Targeting cytokines in asthma therapy: could IL-37 be a solution?

IL‐37 regulates allergic inflammation by counterbalancing pro‐inflammatory IL‐1 and IL‐33

“…[10][11][12][13] On the other hand, they maintain local immuno-homeostasis and so prevent tissue damage by the actions of anti-inflammatory factors including IL-10 and IL-37, and an impairment of this immunoregulatory function could be a central factor in the pathogenesis of chronic inflammatory diseases such as asthma. 14,15 rhIL-37 reduced production of Th2 cytokines in allergen-activated MNCs from wildtype but not from IL-1R1-deficient mice and inhibited IL-33-induced Th2 cytokine release. Furthermore, rhIL-37 attenuated IL-1β-and IL-33-induced pro-inflammatory mediator expression in murine AEC cultures.…”

“…Airway epithelial cells (AECs) and antigen‐presenting cells (APCs) produce factors that amplify or dampen acute inflammatory reactions: On the one hand, they augment allergic airway inflammation and thus formation of pathophysiological hallmarks of asthma by releasing pro‐inflammatory cytokines such as interleukin (IL) 1β and IL‐6, while epithelium‐derived factors such as IL‐33 promote Th2 and innate lymphoid tissue cell 2 (ILC2) differentiation that direct allergic immune responses via release of IL‐4, IL‐5, and IL‐13 10‐13 . On the other hand, they maintain local immuno‐homeostasis and so prevent tissue damage by the actions of anti‐inflammatory factors including IL‐10 and IL‐37, and an impairment of this immuno‐regulatory function could be a central factor in the pathogenesis of chronic inflammatory diseases such as asthma 14,15 …”