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Published on: April 16, 2019
T1/ST2 expression on Th2 cells negatively regulates allergic pulmonary inflammation
Niamh E Mangan1, Ayan Dasvarma, Andrew N J McKenzie
1Institute of Molecular Medicine, Trinity College Dublin, St James's Hospital, Dublin, Ireland.
European Journal of Immunology
|April 5, 2007
Summary
The transmembrane protein ST2 (T1/ST2) normally suppresses allergic lung inflammation in mice. Lacking ST2 on T helper 2 cells exacerbates airway inflammation and hyper-responsiveness.
Area of Science:
- Immunology
- Allergy Research
- Respiratory Medicine
Background:
- Transmembrane T1/ST2 (ST2) is a marker on Th2 cells involved in allergic inflammation.
- The in vivo role of ST2 on T cells in type 2 immune responses remained unclear.
Purpose of the Study:
- To investigate the function of ST2 on T cells in vivo, specifically its role in regulating pulmonary inflammation during allergic responses.
Main Methods:
- Generation of ST2(-/-) mice crossed with ovalbumin (OVA) T cell receptor-transgenic mice.
- In vitro Th2 differentiation and cytokine response assessment.
- Transfer of OVA-specific ST2(-/-) Th2 cells into BALB/c mice to induce pulmonary inflammation.
- Analysis of pulmonary inflammation, airway hyper-responsiveness, and immune cell populations.
Main Results:
- OVA-specific ST2(-/-) Th2 cells showed increased IL-5 production upon stimulation.
- Transfer of these cells led to exacerbated pulmonary inflammation, airway occlusion, and hyper-responsiveness in recipient mice.
- Recipients exhibited increased eosinophils and reduced macrophages in the lungs, with altered Th2 cytokine profiles.
Conclusions:
- ST2 expression on Th2 cells plays a crucial role in down-regulating pulmonary inflammation.
- Targeting ST2 presents a potential therapeutic strategy for allergic airway disorders like asthma.
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