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T cell AIM2 Exacerbates Lung Inflammation in OVA-LPS and HDM-induced Asthma Models
Biorxiv : the Preprint Server for Biology
|July 9, 2025
Summary
AIM2 inflammasome receptor drives allergic asthma by promoting airway hyperresponsiveness and inflammation, particularly through CD4+ T cells. Targeting AIM2 may offer a novel therapeutic strategy for asthma treatment.
Area of Science:
- Immunology
- Respiratory Medicine
- Molecular Biology
Background:
- Asthma is a complex inflammatory airway disease involving immune dysregulation.
- The inflammasome, particularly AIM2, plays a role in asthma pathogenesis.
- AIM2 expression is elevated in severe asthma patients.
Purpose of the Study:
- To investigate the role of AIM2 in allergic asthma models.
- To determine the specific cell types where AIM2 drives asthma pathology.
Main Methods:
- Utilized ovalbumin (OVA)-LPS and house dust mite (HDM)-induced allergic asthma models in mice.
- Employed whole-body and cell-specific Aim2 knockout mouse models.
- Analyzed lung homogenates, bronchoalveolar lavage fluid (BALF), and immune cell populations.
Main Results:
- AIM2 expression increased in allergen-induced asthma models.
- Aim2 deletion reduced airway hyperresponsiveness (AHR), inflammation, and DNA damage in OVA-LPS asthma.
- AIM2 in CD4+ T cells was identified as a key driver of AHR in both models.
- AIM2 in myeloid cells modulated IgG1 levels and IL-13+ CD4+ T cells in HDM-induced asthma.
Conclusions:
- AIM2 plays a significant role in allergic asthma pathogenesis.
- AIM2 in CD4+ T cells is a major contributor to AHR.
- AIM2 in myeloid cells influences specific immune responses in HDM-induced asthma.
- AIM2 represents a potential therapeutic target for allergic asthma.
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