T helper 2-mediated immune response (Th2 response)

The T helper 2 (Th2)-mediated immune response is a complex biological pathway primarily involved in the adaptive immune system's defense against extracellular parasites, such as helminths [3, 5, 20]. It is characterized by the activation of CD4+ T cells that differentiate into Th2 cells, which subsequently secrete a specific profile of cytokines, most notably interleukin-4 (IL-4), IL-5, and IL-13 [1, 6, 18]. These cytokines orchestrate various effector functions, including B cell isotype switching to immunoglobulin E (IgE), recruitment and activation of eosinophils, and stimulation of mucus production by goblet cells [2, 17]. While protective in the context of parasitic infections, a dysregulated or excessive Th2 response is the fundamental driver of type 2 inflammation seen in allergic diseases like asthma, atopic dermatitis, and chronic rhinosinusitis [1, 8, 11]. Modern therapeutic interventions focus on blocking specific components of this pathway using monoclonal antibodies, such as dupilumab (targeting IL-4Rα) and mepolizumab (targeting IL-5), to alleviate symptoms and prevent tissue remodeling [6, 11, 17]. Clinical management often relies on biomarkers like blood eosinophil counts and fractional exhaled nitric oxide (FeNO) to identify patients with a dominant Th2 endotype who are likely to respond to these targeted biologics [4, 9, 10].

Other names

Type 2 immune responseTh2 pathwayTh2-type inflammationT helper 2 response

Inhibition of Th2-associated cytokines (IL-4, IL-5, IL-13, IL-31) or their receptors, neutralization of IgE, and blockade of epithelial-derived alarmins (TSLP, IL-33) to suppress type 2 inflammation.