PD-1 deficiency exacerbates Mycobacteroides abscessus lung infection via metabolic rewiring and dysregulated neutrophil/T cell responses

Background Pulmonary Mycobacteroides abscessus (MAB) infection presents a therapeutic challenge, and while anti-programmed cell death protein 1(PD-1) therapy is clinically associated with increased MAB risk, yet the underlying immunomodulatory mechanisms remain elusive. Methods We established a PD-1-deficient mouse model of MAB infection and assessed bacterial clearance, immune responses, and metabolic alterations using colony counting, histopathology, flow cytometry, multiplex immunofluorescenc