Impacts of Environmental Pollutants on Innate Immunity: The Role of Group 2 Innate Lymphoid Cells

Environmental pollution has emerged as one of the biggest threats to health in the contemporary world. Pollutants modify immune responses and may induce immunotoxicity. In this review, we describe the impact of significant environmental pollutants on the innate immune system, including ozone (O₃), particulate matter (PM), diesel exhaust particles (DEPs) and cigarette smoke (CS), as well as emerging pollutants such as chemical contaminants, nanomaterials, and microplastics, with a particular focus on the regulatory mechanisms of innate lymphoid cells (ILCs). ILCs, tissue-resident lymphocytes without antigen-specific receptors, have been demonstrated to be essential regulators linking environmental detection and immunological responses. Studies indicate that environmental pollutants activate ILCs and alter the immune responses by compromising the epithelial barrier and triggering the release of alarmins, including interleukin (IL)-33, IL-25, and thymic stromal lymphopoietin (TSLP). Among ILCs, group 2 innate lymphoid cells (ILC2s) are highly sensitive to pollutant-induced epithelial signals and play a critical role in type 2 inflammation. Beyond canonical alarmin signaling, accumulating evidence indicates that environmental pollutants regulate ILC2 biology thereby contributing to immune dysregulation and inflammatory diseases. A better understanding of how environmental pollutants regulate ILC2 activation, plasticity, and functional adaptation will facilitate the development of more precise preventive and therapeutic strategies for pollution-associated diseases.