Receptors for IgG complexes activate synthesis of monocyte chemoattractant peptide 1 and colony-stimulating factor

Kazuhiko Hora, Joseph A. Satriano, Arthur Santiago, Tetsuo Mori, E. Richard Stanley, Zihe Shan, Detlef Schlondorff

Research output: Contribution to journalArticle

116 Citations (Scopus)

Abstract

The chemotactic factors responsible for complement-independent macrophage accumulation in immune-complex diseases such as glomerulonephritis remain unknown. Fc receptors for IgG complexes are found on mesangial cells of the kidney, which produce the macrophage growth factor colony-stimulating factor 1 (CSF-1). We therefore investigated the possible stimulation of mesangial-cell expression of CSF-1 and the recently identified monocyte-specific chemoattractant protein 1 (MCP-1) by IgG complexes. IgG complexes, but not monomeric IgG or F(ab′)22 fragments of IgG, rapidly (2-8 h) increased mRNA for both CSF-1 (10-fold) and MCP-1 (20-fold) in cultured mouse mesangial cells. The increase of mRNA for CSF-1 and MCP-1 was not reduced by either cytochalasin B or D, indicating that Fc receptor occupancy is sufficient for signaling and that phagocytosis is not required to elicit this response. IgG complexes also caused a 10-fold increase in the secretion of CSF-1 and a 3- to 5-fold increase in secretion of MCP-1 into the cell culture medium. The synthesis and release of CSF-1 and MCP-1 by mesangial cells as a consequence of Fc receptor occupancy may be responsible for macrophage recruitment and activation at sites of immune-complex deposition.

Original languageEnglish (US)
Pages (from-to)1745-1749
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume89
Issue number5
StatePublished - 1992

Fingerprint

IgG Receptors
Macrophage Colony-Stimulating Factor
Chemotactic Factors
Chemokine CCL2
Monocytes
Mesangial Cells
Immunoglobulin G
Peptides
Fc Receptors
Macrophages
Immune Complex Diseases
Cytochalasin D
Messenger RNA
Cytochalasin B
Macrophage Activation
Glomerulonephritis
Antigen-Antibody Complex
Phagocytosis
Culture Media
Intercellular Signaling Peptides and Proteins

Keywords

  • Glomerulonephritis
  • Immune complexes
  • Mesangial cells

ASJC Scopus subject areas

  • Genetics
  • General

Cite this

Receptors for IgG complexes activate synthesis of monocyte chemoattractant peptide 1 and colony-stimulating factor. / Hora, Kazuhiko; Satriano, Joseph A.; Santiago, Arthur; Mori, Tetsuo; Stanley, E. Richard; Shan, Zihe; Schlondorff, Detlef.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 89, No. 5, 1992, p. 1745-1749.

Research output: Contribution to journalArticle

Hora, Kazuhiko ; Satriano, Joseph A. ; Santiago, Arthur ; Mori, Tetsuo ; Stanley, E. Richard ; Shan, Zihe ; Schlondorff, Detlef. / Receptors for IgG complexes activate synthesis of monocyte chemoattractant peptide 1 and colony-stimulating factor. In: Proceedings of the National Academy of Sciences of the United States of America. 1992 ; Vol. 89, No. 5. pp. 1745-1749.
@article{08307115c9e74c3cae827bddf2c54edd,
title = "Receptors for IgG complexes activate synthesis of monocyte chemoattractant peptide 1 and colony-stimulating factor",
abstract = "The chemotactic factors responsible for complement-independent macrophage accumulation in immune-complex diseases such as glomerulonephritis remain unknown. Fc receptors for IgG complexes are found on mesangial cells of the kidney, which produce the macrophage growth factor colony-stimulating factor 1 (CSF-1). We therefore investigated the possible stimulation of mesangial-cell expression of CSF-1 and the recently identified monocyte-specific chemoattractant protein 1 (MCP-1) by IgG complexes. IgG complexes, but not monomeric IgG or F(ab′)22 fragments of IgG, rapidly (2-8 h) increased mRNA for both CSF-1 (10-fold) and MCP-1 (20-fold) in cultured mouse mesangial cells. The increase of mRNA for CSF-1 and MCP-1 was not reduced by either cytochalasin B or D, indicating that Fc receptor occupancy is sufficient for signaling and that phagocytosis is not required to elicit this response. IgG complexes also caused a 10-fold increase in the secretion of CSF-1 and a 3- to 5-fold increase in secretion of MCP-1 into the cell culture medium. The synthesis and release of CSF-1 and MCP-1 by mesangial cells as a consequence of Fc receptor occupancy may be responsible for macrophage recruitment and activation at sites of immune-complex deposition.",
keywords = "Glomerulonephritis, Immune complexes, Mesangial cells",
author = "Kazuhiko Hora and Satriano, {Joseph A.} and Arthur Santiago and Tetsuo Mori and Stanley, {E. Richard} and Zihe Shan and Detlef Schlondorff",
year = "1992",
language = "English (US)",
volume = "89",
pages = "1745--1749",
journal = "Proceedings of the National Academy of Sciences of the United States of America",
issn = "0027-8424",
number = "5",

