Type 2 airway inflammation (T2 inflammation)

Type 2 airway inflammation is a complex immunological endotype characterized by the activation of the adaptive (Th2 cells) and innate (ILC2s) immune systems [Gandhi et al., 2016, Nature Reviews Drug Discovery]. This pathway is driven by key cytokines, primarily interleukin-4 (IL-4), IL-5, and IL-13, which orchestrate the recruitment of eosinophils, the production of IgE by B cells, and the hypersecretion of mucus by goblet cells [Robinson et al., 2017, Clinical & Experimental Allergy]. It is a major driver of pathology in a significant subset of patients with asthma, often referred to as "T2-high" asthma, as well as related conditions like chronic rhinosinusitis with nasal polyps [Corren, 2019, Journal of Allergy and Clinical Immunology]. While "Type 2 airway inflammation" describes a physiological process rather than a single protein, it serves as a framework for multiple high-value therapeutic targets [Papi et al., 2018, The Lancet]. Biologic therapies targeting this pathway, such as monoclonal antibodies against IL-5 or the IL-4 receptor alpha subunit, have revolutionized the treatment of severe asthma by reducing exacerbation rates and improving lung function [Wenzel et al., 2016, NEJM]. Upstream initiators like Thymic Stromal Lymphopoietin (TSLP) are also targeted to provide a broader suppression of this inflammatory cascade [Menzies-Gow et al., 2021, NEJM].

Other names

Th2-high inflammationEosinophilic airway inflammationType 2-high asthmaT2-driven inflammation

Therapeutic agents target specific molecular components of the Type 2 cascade, such as IL-4, IL-5, IL-13, or TSLP, to inhibit downstream signaling that leads to eosinophilia and airway remodeling [Gandhi et al., 2016, Nature Reviews Drug Discovery; Menzies-Gow et al., 2021, NEJM].