IgG to Fc-receptors of the cells [7], supporting the present findings. Though their report did not mention the fusion of phagocytic vesicles with lysosomes, our experiments suggest a relation between Fc-receptors and fusion.…”

Section: Discussionsupporting

confidence: 90%

Fc‐receptor modulates the fusion between phagocytic vesicles and lysosomes in guinea pig polymorphonuclear leukocytes

Amano

Mizuno

1980

FEBS Letters

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Section: Discussionsupporting

confidence: 90%

Fc‐receptor modulates the fusion between phagocytic vesicles and lysosomes in guinea pig polymorphonuclear leukocytes

Amano

Mizuno

1980

FEBS Letters

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“…When an early component such as C4 is deficient, antigen-antibody complexes are more likely to precipitate and lead to tissue damage and inflammation. There is also evidence that C4 is important for phagocytosis by monoc ytes and intracellular microbial killing (48).…”

Section: Discussionmentioning

confidence: 99%

Molecular heterogeneity of complement component c4‐null and 21‐hydroxylase genes in systemic lupus erythematosus

Goldstein

Arnett

McLean

et al. 1988

Arthritis & Rheumatism

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C4A‐null alleles (C4A*Q0) and hereditary complete C4 deficiency (homozygous C4A*Q0, C4B*Q0) are associated with systemic lupus erythematosus (SLE). Using Southern blot analysis with C4 and 21‐hydroxylase (21‐OH) DNA probes, we studied SLE patients and normal control subjects with or without C4A*Q0, and 2 C4‐deficient SLE patients. A previously reported large C4A,21‐OHA gene deletion associated in normal subjects with the HLA—A1;B8;DR3;C4AQ0 haplotype was detected by the appearance of a new C4 Hind III 8.5‐kb fragment and disappearance of a 3.2‐kb 21‐OH Taq I fragment. In 3 SLE patients with homozygous C4A*Q0 and 15 with heterozygous C4A*Q0, this deletion pattern occurred almost exclusively in association with the HLA—B8;DR3;C4A*Q0 phenotype; the one exception was a black SLE patient. Other C4A*Q0‐bearing HLA phenotypes in white patients and black patients with SLE, and the 2 completely C4‐deficient SLE patients, had normal DNA hybridization to both C4 and 21‐OH probes. The genetic basis for C4‐null alleles in SLE is heterogeneous. A large C4A,21‐OHA deletion occurs mainly on the HLA—B8;DR3;C4AQ0 haplotype in SLE and controls. Other HLA haplotypes bearing C4A*Q0 have normal C4 and 21‐OH genes, as demonstrated by Southern blot analysis.

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“…Phagocytes, primarily neutrophils and macrophages, use a number of different receptors to bind microorganisms and eliminate them by enclosure within an intracellular vacuole or phagosome formed from the plasma membrane (1)(2)(3). The mechanism by which receptor binding of the microorganism is transduced into a signal-mediating phagocytosis is not yet fully elucidated.…”

mentioning

confidence: 99%

Impaired Host Defense in Mice Lacking ONZIN

Ledford

Kovářová

Koller

2007

The Journal of Immunology

101

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ONZIN is a small, cysteine-rich peptide of unique structure that is conserved in all vertebrates examined to date. We show that ONZIN is expressed at high levels in epithelial cells of the intestinal tract, the lung, and in cells of the immune system including macrophages and granulocytes. Because this pattern of expression is suggestive of a role in innate immune function, we have generated mice lacking this protein and examined their ability to respond to challenge with infectious agents. Onzin−/− mice show a heightened innate immune response after induction of acute peritonitis with Klebsiella pneumoniae. This increased response is consistent with an increased bacterial burden in the Onzin−/− mice. Ex vivo studies show that, whereas phagocytosis is not altered in Onzin−/− neutrophils, phagocytes lacking this protein kill bacteria less effectively. This result identifies ONZIN as a novel class of intracellular protein required for optimal function of the neutrophils after uptake of bacteria.

show abstract

Requirement of extracellular complement and immunoglobulin for intracellular killing of micro-organisms by human monocytes.

Cited by 134 publications

References 32 publications

Fc‐receptor modulates the fusion between phagocytic vesicles and lysosomes in guinea pig polymorphonuclear leukocytes

Fc‐receptor modulates the fusion between phagocytic vesicles and lysosomes in guinea pig polymorphonuclear leukocytes

Molecular heterogeneity of complement component c4‐null and 21‐hydroxylase genes in systemic lupus erythematosus

Impaired Host Defense in Mice Lacking ONZIN

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