A possible self-regulating mechanism mediated by C3b-acceptor-bound C3b generated by stimulated macrophages

Z. Fabry, A. Erdei, J. Gergely

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8 Citations (Scopus)

Abstract

Macrophages have been shown to produce C3 and to bear Fc receptors (FcR), and besides the various C3 receptors, they possess C3b acceptors (C3bA) as well as surface proteases capable of cleaving C3. Using the immune adherence method, we demonstrated that the amount of covalently fixed (i.e., C3bA-bound) C3b is markedly increased upon cell stimulation by phorbol myristate acetate or aggregated IgG, even in the absence of C3. The enhancement of nascent C3b (C3b(x)) binding to C3bA on these cells could be reversed by inhibiting the process at different stages, using either cycloheximide, phenyl-methyl-sulphonyl-fluoride, salicyl hydroxamic acid, or methylamine. On the basis of our present results and earlier results, we propose a self-regulatory mechanism by which activated, C3-producing macrophages cleave C3 by their surface proteases. C3b(x) generated in this way fixes covalently to C3bA of the producer cells, resulting in the inhibition of FcR on these cells.

Original languageEnglish
Pages (from-to)549-555
Number of pages7
JournalScandinavian Journal of Immunology
Volume22
Issue number5
Publication statusPublished - 1985

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Macrophages
Fc Receptors
Peptide Hydrolases
Complement 3b Receptors
Hydroxamic Acids
Tetradecanoylphorbol Acetate
Cycloheximide
Immunoglobulin G

ASJC Scopus subject areas

  • Immunology

Cite this

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abstract = "Macrophages have been shown to produce C3 and to bear Fc receptors (FcR), and besides the various C3 receptors, they possess C3b acceptors (C3bA) as well as surface proteases capable of cleaving C3. Using the immune adherence method, we demonstrated that the amount of covalently fixed (i.e., C3bA-bound) C3b is markedly increased upon cell stimulation by phorbol myristate acetate or aggregated IgG, even in the absence of C3. The enhancement of nascent C3b (C3b(x)) binding to C3bA on these cells could be reversed by inhibiting the process at different stages, using either cycloheximide, phenyl-methyl-sulphonyl-fluoride, salicyl hydroxamic acid, or methylamine. On the basis of our present results and earlier results, we propose a self-regulatory mechanism by which activated, C3-producing macrophages cleave C3 by their surface proteases. C3b(x) generated in this way fixes covalently to C3bA of the producer cells, resulting in the inhibition of FcR on these cells.",
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T1 - A possible self-regulating mechanism mediated by C3b-acceptor-bound C3b generated by stimulated macrophages

AU - Fabry, Z.

AU - Erdei, A.

AU - Gergely, J.

PY - 1985

Y1 - 1985

N2 - Macrophages have been shown to produce C3 and to bear Fc receptors (FcR), and besides the various C3 receptors, they possess C3b acceptors (C3bA) as well as surface proteases capable of cleaving C3. Using the immune adherence method, we demonstrated that the amount of covalently fixed (i.e., C3bA-bound) C3b is markedly increased upon cell stimulation by phorbol myristate acetate or aggregated IgG, even in the absence of C3. The enhancement of nascent C3b (C3b(x)) binding to C3bA on these cells could be reversed by inhibiting the process at different stages, using either cycloheximide, phenyl-methyl-sulphonyl-fluoride, salicyl hydroxamic acid, or methylamine. On the basis of our present results and earlier results, we propose a self-regulatory mechanism by which activated, C3-producing macrophages cleave C3 by their surface proteases. C3b(x) generated in this way fixes covalently to C3bA of the producer cells, resulting in the inhibition of FcR on these cells.

AB - Macrophages have been shown to produce C3 and to bear Fc receptors (FcR), and besides the various C3 receptors, they possess C3b acceptors (C3bA) as well as surface proteases capable of cleaving C3. Using the immune adherence method, we demonstrated that the amount of covalently fixed (i.e., C3bA-bound) C3b is markedly increased upon cell stimulation by phorbol myristate acetate or aggregated IgG, even in the absence of C3. The enhancement of nascent C3b (C3b(x)) binding to C3bA on these cells could be reversed by inhibiting the process at different stages, using either cycloheximide, phenyl-methyl-sulphonyl-fluoride, salicyl hydroxamic acid, or methylamine. On the basis of our present results and earlier results, we propose a self-regulatory mechanism by which activated, C3-producing macrophages cleave C3 by their surface proteases. C3b(x) generated in this way fixes covalently to C3bA of the producer cells, resulting in the inhibition of FcR on these cells.

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