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Interleukin 12 (IL-12) is crucial to the development of protective immunity in mice intravenously infected with mycobacterium tuberculosis.

Cooper AM, Magram J, Ferrante J, Orme IM - J. Exp. Med. (1997)

Bottom Line: Immunity to Mycobacterium tuberculosis infection is associated with the emergence of protective CD4 T cells that secrete cytokines, resulting in activation of macrophages and the recruitment of monocytes to initiate granuloma formation.The cytokine-mediating macrophage activation is interferon-gamma (IFN-gamma), which is largely dependent on interleukin-12 (IL-12) for its induction.T cell activation as measured by delayed type hypersensitivity and lymphocyte accumulation at the site of infection were both markedly reduced in the IL-12 p40(-/-) mice.

View Article: PubMed Central - PubMed

Affiliation: Department of Microbiology, Colorado State University, Fort Collins, Colorado 80523, USA.

ABSTRACT
Immunity to Mycobacterium tuberculosis infection is associated with the emergence of protective CD4 T cells that secrete cytokines, resulting in activation of macrophages and the recruitment of monocytes to initiate granuloma formation. The cytokine-mediating macrophage activation is interferon-gamma (IFN-gamma), which is largely dependent on interleukin-12 (IL-12) for its induction. To address the role of IL-12 in immunity to tuberculosis, IL-12 p40(-/-) mice were infected with M. tuberculosis and their capacity to control bacterial growth and other characteristics of their immune response were determined. The IL-12 p40(-/-) mice were unable to control bacterial growth and this appeared to be linked to the absence of both innate and acquired sources of IFN-gamma. T cell activation as measured by delayed type hypersensitivity and lymphocyte accumulation at the site of infection were both markedly reduced in the IL-12 p40(-/-) mice. Therefore, IL-12 is essential to the generation of a protective immune response to M. tuberculosis, with its main functions being the induction of the expression of IFN-gamma and the activation of antigen-specific lymphocytes capable of creating a protective granuloma.

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IL-12 p40−/− mice have defective granuloma formation. Tissue from infected control (A) and IL-12 p40−/− (B) mice was fixed in formal saline, sectioned, and stained with hematoxylin and eosin. At sites of mononuclear accumulation in the lung tissue there are more lymphocytes in the control (A) tissue compared with IL-12 p40−/− (B) tissue. Original magnification ×200.
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Figure 5: IL-12 p40−/− mice have defective granuloma formation. Tissue from infected control (A) and IL-12 p40−/− (B) mice was fixed in formal saline, sectioned, and stained with hematoxylin and eosin. At sites of mononuclear accumulation in the lung tissue there are more lymphocytes in the control (A) tissue compared with IL-12 p40−/− (B) tissue. Original magnification ×200.

Mentions: The absence of a strong DTH in the IL-12 p40−/− mice was mirrored in the lower number of lymphocytes in the lung granulomas of IL-12–deficient animals (Fig. 5). Many macrophages in the IL-12 p40−/− tissues appeared vacuolated due to the presence of large numbers of bacteria, whereas bacteria are very sparse in the tissues of C57BL/6 control mice.


Interleukin 12 (IL-12) is crucial to the development of protective immunity in mice intravenously infected with mycobacterium tuberculosis.

Cooper AM, Magram J, Ferrante J, Orme IM - J. Exp. Med. (1997)

IL-12 p40−/− mice have defective granuloma formation. Tissue from infected control (A) and IL-12 p40−/− (B) mice was fixed in formal saline, sectioned, and stained with hematoxylin and eosin. At sites of mononuclear accumulation in the lung tissue there are more lymphocytes in the control (A) tissue compared with IL-12 p40−/− (B) tissue. Original magnification ×200.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2198958&req=5

Figure 5: IL-12 p40−/− mice have defective granuloma formation. Tissue from infected control (A) and IL-12 p40−/− (B) mice was fixed in formal saline, sectioned, and stained with hematoxylin and eosin. At sites of mononuclear accumulation in the lung tissue there are more lymphocytes in the control (A) tissue compared with IL-12 p40−/− (B) tissue. Original magnification ×200.
Mentions: The absence of a strong DTH in the IL-12 p40−/− mice was mirrored in the lower number of lymphocytes in the lung granulomas of IL-12–deficient animals (Fig. 5). Many macrophages in the IL-12 p40−/− tissues appeared vacuolated due to the presence of large numbers of bacteria, whereas bacteria are very sparse in the tissues of C57BL/6 control mice.

Bottom Line: Immunity to Mycobacterium tuberculosis infection is associated with the emergence of protective CD4 T cells that secrete cytokines, resulting in activation of macrophages and the recruitment of monocytes to initiate granuloma formation.The cytokine-mediating macrophage activation is interferon-gamma (IFN-gamma), which is largely dependent on interleukin-12 (IL-12) for its induction.T cell activation as measured by delayed type hypersensitivity and lymphocyte accumulation at the site of infection were both markedly reduced in the IL-12 p40(-/-) mice.

View Article: PubMed Central - PubMed

Affiliation: Department of Microbiology, Colorado State University, Fort Collins, Colorado 80523, USA.

ABSTRACT
Immunity to Mycobacterium tuberculosis infection is associated with the emergence of protective CD4 T cells that secrete cytokines, resulting in activation of macrophages and the recruitment of monocytes to initiate granuloma formation. The cytokine-mediating macrophage activation is interferon-gamma (IFN-gamma), which is largely dependent on interleukin-12 (IL-12) for its induction. To address the role of IL-12 in immunity to tuberculosis, IL-12 p40(-/-) mice were infected with M. tuberculosis and their capacity to control bacterial growth and other characteristics of their immune response were determined. The IL-12 p40(-/-) mice were unable to control bacterial growth and this appeared to be linked to the absence of both innate and acquired sources of IFN-gamma. T cell activation as measured by delayed type hypersensitivity and lymphocyte accumulation at the site of infection were both markedly reduced in the IL-12 p40(-/-) mice. Therefore, IL-12 is essential to the generation of a protective immune response to M. tuberculosis, with its main functions being the induction of the expression of IFN-gamma and the activation of antigen-specific lymphocytes capable of creating a protective granuloma.

Show MeSH
Related in: MedlinePlus