Correction of defective macrophage differentiation in C3H/HeJ mice by an interferon-like molecule

S. N. Vogel, L. L. Weedon, R. N. Moore, David L. Rosenstreich

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

C3H/HeJ mice possess macrophages that lose the capacity to bind and phagocytose opsonized sheep erythrocytes (EA) when cultured. This defect in Fc receptor capacity is completely overcome by treatment of macrophage monolayers with extremely low concentrations of a lymphokine-rich, Con A-stimulated spleen cell supernatant. In this study we have pursued a biochemical and functional analysis of the lymphokine-rich supernatant to determine the nature of the specific factor responsible for the restoration of Fc receptor function. The chromatographic behavior and physical properties, its co-elution with anti-viral activity through a sequential purification scheme, the parallel activity of purified β-interferon in enhancing both the binding and phagocytosis of EA, and the abrogation of factor-induced Fc-mediated phagocytosis with anti-Type II interferon antiserum, strongly support the hypothesis that the active factor is γ- (Type II or immune) interferon (IFN). These studies suggest γ-IFN may act as a differentiative signal to the macrophage by facilitating enhanced expression of macrophage surface membrane components.

Original languageEnglish (US)
Pages (from-to)380-387
Number of pages8
JournalJournal of Immunology
Volume128
Issue number1
StatePublished - 1982
Externally publishedYes

Fingerprint

Inbred C3H Mouse
Interferons
Macrophages
Phagocytosis
Fc Receptors
Lymphokines
Interferon-gamma
Immune Sera
Sheep
Spleen
Erythrocytes
Membranes

ASJC Scopus subject areas

  • Immunology

Cite this

Correction of defective macrophage differentiation in C3H/HeJ mice by an interferon-like molecule. / Vogel, S. N.; Weedon, L. L.; Moore, R. N.; Rosenstreich, David L.

In: Journal of Immunology, Vol. 128, No. 1, 1982, p. 380-387.

Research output: Contribution to journalArticle

@article{95def1ac0795418aafccc891345c7375,
title = "Correction of defective macrophage differentiation in C3H/HeJ mice by an interferon-like molecule",
abstract = "C3H/HeJ mice possess macrophages that lose the capacity to bind and phagocytose opsonized sheep erythrocytes (EA) when cultured. This defect in Fc receptor capacity is completely overcome by treatment of macrophage monolayers with extremely low concentrations of a lymphokine-rich, Con A-stimulated spleen cell supernatant. In this study we have pursued a biochemical and functional analysis of the lymphokine-rich supernatant to determine the nature of the specific factor responsible for the restoration of Fc receptor function. The chromatographic behavior and physical properties, its co-elution with anti-viral activity through a sequential purification scheme, the parallel activity of purified β-interferon in enhancing both the binding and phagocytosis of EA, and the abrogation of factor-induced Fc-mediated phagocytosis with anti-Type II interferon antiserum, strongly support the hypothesis that the active factor is γ- (Type II or immune) interferon (IFN). These studies suggest γ-IFN may act as a differentiative signal to the macrophage by facilitating enhanced expression of macrophage surface membrane components.",
author = "Vogel, {S. N.} and Weedon, {L. L.} and Moore, {R. N.} and Rosenstreich, {David L.}",
year = "1982",
language = "English (US)",
volume = "128",
pages = "380--387",
journal = "Journal of Immunology",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "1",

}

TY - JOUR

T1 - Correction of defective macrophage differentiation in C3H/HeJ mice by an interferon-like molecule

AU - Vogel, S. N.

AU - Weedon, L. L.

AU - Moore, R. N.

AU - Rosenstreich, David L.

PY - 1982

Y1 - 1982

N2 - C3H/HeJ mice possess macrophages that lose the capacity to bind and phagocytose opsonized sheep erythrocytes (EA) when cultured. This defect in Fc receptor capacity is completely overcome by treatment of macrophage monolayers with extremely low concentrations of a lymphokine-rich, Con A-stimulated spleen cell supernatant. In this study we have pursued a biochemical and functional analysis of the lymphokine-rich supernatant to determine the nature of the specific factor responsible for the restoration of Fc receptor function. The chromatographic behavior and physical properties, its co-elution with anti-viral activity through a sequential purification scheme, the parallel activity of purified β-interferon in enhancing both the binding and phagocytosis of EA, and the abrogation of factor-induced Fc-mediated phagocytosis with anti-Type II interferon antiserum, strongly support the hypothesis that the active factor is γ- (Type II or immune) interferon (IFN). These studies suggest γ-IFN may act as a differentiative signal to the macrophage by facilitating enhanced expression of macrophage surface membrane components.

AB - C3H/HeJ mice possess macrophages that lose the capacity to bind and phagocytose opsonized sheep erythrocytes (EA) when cultured. This defect in Fc receptor capacity is completely overcome by treatment of macrophage monolayers with extremely low concentrations of a lymphokine-rich, Con A-stimulated spleen cell supernatant. In this study we have pursued a biochemical and functional analysis of the lymphokine-rich supernatant to determine the nature of the specific factor responsible for the restoration of Fc receptor function. The chromatographic behavior and physical properties, its co-elution with anti-viral activity through a sequential purification scheme, the parallel activity of purified β-interferon in enhancing both the binding and phagocytosis of EA, and the abrogation of factor-induced Fc-mediated phagocytosis with anti-Type II interferon antiserum, strongly support the hypothesis that the active factor is γ- (Type II or immune) interferon (IFN). These studies suggest γ-IFN may act as a differentiative signal to the macrophage by facilitating enhanced expression of macrophage surface membrane components.

UR - http://www.scopus.com/inward/record.url?scp=0020081109&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0020081109&partnerID=8YFLogxK

M3 - Article

VL - 128

SP - 380

EP - 387

JO - Journal of Immunology

JF - Journal of Immunology

SN - 0022-1767

IS - 1

ER -