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The Interleukin 1 receptor-like 1 (ST2), also known as the Interleukin-33 receptor, is a member of the interleukin-1 receptor family that plays a critical role in Type 2 innate and adaptive immunity [1, 2]. It exists in two main isoforms: a membrane-bound form (ST2L) that mediates cellular signaling and a soluble form (sST2) that acts as a decoy receptor to regulate IL-33 activity [3]. Upon binding its ligand, IL-33, the receptor recruits the IL-1 receptor accessory protein (IL-1RAcP) to initiate downstream signaling through the MyD88 pathway, leading to the production of pro-inflammatory cytokines [1, 3]. This pathway is heavily implicated in the pathogenesis of allergic and inflammatory diseases such as asthma, chronic obstructive pulmonary disease (COPD), and atopic dermatitis [4, 5]. In clinical practice, soluble ST2 is also utilized as a significant prognostic biomarker for heart failure and cardiovascular stress [6]. Therapeutic strategies targeting this receptor, such as monoclonal antibodies like astegolimab, aim to block the IL-33/ST2 axis to reduce chronic airway inflammation and exacerbations in respiratory conditions [7, 8].
Antagonist; monoclonal antibody that binds to the extracellular domain of the ST2 receptor, blocking the binding of IL-33 and preventing the formation of the ST2/IL-1RAcP signaling complex [7, 8].
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