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Exosomal programmed death ligand 1 in patients with Mycobacterium avium complex lung disease
Chi-Yu Hsu1, Bo-Shiun Yan2, Juo-Hsin Lai1
1National Taiwan University College of Medicine, Taipei, Taiwan.
Background:
Mycobacterium avium complex lung disease (MAC-LD) is increasing worldwide. Exosomal programmed death-ligand 1 (PD-L1) has been scarcely investigated in MAC-LD.
Methods:
Plasma exosomes and their PD-L1 from MAC-LD patients and healthy controls were measured and used for co-culturing Jurkat cells with or without PD-L1/PD-1 blocking antibodies. MAC-infected mice were treated with exosome inhibitors to assess exosomal PD-L1 and bacterial burden.
Results:
Plasma exosomal PD-L1 levels were significantly higher in MAC-LD patients (1,477±1,243 pg/mL) vs. controls (183.8±113.9 pg/mL; P < .001), correlated with cavitary disease (2,415±1,309 vs. 844.1±652.2 pg/mL; P = .008) and decreased after treatment (1,474±961.3 vs. 738.5±820.4 pg/mL; P = .03). MAC-infected macrophage exosomes decreased Jurkat cell survival (72.9±11.5% vs. 98.2±0.6%; P < .01), which could be reversed by PD-L1/PD-1 antibodies. In the mouse study, GW4869 (an exosome biogenesis inhibitor) reduced lung exosomal PD-L1 (497.6±123.1 to 197.7±116.4 pg/mL; P = .008) and bacterial load (996,400±96,316 to 116,400±18,528 CFU; P = .008), whereas DMA (an exosome release inhibitor) showed no significant effect on lung exosome and bacterial load.
Conclusions:
Exosomal PD-L1 promotes immune suppression and reflects disease severity in MAC-LD. Inhibition of exosome biogenesis reduced exosomal PD-L1 levels and MAC burden in lung, supporting a potential therapeutic avenue that requires further validation.
Insights
Exosomal PD-L1 is elevated in Mycobacterium avium complex lung disease (MAC-LD), suppressing immune responses. Inhibiting exosome production may reduce MAC-LD severity and bacterial load.
Area of Science:
- Immunology
- Pulmonology
- Cell Biology
Background:
- Mycobacterium avium complex lung disease (MAC-LD) is a growing global health concern.
- The role of exosomal programmed death-ligand 1 (PD-L1) in MAC-LD remains largely unexplored.
Purpose of the Study:
- To investigate the levels and function of exosomal PD-L1 in MAC-LD.
- To explore the therapeutic potential of targeting exosomal PD-L1 in MAC-LD.
Main Methods:
- Quantified plasma exosomal PD-L1 in MAC-LD patients and healthy controls.
- Co-cultured Jurkat cells with patient-derived exosomes and PD-1/PD-L1 blocking antibodies.
- Administered exosome inhibitors to MAC-infected mice to assess exosomal PD-L1 and bacterial burden.
Main Results:
- Plasma exosomal PD-L1 was significantly higher in MAC-LD patients, correlating with disease severity and decreasing post-treatment.
- MAC-infected macrophage exosomes impaired Jurkat cell survival, an effect reversed by PD-L1/PD-1 blockade.
- In vivo, GW4869 (exosome biogenesis inhibitor) reduced lung exosomal PD-L1 and bacterial load, while DMA (exosome release inhibitor) had no significant effect.
Conclusions:
- Exosomal PD-L1 contributes to immune suppression and indicates MAC-LD severity.
- Inhibiting exosome biogenesis offers a potential therapeutic strategy for MAC-LD by reducing exosomal PD-L1 and bacterial burden.
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