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PTP1B deficiency in myeloid cells increases susceptibility to Candida albicans systemic infection by modulating antifungal immunity

Summary

This research shows that a protein called PTP1B plays an important role in protecting the body against dangerous yeast infections caused by Candida albicans. When this protein is missing from immune cells, mice become much more susceptible to severe fungal infections. The study found that PTP1B helps immune cells called macrophages and neutrophils kill fungi effectively, and when it’s absent, these immune cells work poorly. This discovery suggests that targeting PTP1B could be a new way to help patients fight off serious fungal infections.

Background

Invasive candidiasis caused by Candida albicans poses significant threat to immunocompromised patients with high mortality rates. Protein tyrosine phosphatase 1B (PTP1B) is a regulator of immunoreceptor signaling and inflammatory responses. Understanding immune mechanisms against fungal infection is fundamental for developing therapeutic strategies.

Objective

To reveal the critical role of myeloid cell-intrinsic PTP1B in antifungal immunity and determine how PTP1B deficiency alters susceptibility to systemic C. albicans infection. The study aimed to identify mechanisms by which PTP1B modulates immune cell functions during host defense against fungal pathogens.

Results

LysM PTP1B−/− mice were significantly more susceptible to systemic C. albicans infection with impaired survival, increased weight loss, and elevated fungal burdens in organs. PTP1B-deficient neutrophils and macrophages showed impaired phagocytosis, reduced killing capacity, and lower ROS production. Proteomic analysis revealed enrichment of type I interferon-regulated proteins in infected macrophages lacking PTP1B.

Conclusion

PTP1B functions as a critical modulator of innate immune responses to C. albicans, balancing antifungal activity with systemic toxicity and immunopathology. Boosting specific PTP1B-dependent pathways may offer new strategies for enhancing host defense against fungal infections while minimizing immunopathology.
  • Published in:mBio,
  • Study Type:Experimental Research,
  • Source: PMID: 40879376; DOI: 10.1128/mbio.01516-25
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