| T136 |
134-1426 |
Sentence |
denotes |
In a mouse model of influenza virus-induced asthma exacerbation,58 administration of an anti-ST2 antibody significantly reduced airway hyper-responsiveness and bodyweight loss, lowered inflammatory cell numbers in the lungs, and eliminated neutrophil extracellular traps in the airway lumen; moreover, anti-ST2 treatment restored lung expression of IFNβ, IL-12p35, and IL-12p70, and reduced viral load.58 There are several ongoing phase 2 trials using anti-ST2 therapy for inflammatory lung diseases such as chronic obstructive pulmonary disease and asthma.12 In the IFNγ-deficient mouse model of atypical MAS, blocking ST2 provided significant protection against weight loss, increased survival, reduced serum ferritin and soluble CD25 concentrations, and lowered CD8+ T-cell frequencies and neutrophilia.32 By contrast, individually blocking IL-6, IL-1β, or GM-CSF did not provide major protection against disease, suggesting that dampening IL-33–ST2 signalling, rather than individual downstream effector cytokines, might be more effective in treating either canonical MAS or atypical MAS-like diseases,32 such as COVID-19.2 A study evaluating the safety and efficacy of astegolimab (MSTT1041A) in severe COVID-19 pneumonia is recruiting participants (NCT04386616; EudraCT 2020-002713-17). |
