The roles of tumor necrosis factor-α, interleukin-1 and interleukin-12 in murine cytomegalovirus infection

S. T. Yerkovich, S. D. Olver, J. C. Lenzo, C. D. Peacock, P. Price

Research output: Contribution to journalArticle

Abstract

The roles of the inflammatory cytokines tumour necrosis factor-α (TNF-α), interleukin-1 (IL-1) and IL-12, in murine cytomegalovirus (MCMV) disease were investigated in susceptible BALB/c and resistant C57BL/6 mice. MCMV infection induced IL-1 and TNF-α production by peritoneal cells from BALB/c mice, as demonstrated previously in C57BL/6 mice. Overt ill-health and viral replication in the spleens of BALB/c mice were increased by in vivo treatment with soluble TNFα receptors to inhibit the activity of this cytokine, whilst antibodies to IL-12 had a similar but more restricted effect. C57BL/6 mice were not affected by either treatment, suggesting TNF-α and IL-12 are not critical for natural killer cell-mediated restriction of viral replication in the spleen. Soluble TNF-α receptors and antibodies to IL-12 also enhanced MCMV titres and numbers of viral antigen-positive cells in the livers of BALB/c mice and TNF-α receptors have similar effects in C57BL/6 livers. In contrast, IL-1 receptors improved the health of MCMV-infected BALB/c mice and reduced viral replication and hepatitis at some time-points. Mechanisms which may underlie these changes are discussed.

Original languageEnglish (US)
Pages (from-to)45-52
Number of pages8
JournalImmunology
Volume91
Issue number1
StatePublished - 1997
Externally publishedYes

Fingerprint

Muromegalovirus
Cytomegalovirus Infections
Interleukin-12
Interleukin-1
Tumor Necrosis Factor Receptors
Tumor Necrosis Factor-alpha
Inbred C57BL Mouse
Spleen
Cytokines
Interleukin-1 Receptors
Viral Antigens
Antibodies
Liver
Health
Natural Killer Cells
Hepatitis

ASJC Scopus subject areas

  • Immunology

Cite this

Yerkovich, S. T., Olver, S. D., Lenzo, J. C., Peacock, C. D., & Price, P. (1997). The roles of tumor necrosis factor-α, interleukin-1 and interleukin-12 in murine cytomegalovirus infection. Immunology, 91(1), 45-52.

The roles of tumor necrosis factor-α, interleukin-1 and interleukin-12 in murine cytomegalovirus infection. / Yerkovich, S. T.; Olver, S. D.; Lenzo, J. C.; Peacock, C. D.; Price, P.

In: Immunology, Vol. 91, No. 1, 1997, p. 45-52.

Research output: Contribution to journalArticle

Yerkovich, ST, Olver, SD, Lenzo, JC, Peacock, CD & Price, P 1997, 'The roles of tumor necrosis factor-α, interleukin-1 and interleukin-12 in murine cytomegalovirus infection', Immunology, vol. 91, no. 1, pp. 45-52.
Yerkovich, S. T. ; Olver, S. D. ; Lenzo, J. C. ; Peacock, C. D. ; Price, P. / The roles of tumor necrosis factor-α, interleukin-1 and interleukin-12 in murine cytomegalovirus infection. In: Immunology. 1997 ; Vol. 91, No. 1. pp. 45-52.
@article{8b9b8dd07c98403cb7ed57420d317223,
title = "The roles of tumor necrosis factor-α, interleukin-1 and interleukin-12 in murine cytomegalovirus infection",
abstract = "The roles of the inflammatory cytokines tumour necrosis factor-α (TNF-α), interleukin-1 (IL-1) and IL-12, in murine cytomegalovirus (MCMV) disease were investigated in susceptible BALB/c and resistant C57BL/6 mice. MCMV infection induced IL-1 and TNF-α production by peritoneal cells from BALB/c mice, as demonstrated previously in C57BL/6 mice. Overt ill-health and viral replication in the spleens of BALB/c mice were increased by in vivo treatment with soluble TNFα receptors to inhibit the activity of this cytokine, whilst antibodies to IL-12 had a similar but more restricted effect. C57BL/6 mice were not affected by either treatment, suggesting TNF-α and IL-12 are not critical for natural killer cell-mediated restriction of viral replication in the spleen. Soluble TNF-α receptors and antibodies to IL-12 also enhanced MCMV titres and numbers of viral antigen-positive cells in the livers of BALB/c mice and TNF-α receptors have similar effects in C57BL/6 livers. In contrast, IL-1 receptors improved the health of MCMV-infected BALB/c mice and reduced viral replication and hepatitis at some time-points. Mechanisms which may underlie these changes are discussed.",
author = "Yerkovich, {S. T.} and Olver, {S. D.} and Lenzo, {J. C.} and Peacock, {C. D.} and P. Price",
year = "1997",
language = "English (US)",
volume = "91",
pages = "45--52",
journal = "Immunology",
issn = "0019-2805",
publisher = "Wiley-Blackwell",
number = "1",

