Type 2 and Th17 inflammatory pathway (T2/Th17 response)

The Type 2 cytokines and Th2/Th17-skewed inflammatory response refers to a complex immune signaling network characterized by the coordinated activity of T-helper 2 (Th2) and T-helper 17 (Th17) pathways. Type 2 inflammation is primarily driven by cytokines such as Interleukin-4 (IL-4), IL-5, and IL-13, which promote eosinophil activation, IgE synthesis, and goblet cell hyperplasia (Gandhi et al., 2016, Nature Reviews Drug Discovery). The Th17 component involves cytokines like IL-17A and IL-22, which contribute to neutrophilic recruitment and structural changes in tissues, often complicating the clinical presentation of allergic diseases (McGeachy et al., 2019, Immunity). This dual-skewed response is a hallmark of severe, treatment-resistant forms of asthma, atopic dermatitis, and chronic rhinosinusitis, where it often correlates with corticosteroid resistance (Fahy, 2015, Nature Reviews Immunology). Therapeutic strategies targeting this response include monoclonal antibodies that neutralize specific cytokines or block their receptors, such as Dupilumab for IL-4/IL-13 signaling and Secukinumab for IL-17A (Guttman-Yassky et al., 2018, JACI). Effective management of this response requires identifying specific patient endotypes through biomarkers like blood eosinophils and FeNO to optimize treatment outcomes.

Other names

Type 2 inflammationTh2/Th17-mediated inflammationType 2/Type 17 immune responseT2/Th17-high endotype

Inhibition of pro-inflammatory cytokine signaling through monoclonal antibody-mediated neutralization or receptor blockade to reduce inflammatory cell recruitment and tissue damage.