IL-24 modulates IFN-γ expression in patients with tuberculosis

Bo Wu; Chunhong Huang; Midori Kato-Maeda; Philip C. Hopewell; Charles L. Daley; Alan M. Krensky; Carol Clayberger

doi:10.1016/j.imlet.2007.11.018

IL-24 modulates IFN-γ expression in patients with tuberculosis

Bo Wu, Chunhong Huang, Midori Kato-Maeda, Philip C. Hopewell, Charles L. Daley, Alan M. Krensky, Carol Clayberger^*

^*Corresponding author for this work

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

13 Scopus citations

Abstract

IL-24 is a newly described member of the IL-10 family. We previously demonstrated that PBMC from TB patients exhibited low levels of IL-24 and IFN-γ compared to subjects with latent tuberculosis infection (LTBI). In order to investigate the role of IL-24 in IFN-γ expression in TB patients, we stimulated PBMC from individuals with LTBI or TB patients with the Mtb-specific antigen, early secretory antigenic target-6 (ESAT-6) and measured cytokine expression using quantitative real-time PCR (qPCR). Exogenous IL-24 increased IFN-γ expression in PBMC obtained from TB patients while neutralization of IL-24 reduced IFN-γ expression in PBMC from subjects with LTBI. Exogenous IL-24 enhanced IFN-γ expression by increasing expression of IL-12 family cytokines, including IL-12α, IL-12β, IL-23α and IL-27, and by reducing FOXP3 expression in PBMC from TB patients. This is the first demonstration that IL-24 may play an important role in IFN-γ expression following infection with Mtb.

Original language	English (US)
Pages (from-to)	57-62
Number of pages	6
Journal	Immunology Letters
Volume	117
Issue number	1
DOIs	https://doi.org/10.1016/j.imlet.2007.11.018
State	Published - Apr 15 2008

Keywords

Cytokine
Human
Mycobacterium tuberculosis

ASJC Scopus subject areas

Immunology and Allergy
Immunology

UN SDGs

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

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10.1016/j.imlet.2007.11.018

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title = "IL-24 modulates IFN-γ expression in patients with tuberculosis",

abstract = "IL-24 is a newly described member of the IL-10 family. We previously demonstrated that PBMC from TB patients exhibited low levels of IL-24 and IFN-γ compared to subjects with latent tuberculosis infection (LTBI). In order to investigate the role of IL-24 in IFN-γ expression in TB patients, we stimulated PBMC from individuals with LTBI or TB patients with the Mtb-specific antigen, early secretory antigenic target-6 (ESAT-6) and measured cytokine expression using quantitative real-time PCR (qPCR). Exogenous IL-24 increased IFN-γ expression in PBMC obtained from TB patients while neutralization of IL-24 reduced IFN-γ expression in PBMC from subjects with LTBI. Exogenous IL-24 enhanced IFN-γ expression by increasing expression of IL-12 family cytokines, including IL-12α, IL-12β, IL-23α and IL-27, and by reducing FOXP3 expression in PBMC from TB patients. This is the first demonstration that IL-24 may play an important role in IFN-γ expression following infection with Mtb.",

keywords = "Cytokine, Human, Mycobacterium tuberculosis",

author = "Bo Wu and Chunhong Huang and Midori Kato-Maeda and Hopewell, {Philip C.} and Daley, {Charles L.} and Krensky, {Alan M.} and Carol Clayberger",

note = "Funding Information: We are grateful to Colorado State University and the NIH, NIAID Contract NO 1 AI-75320, entitled “Tuberculosis Research Materials and Vaccine Testing” for providing ESAT-6 used in this study and to the TB Clinic at the San Francisco Department of Public Health. We thank Irina Rudoy and Cynthia Merrifield for recruitment of TB patients, blood drawing and data collection, Shu-Chen Lyu for technical assistance, and Gary Schoolnik and Peter Small for helpful discussions. ",

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AU - Wu, Bo

AU - Huang, Chunhong

AU - Kato-Maeda, Midori

AU - Hopewell, Philip C.

AU - Daley, Charles L.

AU - Krensky, Alan M.

AU - Clayberger, Carol

N1 - Funding Information: We are grateful to Colorado State University and the NIH, NIAID Contract NO 1 AI-75320, entitled “Tuberculosis Research Materials and Vaccine Testing” for providing ESAT-6 used in this study and to the TB Clinic at the San Francisco Department of Public Health. We thank Irina Rudoy and Cynthia Merrifield for recruitment of TB patients, blood drawing and data collection, Shu-Chen Lyu for technical assistance, and Gary Schoolnik and Peter Small for helpful discussions.

PY - 2008/4/15

Y1 - 2008/4/15

N2 - IL-24 is a newly described member of the IL-10 family. We previously demonstrated that PBMC from TB patients exhibited low levels of IL-24 and IFN-γ compared to subjects with latent tuberculosis infection (LTBI). In order to investigate the role of IL-24 in IFN-γ expression in TB patients, we stimulated PBMC from individuals with LTBI or TB patients with the Mtb-specific antigen, early secretory antigenic target-6 (ESAT-6) and measured cytokine expression using quantitative real-time PCR (qPCR). Exogenous IL-24 increased IFN-γ expression in PBMC obtained from TB patients while neutralization of IL-24 reduced IFN-γ expression in PBMC from subjects with LTBI. Exogenous IL-24 enhanced IFN-γ expression by increasing expression of IL-12 family cytokines, including IL-12α, IL-12β, IL-23α and IL-27, and by reducing FOXP3 expression in PBMC from TB patients. This is the first demonstration that IL-24 may play an important role in IFN-γ expression following infection with Mtb.

AB - IL-24 is a newly described member of the IL-10 family. We previously demonstrated that PBMC from TB patients exhibited low levels of IL-24 and IFN-γ compared to subjects with latent tuberculosis infection (LTBI). In order to investigate the role of IL-24 in IFN-γ expression in TB patients, we stimulated PBMC from individuals with LTBI or TB patients with the Mtb-specific antigen, early secretory antigenic target-6 (ESAT-6) and measured cytokine expression using quantitative real-time PCR (qPCR). Exogenous IL-24 increased IFN-γ expression in PBMC obtained from TB patients while neutralization of IL-24 reduced IFN-γ expression in PBMC from subjects with LTBI. Exogenous IL-24 enhanced IFN-γ expression by increasing expression of IL-12 family cytokines, including IL-12α, IL-12β, IL-23α and IL-27, and by reducing FOXP3 expression in PBMC from TB patients. This is the first demonstration that IL-24 may play an important role in IFN-γ expression following infection with Mtb.

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KW - Human

KW - Mycobacterium tuberculosis

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IL-24 modulates IFN-γ expression in patients with tuberculosis

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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