Dichotomous role of TGF-β controls inducible regulatory T-cell fate in allergic airway disease through Smad3 and TGF-β–activated kinase 1

2020 ◽  
Vol 145 (3) ◽  
pp. 933-946.e4
Author(s):  
Anthony Joetham ◽  
Michaela Schedel ◽  
Fangkun Ning ◽  
Meiqin Wang ◽  
Katsuyuki Takeda ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Fate ◽  
Regulatory T Cell ◽  
Airway Disease ◽  
Allergic Airway Disease

Eotaxin/CCL11 is involved in acute, but not chronic, allergic airway responses toAspergillus fumigatus

2002 ◽  
Vol 283 (1) ◽  
pp. L198-L204 ◽  
Author(s):  
Jane M. Schuh ◽  
Kate Blease ◽  
Steven L. Kunkel ◽  
Cory M. Hogaboam
Keyword(s):  
T Cell ◽  
Airway Hyperresponsiveness ◽  
Airway Disease ◽  
Allergic Airway Disease ◽  
Th2 Cells ◽  
Wild Type ◽  
Cell Recruitment ◽  
Chronic Model ◽  
Airway Responses

Eotaxin/CCL11 is a major chemoattractant for eosinophils and Th2 cells. As such, it represents an attractive target in the treatment of allergic disease. The present study addresses the role of eotaxin/CCL11 during acute and chronic allergic airway responses to the fungus Aspergillus fumigatus. Mice lacking the eotaxin gene (Eo−/−) and wild-type mice (Eo+/+) were sensitized to A. fumigatus and received either an intratracheal challenge with soluble A. fumigatusantigens (acute model) or an intratracheal challenge with live A. fumigatus spores or conidia (chronic model). Airway hyperresponsiveness and eosinophil, but not T cell, recruitment were significantly decreased at 24 h after the soluble allergen in A. fumigatus-sensitized Eo−/− mice compared with similarly sensitized Eo+/+ mice. In contrast, the development of chronic allergic airway disease due to A. fumigatus conidia was not altered by the lack of eotaxin. Together, these data suggest that eotaxin initiates allergic airway disease due to A. fumigatus, but this chemokine did not appear to contribute to the maintenance of A. fumigatus-induced allergic airway disease.

scholarly journals Role of conserved non-coding DNA elements in the Foxp3 gene in regulatory T-cell fate

Nature ◽  
2010 ◽  
Vol 463 (7282) ◽  
pp. 808-812 ◽  
Author(s):  
Ye Zheng ◽  
Steven Josefowicz ◽  
Ashutosh Chaudhry ◽  
Xiao P. Peng ◽  
Katherine Forbush ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Fate ◽  
Regulatory T Cell ◽  
Foxp3 Gene ◽  
Dna Elements

scholarly journals Role of Macrophage Migration Inhibitory Factor in the Regulatory T Cell Response of Tumor-Bearing Mice

2012 ◽  
Vol 189 (8) ◽  
pp. 3905-3913 ◽  
Author(s):  
Susanna Choi ◽  
Hang-Rae Kim ◽  
Lin Leng ◽  
Insoo Kang ◽  
William L. Jorgensen ◽  
...  
Keyword(s):  
T Cell ◽  
Migration Inhibitory Factor ◽  
Regulatory T Cell ◽  
Cell Response ◽  
Macrophage Migration Inhibitory Factor ◽  
T Cell Response ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Tumor Bearing

scholarly journals Maternal endotoxin exposure attenuates allergic airway disease in infant rats

2010 ◽  
Vol 298 (5) ◽  
pp. L670-L677 ◽  
Author(s):  
Lei Cao ◽  
Jinxia Wang ◽  
Yingchun Zhu ◽  
Irene Tseu ◽  
Martin Post
Keyword(s):  
Transcription Factors ◽  
Cell Differentiation ◽  
T Cell ◽  
Airway Disease ◽  
Positive Control ◽  
Allergic Airway Disease ◽  
T Helper ◽  
T Helper 1 ◽  
Pregnant Rats ◽  
Neonatal Immune System

Prenatal exposures to immunogenic stimuli, such as bacterial LPS, have shown to influence the neonatal immune system and lung function. However, no detailed analysis of the immunomodulatory effects of LPS on postnatal T helper cell differentiation has been performed. Using a rat model, we investigated the effect of prenatal LPS exposure on postnatal T cell differentiation and experimental allergic airway disease. Pregnant rats were injected with LPS on day 20 and 21 (term = 22 days). Some of the offspring were sensitized and challenged with ovalbumin. Positive control animals were placebo exposed to saline instead of LPS, whereas negative controls were sensitized with saline. Expression of T cell-related transcription factors and cytokines was quantified in the lung, and airway hyperresponsiveness was measured. Prenatal LPS exposure induced a T helper 1 (TH1) immune milieu in the offspring of rats [i.e., increased T-bet and TH1 cytokine expression while expression of TH2-associated transcription factors (GATA3 and STAT6) and cytokines was decreased]. Prenatal LPS exposure did not trigger TH17 cell differentiation in the offspring. Furthermore, prenatal LPS exposure reduced ovalbumin-induced (TH2-mediated) airway inflammation, eosinophilia, and airway responsiveness. Thus, in utero exposure to endotoxin promotes a TH1 immune environment, which suppresses the development of allergic airway disease later in life.

Investigating the Role of Relaxin in the Regulation of Airway Fibrosis in Animal Models of Acute and Chronic Allergic Airway Disease

2005 ◽  
Vol 1041 (1) ◽  
pp. 194-196 ◽  
Author(s):  
ISHANEE MOOKERJEE ◽  
MIMI L.K. TANG ◽  
NATASHA SOLLY ◽  
GEOFFREY W. TREGEAR ◽  
CHRISHAN S. SAMUEL
Keyword(s):  
Animal Models ◽  
Airway Disease ◽  
Allergic Airway Disease ◽  
Airway Fibrosis
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