}

TY - JOUR

T1 - The roles of tumor necrosis factor-α, interleukin-1 and interleukin-12 in murine cytomegalovirus infection

AU - Yerkovich, S. T.

AU - Olver, S. D.

AU - Lenzo, J. C.

AU - Peacock, C. D.

AU - Price, P.

PY - 1997

Y1 - 1997

N2 - The roles of the inflammatory cytokines tumour necrosis factor-α (TNF-α), interleukin-1 (IL-1) and IL-12, in murine cytomegalovirus (MCMV) disease were investigated in susceptible BALB/c and resistant C57BL/6 mice. MCMV infection induced IL-1 and TNF-α production by peritoneal cells from BALB/c mice, as demonstrated previously in C57BL/6 mice. Overt ill-health and viral replication in the spleens of BALB/c mice were increased by in vivo treatment with soluble TNFα receptors to inhibit the activity of this cytokine, whilst antibodies to IL-12 had a similar but more restricted effect. C57BL/6 mice were not affected by either treatment, suggesting TNF-α and IL-12 are not critical for natural killer cell-mediated restriction of viral replication in the spleen. Soluble TNF-α receptors and antibodies to IL-12 also enhanced MCMV titres and numbers of viral antigen-positive cells in the livers of BALB/c mice and TNF-α receptors have similar effects in C57BL/6 livers. In contrast, IL-1 receptors improved the health of MCMV-infected BALB/c mice and reduced viral replication and hepatitis at some time-points. Mechanisms which may underlie these changes are discussed.

AB - The roles of the inflammatory cytokines tumour necrosis factor-α (TNF-α), interleukin-1 (IL-1) and IL-12, in murine cytomegalovirus (MCMV) disease were investigated in susceptible BALB/c and resistant C57BL/6 mice. MCMV infection induced IL-1 and TNF-α production by peritoneal cells from BALB/c mice, as demonstrated previously in C57BL/6 mice. Overt ill-health and viral replication in the spleens of BALB/c mice were increased by in vivo treatment with soluble TNFα receptors to inhibit the activity of this cytokine, whilst antibodies to IL-12 had a similar but more restricted effect. C57BL/6 mice were not affected by either treatment, suggesting TNF-α and IL-12 are not critical for natural killer cell-mediated restriction of viral replication in the spleen. Soluble TNF-α receptors and antibodies to IL-12 also enhanced MCMV titres and numbers of viral antigen-positive cells in the livers of BALB/c mice and TNF-α receptors have similar effects in C57BL/6 livers. In contrast, IL-1 receptors improved the health of MCMV-infected BALB/c mice and reduced viral replication and hepatitis at some time-points. Mechanisms which may underlie these changes are discussed.

UR - http://www.scopus.com/inward/record.url?scp=0030612172&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030612172&partnerID=8YFLogxK

M3 - Article

C2 - 9203964

AN - SCOPUS:0030612172

VL - 91

SP - 45

EP - 52

JO - Immunology

JF - Immunology

SN - 0019-2805

IS - 1

ER -