This study investigates the role of PD-1 in regulating acute neutrophilic inflammation in a murine model of airway hyperreactivity (AHR). Using a humanized PD-1 Knockin mouse model, where the extracellular domain of PD-1 is humanized, the researchers demonstrated that treatment with a human PD-1 agonist dampens AHR, decreases neutrophil recruitment, and modulates cytokine production. Mechanistically, the PD-1 agonist reprograms pulmonary effector T cells, reducing their number and activation, thereby alleviating neutrophilic asthma symptoms.
PD-1 agonist treatment effectively reduces neutrophilic airway inflammation and hyperreactivity by reprogramming effector T cells in a humanized mouse model, highlighting its therapeutic potential for neutrophilic asthma.
Humanized PD-1 Knockin (hPD-1 KI) mouse model, engineered to express the human extracellular domain of PD-1, allowing for the evaluation of human PD-1-targeting therapeutics in vivo.
Neutrophilic asthma, PD-1 agonist therapy, T cell modulation, Airway hyperreactivity, Humanized mouse model
Humanized Knockin model, PD-1 extracellular domain replacement, Immunotherapy evaluation, T cell reprogramming
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