Tumor necrosis factor-α is required in the protective immune response against mycobacterium tuberculosis in mice

Jo Anne L. Flynn; Marsha M. Goldstein; John Chan; Karla J. Triebold; Klaus Pfeffer; Charles J. Lowenstein; Robert Schrelber; Tak W. Mak; Barry R. Bloom

doi:10.1016/1074-7613(95)90001-2

Tumor necrosis factor-α is required in the protective immune response against mycobacterium tuberculosis in mice

Jo Anne L. Flynn, Marsha M. Goldstein, John Chan, Karla J. Triebold, Klaus Pfeffer, Charles J. Lowenstein, Robert Schrelber, Tak W. Mak, Barry R. Bloom

Medicine

Research output: Contribution to journal › Article › peer-review

1410 Scopus citations

Abstract

Understanding the immunological mechanisms of protection and pathogenesis in tuberculosis remains problematic. We have examined the extent to which tumor necrosis factor-α (TNFα) contributes to this disease using murine models In which the action of TNFα is inhibited. TNFa was neutralized In vivo by monoclonal antibody; in addition, a mouse strain with a disruption in the gene for the 55 kDa TNF receptor was used. The data from both models established that TNFα and the 55 kDa TNF receptor are essential for protection against tuberculosis in mice, and for reactive nitrogen production by macrophages early in infection. Granulomas were formed in equal numbers in control and experimental mice, but necrosis was observed only in mice deficient in TNFα or TNF receptor. TNFα and the 55 kDa TNF receptor are necessary conditions for protection against murine M. tuberculosis infection, but are not solely responsible for the tissue damage observed.

Original language	English (US)
Pages (from-to)	561-572
Number of pages	12
Journal	Immunity
Volume	2
Issue number	6
DOIs	https://doi.org/10.1016/1074-7613(95)90001-2
State	Published - Jun 1995

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Infectious Diseases

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/1074-7613(95)90001-2

Cite this

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title = "Tumor necrosis factor-α is required in the protective immune response against mycobacterium tuberculosis in mice",

abstract = "Understanding the immunological mechanisms of protection and pathogenesis in tuberculosis remains problematic. We have examined the extent to which tumor necrosis factor-α (TNFα) contributes to this disease using murine models In which the action of TNFα is inhibited. TNFa was neutralized In vivo by monoclonal antibody; in addition, a mouse strain with a disruption in the gene for the 55 kDa TNF receptor was used. The data from both models established that TNFα and the 55 kDa TNF receptor are essential for protection against tuberculosis in mice, and for reactive nitrogen production by macrophages early in infection. Granulomas were formed in equal numbers in control and experimental mice, but necrosis was observed only in mice deficient in TNFα or TNF receptor. TNFα and the 55 kDa TNF receptor are necessary conditions for protection against murine M. tuberculosis infection, but are not solely responsible for the tissue damage observed.",

author = "Flynn, {Jo Anne L.} and Goldstein, {Marsha M.} and John Chan and Triebold, {Karla J.} and Klaus Pfeffer and Lowenstein, {Charles J.} and Robert Schrelber and Mak, {Tak W.} and Bloom, {Barry R.}",

year = "1995",

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language = "English (US)",

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journal = "Immunity",

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publisher = "Cell Press",

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T1 - Tumor necrosis factor-α is required in the protective immune response against mycobacterium tuberculosis in mice

AU - Flynn, Jo Anne L.

AU - Goldstein, Marsha M.

AU - Chan, John

AU - Triebold, Karla J.

AU - Pfeffer, Klaus

AU - Lowenstein, Charles J.

AU - Schrelber, Robert

AU - Mak, Tak W.

AU - Bloom, Barry R.

PY - 1995/6

Y1 - 1995/6

N2 - Understanding the immunological mechanisms of protection and pathogenesis in tuberculosis remains problematic. We have examined the extent to which tumor necrosis factor-α (TNFα) contributes to this disease using murine models In which the action of TNFα is inhibited. TNFa was neutralized In vivo by monoclonal antibody; in addition, a mouse strain with a disruption in the gene for the 55 kDa TNF receptor was used. The data from both models established that TNFα and the 55 kDa TNF receptor are essential for protection against tuberculosis in mice, and for reactive nitrogen production by macrophages early in infection. Granulomas were formed in equal numbers in control and experimental mice, but necrosis was observed only in mice deficient in TNFα or TNF receptor. TNFα and the 55 kDa TNF receptor are necessary conditions for protection against murine M. tuberculosis infection, but are not solely responsible for the tissue damage observed.

AB - Understanding the immunological mechanisms of protection and pathogenesis in tuberculosis remains problematic. We have examined the extent to which tumor necrosis factor-α (TNFα) contributes to this disease using murine models In which the action of TNFα is inhibited. TNFa was neutralized In vivo by monoclonal antibody; in addition, a mouse strain with a disruption in the gene for the 55 kDa TNF receptor was used. The data from both models established that TNFα and the 55 kDa TNF receptor are essential for protection against tuberculosis in mice, and for reactive nitrogen production by macrophages early in infection. Granulomas were formed in equal numbers in control and experimental mice, but necrosis was observed only in mice deficient in TNFα or TNF receptor. TNFα and the 55 kDa TNF receptor are necessary conditions for protection against murine M. tuberculosis infection, but are not solely responsible for the tissue damage observed.

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Tumor necrosis factor-α is required in the protective immune response against mycobacterium tuberculosis in mice

Abstract

ASJC Scopus subject areas

UN SDGs

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