T-helper 2 and T-helper 17 cytokine pathways (Th2/Th17 pathways)

The Th2 and Th17 cytokine pathways represent two distinct but often overlapping arms of the adaptive immune system involved in chronic inflammatory and autoimmune diseases. The Th2 pathway is characterized by the production of cytokines such as IL-4, IL-5, and IL-13, which drive allergic inflammation, eosinophil recruitment, and IgE production, playing a central role in conditions like asthma and atopic dermatitis [1]. Conversely, the Th17 pathway involves cytokines like IL-17A, IL-17F, and IL-23, which are critical for host defense against extracellular pathogens but also drive the pathogenesis of psoriasis, psoriatic arthritis, and ankylosing spondylitis [2]. Therapeutic targeting of these pathways has revolutionized the treatment of moderate-to-severe inflammatory diseases through the use of monoclonal antibodies that neutralize specific cytokines or block their respective receptors [3]. While highly effective, modulating these pathways requires careful monitoring for potential side effects, such as increased susceptibility to certain infections or the paradoxical worsening of other inflammatory conditions [4]. Understanding the interplay between Th2 and Th17 signaling is essential for developing personalized treatment strategies in heterogeneous diseases like severe asthma, where both pathways may contribute to the clinical phenotype [5]. Sources: [1] Gandhi NA, et al. Nature Reviews Drug Discovery. 2016;15(1):35-50. [2] McGeachy MJ, et al. Immunity. 2019;50(4):832-848. [3] StatPearls. T Helper Cells. 2023. [4] Blauvelt A, et al. Journal of the American Academy of Dermatology. 2018;79(1):11-23. [5] Cosmi L, et al. European Journal of Immunology. 2014;44(12):3621-3631.

Other names

Type 2 and Type 17 immune responseTh2/Th17 axisT-helper cell type 2 and 17 signalingIL-4/IL-5/IL-13 and IL-17/IL-23 pathways

Monoclonal antibody-mediated neutralization of specific interleukins (e.g., IL-4, IL-5, IL-13, IL-17A, IL-23) or blockade of their respective receptors (e.g., IL-4Rα, IL-5Rα, IL-17RA) to inhibit downstream inflammatory signaling.