August 20, 2023|,

Preprint Highlight: The pore-forming apolipoprotein APOL7C drives phagosomal rupture and antigen cross-presentation by dendritic cells

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Highlighted By: Adriana Mantegazza, Thomas Jefferson University

Preprint DOI: https://doi.org/https://doi.org/10.1101/2023.08.11.553042
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Significance Statement:

  • Conventional dendritic cells type 1 (cDC1s) specialize in antigen “cross-presentation”, a mechanism that involves the presentation of exogenous antigens on major histocompatibility complex class I (MHC-I) proteins. While this process is essential in triggering anti-viral and anti-tumor immunity, the molecular mechanisms that facilitate cargo export to the cytosol to promote MHC-I presentation after phagocytosis are largely unknown.
  • Using correlative confocal and focused ion beam scanning electron microscopy, along with FRET and FRAP approaches, the authors show that phagosomal recruitment of the pore-forming protein apolipoprotein 7C (APOL7C) leads to phagosomal membrane rupture, leading to phagosomal content exit. Notably, APOL7C recruitment is dependent on NADPH oxidase-induced phagosomal membrane depolarization.
  • These findings suggest APOL7C as a novel phagosomal effector required for efficient phagosomal cargo exit and subsequent antigen cross-presentation in cDC1s.

Read the Preprint:

The pore-forming apolipoprotein APOL7C drives phagosomal rupture and antigen cross-presentation by dendritic cells.
Gerone A. Gonzales, Song Huang, Jahanara Rajwani, Liam Wilkinson, Jenny A. Nguyen, Cassandra M. Wood, Melanie Moore, Eymi Cedeño, Saif Sikdar, Neil McKenna, Vincent Ebacher, Nicole L. Rosin, Matheus B. Carneiro, Bas Surewaard, Nathan C. Peters, Jeff Biernaskie, Douglas J. Mahoney, Robin M. Yates, Johnathan Canton
bioRxiv 2023.08.11.553042; doi: https://doi.org/10.1101/2023.08.11.553042

 

 

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