Human PD-1 agonist treatment alleviates neutrophilic asthma by reprogramming T cells

January 1, 2023
J Allergy Clin Immunol
https://pubmed.ncbi.nlm.nih.gov/35963455

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/35963455

Research summary

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.

Key outcome of the study

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.

Mouse model

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.

TARGET:
PDCD1
PD-1, CD279

Keywords

Neutrophilic asthma, PD-1 agonist therapy, T cell modulation, Airway hyperreactivity, Humanized mouse model

Technical specifications

Humanized Knockin model, PD-1 extracellular domain replacement, Immunotherapy evaluation, T cell reprogramming

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