- D3.515 - PM2.5 exposure shapes monocyte and T cell immune reprogramming in allergic airway disease

Fine particulate matter (PM2.5) is a major environmental risk factor for allergic airway diseases such as allergic rhinitis and asthma. Although these conditions are classically characterized by type 2 (Th2)–biased immunity, environmental exposures may promote additional inflammatory pathways, including Th17-associated responses.

PM2.5 exposure was assessed using personal monitoring. Peripheral blood mononuclear cells (PBMCs) from 16 patients with allergic rhinitis and asthma were profiled by single-cell RNA sequencing. Data were processed, integrated, and clustered in Seurat; monocytes and T cells were subsetted for refined clustering, followed by differential gene expression and pathway enrichment analyses (GO/KEGG) comparing high- and low-exposure groups. Cell–cell communication, including monocyte–T cell crosstalk, was inferred using CellChat.

High PM2.5 exposure was associated with transcriptional remodeling and exposure-dependent shifts in inferred intercellular communication networks in PBMCs.  In monocytes, inflammatory classical monocytes showed up-regulation of danger/pro-inflammatory signaling pathways, whereas steady-state classical monocytes demonstrated down-regulation of pathways related to phagocytosis, antigen processing/presentation, and antiviral immune functions, consistent with attenuation of homeostatic clearance programs.  In T cells, CD4+ subsets were enriched for T-cell differentiation pathways and IL-17–associated immune programs, while CD8+ subsets exhibited enhanced differentiation and cytotoxic inflammatory signatures, including TNF-related pathways.  Together, these findings are consistent with the emergence of Th17-associated inflammation superimposed on an underlying Th2-biased allergic immune background, with altered monocyte–T cell communication suggested at the network level.

PM2.5 exposure is linked to systemic immune reprogramming characterized by inflammatory monocyte priming, attenuation of steady-state monocyte functions, and IL-17–linked T-cell program remodeling. CellChat-based inference further suggests exposure-dependent alterations in monocyte–T cell communication in PBMCs; functional and tissue-level validation is warranted.