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Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2026,8,11]]},"abstract":"<jats:p>\n                    Asthma is a heterogeneous inflammatory airway disease characterized by immune dysregulation, airway hyperresponsiveness (AHR), and excessive immune activation. Although NLRP3 (NOD-like receptor family pyrin domain-containing 3) has been extensively studied in asthma, its role remains controversial, and the contribution of DNA sensor AIM2 (Absent in Melanoma 2) is less well defined. To assess AIM2\u2019s relevance in asthma, we analyzed public human datasets and found increased\n                    <jats:italic toggle=\"yes\">AIM2<\/jats:italic>\n                    , but not\n                    <jats:italic toggle=\"yes\">NLRP3<\/jats:italic>\n                    , expression in severe asthma and in neutrophilic compared with paucigranulocytic asthma. In allergic asthma models induced by ovalbumin (OVA)-lipopolysaccharide (LPS) or house dust mite (HDM), AIM2 expression was increased in lung homogenates and bronchoalveolar lavage fluid cells. Analysis of a published single-cell RNA-seq dataset from the HDM model further showed increased\n                    <jats:italic toggle=\"yes\">Aim2<\/jats:italic>\n                    , but not\n                    <jats:italic toggle=\"yes\">Nlrp3<\/jats:italic>\n                    , expression in T helper cells, with most\n                    <jats:italic toggle=\"yes\">Aim2<\/jats:italic>\n                    -expressing cells coexpressing\n                    <jats:italic toggle=\"yes\">Gata3<\/jats:italic>\n                    . In the OVA-LPS model, whole-body\n                    <jats:italic toggle=\"yes\">Aim2<\/jats:italic>\n                    deficiency reduced AHR, inflammatory cytokine production, airway smooth muscle actin, and \u03b3H2A.X, consistent with decreased airway remodeling and tissue stress. Unexpectedly, CD4-specific, but not Treg- or myeloid-specific,\n                    <jats:italic toggle=\"yes\">Aim2<\/jats:italic>\n                    deletion significantly attenuated disease, identifying AIM2 in CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells as a major driver of pathogenesis. In the HDM model,\n                    <jats:italic toggle=\"yes\">Aim2<\/jats:italic>\n                    deficiency similarly reduced AHR. Cell-specific deletion showed that AIM2 in CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells promotes AHR and cytokine production, whereas AIM2 in myeloid cells modulates IgG1, IL-13-producing CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells, and alveolar macrophages. These findings identify AIM2 as a regulator of allergic asthma acting predominantly through T cells, with an additional context-dependent contribution from myeloid cells.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2520215123","type":"journal-article","created":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T17:46:06Z","timestamp":1786124766000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":1,"title":["T cell\u2013intrinsic AIM2 exacerbates lung inflammation in OVA-LPS- and HDM-induced asthma models"],"prefix":"10.1073","volume":"123","author":[{"given":"Wei-Chun","family":"Chou","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/043ehm030","id-type":"ROR","asserted-by":"publisher"}],"name":"Lineberger Comprehensive Cancer Center, University of North Carolina","place":["Chapel Hill"]},{"name":"Department of Genetics, University of North Carolina","place":["Chapel 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Bigler M. Timour M. Boedigheimer Expression profiling in blood from subjects with severe asthma moderate asthma and non-asthmatics collected in the U-BIOPRED study. Gene Expression Omnibus (GEO). https:\/\/www.ncbi.nlm.nih.gov\/geo\/query\/acc.cgi?acc=GSE69683. Accessed 27 February 2024."},{"key":"e_1_3_4_77_2","unstructured":"S. S\u00e1nchez-Ovando J. L. Simpson K. J. Baines D. Barker P. A. Wark Transcriptomic profiling of inflammatory phenotypes of severe asthma using endobronchial biopsies. Gene Expression Omnibus (GEO). https:\/\/www.ncbi.nlm.nih.gov\/geo\/query\/acc.cgi?acc=GSE143303. Accessed 28 April 2022."},{"key":"e_1_3_4_78_2","unstructured":"C. A. Tibbitt J. M. Coquet Identification of novel regulators of Th2 cells in HDM model (RNA- Seq). Gene Expression Omnibus (GEO). https:\/\/www.ncbi.nlm.nih.gov\/geo\/query\/acc.cgi?acc=GSE131935. 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