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Updated: Sep 19, 2025

Establishment of an In vitro System to Study Intracellular Behavior of Candida glabrata in Human THP-1 Macrophages
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EPHA5 regulates antifungal innate immunity by phosphorylating EPHB2 and Dectin-1

Ru Gao1, Heping Wang1, Zhihui Cui1

  • 1Key Laboratory of Molecular Biophysics of the Ministry of Education, National Engineering Research Center for Nanomedicine, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China.

Plos Pathogens
|June 9, 2025
PubMed

Insights

Ephrin receptor A5 (EPHA5) is crucial for antifungal immunity. It activates EPH receptor B2 (EPHB2) and Dectin-1, enhancing immune cell response against fungal pathogens like Candida albicans.

Area of Science:

  • Immunology
  • Molecular Biology
  • Mycology

Background:

  • Invasive fungal infections (IFIs) cause millions of deaths globally.
  • Understanding immune responses to fungi is key for developing new antifungal therapies.
  • Ephrin receptor B2 (EPHB2) was previously identified as a coreceptor for β-glucan, activating antifungal signaling.

Purpose of the Study:

  • To elucidate the mechanism of EPHB2 activation during fungal infection.
  • To identify upstream regulators of EPHB2 and Dectin-1 in antifungal immunity.
  • To investigate the role of EPHA5 in host defense against invasive fungal pathogens.

Main Methods:

  • Cell-based assays to study protein phosphorylation and signaling.
  • Analysis of immune cell recruitment and activation in vitro.
  • Phenotypic analysis of EphA5-deficient mice infected with Candida albicans.

Main Results:

  • Ephrin receptor A5 (EPHA5) phosphorylates both EPHB2 and Dectin-1 upon fungal infection.
  • EPHA5 activation leads to Syk recruitment and activation, initiating downstream antifungal signaling.
  • EphA5-deficient mice show increased susceptibility to Candida albicans, with higher fungal loads and impaired immune cell infiltration.

Conclusions:

  • EPHA5 is a critical upstream activator of EPHB2 and Dectin-1 in antifungal immunity.
  • The EPHA5-EPHB2-Dectin-1 axis is essential for effective host defense against invasive fungal infections.
  • Targeting this pathway may offer novel therapeutic strategies for treating IFIs.

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