IL-9 is associated with an impaired Th1 immune response 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.clim.2007.09.009

IL-9 is associated with an impaired Th1 immune response 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

55 Scopus citations

Abstract

Although a defective Th1 response has been demonstrated in patients infected with Mycobacterium tuberculosis (Mtb), the mechanisms leading to this defect are not well understood. To study the immune response to Mtb infection, we stimulated PBMC from individuals with latent tuberculosis infection (LTBI) or patients with tuberculosis (TB) with the Mtb specific antigen early secretory antigenic target-6 (ESAT-6). mRNAs for a panel of cytokines were measured using quantitative real-time PCR (qPCR). PBMC from TB patients exhibited low levels of IFN-γ, IL-12α, IL-12β, and IL-23 mRNA but high levels of IL-9 mRNA. Sera from TB patients blocked the differentiation and function of dendritic cells from TST negative (TST-) donors. Exogenous IL-9 reduced IFN-γ mRNA expression in PBMC from LTBI by 30% (n = 4) and neutralization of IL-9 restored the IFN-γ mRNA expression in PBMC from TB patients by 66% (n = 8). Thus, increased expression of IL-9 may contribute to the development of TB.

Original language	English (US)
Pages (from-to)	202-210
Number of pages	9
Journal	Clinical Immunology
Volume	126
Issue number	2
DOIs	https://doi.org/10.1016/j.clim.2007.09.009
State	Published - Feb 2008

Keywords

Cytokines;
Dendritic cell;
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.clim.2007.09.009

Cite this

@article{73a1c467208540dc89764e6858658084,

title = "IL-9 is associated with an impaired Th1 immune response in patients with tuberculosis",

abstract = "Although a defective Th1 response has been demonstrated in patients infected with Mycobacterium tuberculosis (Mtb), the mechanisms leading to this defect are not well understood. To study the immune response to Mtb infection, we stimulated PBMC from individuals with latent tuberculosis infection (LTBI) or patients with tuberculosis (TB) with the Mtb specific antigen early secretory antigenic target-6 (ESAT-6). mRNAs for a panel of cytokines were measured using quantitative real-time PCR (qPCR). PBMC from TB patients exhibited low levels of IFN-γ, IL-12α, IL-12β, and IL-23 mRNA but high levels of IL-9 mRNA. Sera from TB patients blocked the differentiation and function of dendritic cells from TST negative (TST-) donors. Exogenous IL-9 reduced IFN-γ mRNA expression in PBMC from LTBI by 30% (n = 4) and neutralization of IL-9 restored the IFN-γ mRNA expression in PBMC from TB patients by 66% (n = 8). Thus, increased expression of IL-9 may contribute to the development of TB.",

keywords = "Cytokines;, Dendritic cell;, 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 the recombinant proteins 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. This work was supported by grants from the National Institutes of Health (RO1 AI051356, to C.C., and RO1 AI034238 to P.C.H.).",

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doi = "10.1016/j.clim.2007.09.009",

language = "English (US)",

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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 the recombinant proteins 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. This work was supported by grants from the National Institutes of Health (RO1 AI051356, to C.C., and RO1 AI034238 to P.C.H.).

PY - 2008/2

Y1 - 2008/2

N2 - Although a defective Th1 response has been demonstrated in patients infected with Mycobacterium tuberculosis (Mtb), the mechanisms leading to this defect are not well understood. To study the immune response to Mtb infection, we stimulated PBMC from individuals with latent tuberculosis infection (LTBI) or patients with tuberculosis (TB) with the Mtb specific antigen early secretory antigenic target-6 (ESAT-6). mRNAs for a panel of cytokines were measured using quantitative real-time PCR (qPCR). PBMC from TB patients exhibited low levels of IFN-γ, IL-12α, IL-12β, and IL-23 mRNA but high levels of IL-9 mRNA. Sera from TB patients blocked the differentiation and function of dendritic cells from TST negative (TST-) donors. Exogenous IL-9 reduced IFN-γ mRNA expression in PBMC from LTBI by 30% (n = 4) and neutralization of IL-9 restored the IFN-γ mRNA expression in PBMC from TB patients by 66% (n = 8). Thus, increased expression of IL-9 may contribute to the development of TB.

AB - Although a defective Th1 response has been demonstrated in patients infected with Mycobacterium tuberculosis (Mtb), the mechanisms leading to this defect are not well understood. To study the immune response to Mtb infection, we stimulated PBMC from individuals with latent tuberculosis infection (LTBI) or patients with tuberculosis (TB) with the Mtb specific antigen early secretory antigenic target-6 (ESAT-6). mRNAs for a panel of cytokines were measured using quantitative real-time PCR (qPCR). PBMC from TB patients exhibited low levels of IFN-γ, IL-12α, IL-12β, and IL-23 mRNA but high levels of IL-9 mRNA. Sera from TB patients blocked the differentiation and function of dendritic cells from TST negative (TST-) donors. Exogenous IL-9 reduced IFN-γ mRNA expression in PBMC from LTBI by 30% (n = 4) and neutralization of IL-9 restored the IFN-γ mRNA expression in PBMC from TB patients by 66% (n = 8). Thus, increased expression of IL-9 may contribute to the development of TB.

KW - Cytokines;

KW - Dendritic cell;

KW - Human

KW - Mycobacterium tuberculosis;

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IL-9 is associated with an impaired Th1 immune response in patients with tuberculosis

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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