Comparison of C1q-receptors on rat microglia and peritoneal macrophages

Wing, Mark; Seilly, David J.; Nicholas, Richard; Rahman, S.M. Jamshedur; Zajicek, John; Lachmann, P. J.; Compston, D. A. S.

doi:10.1016/s0165-5728(98)00227-6

Cited by 9 publications

(5 citation statements)

References 43 publications

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“…Previous work has shown that C1qR P recognizes a site in the collagen-like region of C1q [reviewed in ref. 54], and the recent demonstration by Wing et al [55] that microglia express a surface binding site for the collagen-like region of C1q, which exhibits the characteristics of a receptor, further supports our demonstration of a microglial C1qR P . In addition, soluble C1q does not enhance phagocytosis in microglia [S. Webster, unpublished observations], consistent with the requirement of C1qR P for immobilized C1q [54].…”

Section: Discussionsupporting

confidence: 90%

Structural and functional evidence for microglial expression of C1qRP, the C1q receptor that enhances phagocytosis

Webster

Park

Fonseca

et al. 2000

Journal of Leukocyte Biology

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Microglial activation has been associated with several degenerative diseases of the central nervous system (CNS). One consequence of activation is the induction of a more efficient phagocytic response, and it is therefore important to determine what factors regulate microglial phagocytosis and whether this capacity influences the progression of neurodegenerative changes. Previous studies have demonstrated that complement component C1q enhances Fc receptor-and CR1-mediated phagocytosis in cells of the myeloid lineage via a cell surface receptor, C1qR P . Because C1q has been found in the area of lesions in several degenerative CNS diseases, the current investigations were carried out to characterize the effects of C1q on microglial phagocytosis. Neonatal rat microglia were shown to express C1qR P as assessed by flow cytometry and immunocytochemistry. Interaction of these cells with substrate-bound C1q was shown to enhance both FcRand CR1-mediated phagocytosis two-to fourfold. In addition, introduction of an antibody raised against the carboxy-terminal, cytoplasmic domain of C1qR P into microglia by electroporation markedly diminished the ability of C1q to enhance uptake of IgG-coated targets, whereas nonspecific IgG had no such effect. These results suggest that C1q in areas of active degeneration may promote the phagocytic capacity of microglia via interaction with microglial C1qR P . J. Leukoc. Biol. 67: 109-116; 2000.

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Section: Discussionsupporting

confidence: 90%

Structural and functional evidence for microglial expression of C1qRP, the C1q receptor that enhances phagocytosis

Webster

Park

Fonseca

et al. 2000

Journal of Leukocyte Biology

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“…Although the CNS is considered to be an immune-privileged organ, the brain represents a major site of complement synthesis (74). All classical-and alternative-pathway complement components can be synthesized in the CNS (6), and functional receptors for complement proteins are expressed by several cell types of the CNS (6,20,92). Local activation of the complement cascade has been demonstrated both in experimental meningitis (75) and in CSF from patients with bacterial meningitis (9,16,76,90,97).…”

Section: Complementmentioning

confidence: 99%

Chemotactic Factors in Cerebrospinal Fluid during Bacterial Meningitis

et al. 2006

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“…Although the CNS is considered to be an immuneprivileged organ, the brain represents a significant site of complement synthesis [6]. All classical and alternative pathway complement components can be synthesized in the CNS [7], and functional receptors for complement proteins are present on several cell populations in the CNS [7][8][9]. Local activation of complement occurs both in experimental meningitis [10] and in CSF from patients with bacterial meningitis [11][12][13].…”

mentioning

confidence: 99%

C1 Inhibitor Treatment Improves Host Defense in Pneumococcal Meningitis in Rats and Mice

et al. 2007

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In spite of antibiotic treatment, pneumococcal meningitis continues to be associated with significant morbidity and mortality. The complement system is a key component of innate immunity against invading pathogens. However, activation of complement is also involved in tissue damage, and complement inhibition by C1 inhibitor (C1-inh) is beneficial in animal models of endotoxemia and sepsis. In the present study, we demonstrate classical pathway complement activation during pneumococcal meningitis in rats. We also evaluate the effect of C1-inh treatment on clinical illness, bacterial clearance, and inflammatory responses in rats and mice with pneumococcal meningitis. C1-inh treatment was associated with reduced clinical illness, a less-pronounced inflammatory infiltrate around the meninges, and lower brain levels of proinflammatory cytokines and chemokines. C1-inh treatment increased bacterial clearance, possibly through an up-regulation of CR3. Hence, C1-inh may be a useful agent in the treatment of pneumococcal meningitis.

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Comparison of C1q-receptors on rat microglia and peritoneal macrophages

Cited by 9 publications

References 43 publications

Structural and functional evidence for microglial expression of C1qRP, the C1q receptor that enhances phagocytosis

Structural and functional evidence for microglial expression of C1qRP, the C1q receptor that enhances phagocytosis

Chemotactic Factors in Cerebrospinal Fluid during Bacterial Meningitis

C1 Inhibitor Treatment Improves Host Defense in Pneumococcal Meningitis in Rats and Mice

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