Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 105, Issue 1, Pages 61-70Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI7589
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Funding
- NATIONAL CANCER INSTITUTE [T32CA009302] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI024571, R01AI026322] Funding Source: NIH RePORTER
- NCI NIH HHS [T32 CA009302, CA-09302] Funding Source: Medline
- NIAID NIH HHS [R01 AI026322, R01AI24571, R01AI26322] Funding Source: Medline
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T helper 2 (Th2) cells play a critical role in the pathogenesis of asthma, but the precise immunological mechanisms that inhibit Th2 cell function in vivo are not well understood Using gene therapy, we demonstrated that ovalbumin-specific (OVA-specific) Th cells engineered to express latent TGF-beta abolished airway hyperreactivity and airway inflammation induced by OVA-specific Th2 effector cells in SCID and BALB/c mice. These effects correlated with increased concentrations of active TGF-beta in the bronchoalveolar lavage (BAL) fluid, demonstrating that latent TGF-beta was activated in the inflammatory environment. In contrast, OVA-specific Th1 cells failed to inhibit airway hyperreactivity and inflammation in this system. The inhibitory effect of TGF-beta-secreting Th cells was antigen-specific and was reversed by neutralization of TGF-beta. Our results demonstrate that T cells secreting TGF-beta in the respiratory mucosa can indeed regulate Th2-induced airway hyperreactivity and inflammation and suggest that TGF-beta-producing T cells play an important regulatory role in asthma.
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