}

TY - JOUR

T1 - Receptors for IgG complexes activate synthesis of monocyte chemoattractant peptide 1 and colony-stimulating factor

AU - Hora, Kazuhiko

AU - Satriano, Joseph A.

AU - Santiago, Arthur

AU - Mori, Tetsuo

AU - Stanley, E. Richard

AU - Shan, Zihe

AU - Schlondorff, Detlef

PY - 1992

Y1 - 1992

N2 - The chemotactic factors responsible for complement-independent macrophage accumulation in immune-complex diseases such as glomerulonephritis remain unknown. Fc receptors for IgG complexes are found on mesangial cells of the kidney, which produce the macrophage growth factor colony-stimulating factor 1 (CSF-1). We therefore investigated the possible stimulation of mesangial-cell expression of CSF-1 and the recently identified monocyte-specific chemoattractant protein 1 (MCP-1) by IgG complexes. IgG complexes, but not monomeric IgG or F(ab′)22 fragments of IgG, rapidly (2-8 h) increased mRNA for both CSF-1 (10-fold) and MCP-1 (20-fold) in cultured mouse mesangial cells. The increase of mRNA for CSF-1 and MCP-1 was not reduced by either cytochalasin B or D, indicating that Fc receptor occupancy is sufficient for signaling and that phagocytosis is not required to elicit this response. IgG complexes also caused a 10-fold increase in the secretion of CSF-1 and a 3- to 5-fold increase in secretion of MCP-1 into the cell culture medium. The synthesis and release of CSF-1 and MCP-1 by mesangial cells as a consequence of Fc receptor occupancy may be responsible for macrophage recruitment and activation at sites of immune-complex deposition.

AB - The chemotactic factors responsible for complement-independent macrophage accumulation in immune-complex diseases such as glomerulonephritis remain unknown. Fc receptors for IgG complexes are found on mesangial cells of the kidney, which produce the macrophage growth factor colony-stimulating factor 1 (CSF-1). We therefore investigated the possible stimulation of mesangial-cell expression of CSF-1 and the recently identified monocyte-specific chemoattractant protein 1 (MCP-1) by IgG complexes. IgG complexes, but not monomeric IgG or F(ab′)22 fragments of IgG, rapidly (2-8 h) increased mRNA for both CSF-1 (10-fold) and MCP-1 (20-fold) in cultured mouse mesangial cells. The increase of mRNA for CSF-1 and MCP-1 was not reduced by either cytochalasin B or D, indicating that Fc receptor occupancy is sufficient for signaling and that phagocytosis is not required to elicit this response. IgG complexes also caused a 10-fold increase in the secretion of CSF-1 and a 3- to 5-fold increase in secretion of MCP-1 into the cell culture medium. The synthesis and release of CSF-1 and MCP-1 by mesangial cells as a consequence of Fc receptor occupancy may be responsible for macrophage recruitment and activation at sites of immune-complex deposition.

KW - Glomerulonephritis

KW - Immune complexes

KW - Mesangial cells

UR - http://www.scopus.com/inward/record.url?scp=0026556862&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026556862&partnerID=8YFLogxK

M3 - Article

C2 - 1542668

AN - SCOPUS:0026556862

VL - 89

SP - 1745

EP - 1749

JO - Proceedings of the National Academy of Sciences of the United States of America

JF - Proceedings of the National Academy of Sciences of the United States of America

SN - 0027-8424

IS - 5

ER -