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RNF41 regulates the damage recognition receptor Clec9A and antigen cross-presentation in mouse dendritic cells

Title: RNF41 regulates the damage recognition receptor Clec9A and antigen cross-presentation in mouse dendritic cells
Authors: Kirsteen M Tullett; Peck Szee Tan; Hae-Young Park; Ralf B Schittenhelm; Nicole Michael; Rong Li; Antonia N Policheni; Emily Gruber; Cheng Huang; Alex J Fulcher; Jillian C Danne; Peter E Czabotar; Linda M Wakim; Justine D Mintern; Georg Ramm; Kristen J Radford; Irina Caminschi; Meredith O'Keeffe; Jose A Villadangos; Mark D Wright; Marnie E Blewitt; William R Heath; Ken Shortman; Anthony W Purcell; Nicos A Nicola; Jian-Guo Zhang; Mireille H Lahoud
Source: eLife, Vol 9 (2020)
Publisher Information: eLife Sciences Publications Ltd, 2020.
Publication Year: 2020
Collection: LCC:Medicine; LCC:Science; LCC:Biology (General)
Subject Terms: dendritic cells; DAMP recognition; E3 ubiquitin ligase; ubiquitination; antigen presentation; Medicine; Science; Biology (General); QH301-705.5
Description: The dendritic cell receptor Clec9A facilitates processing of dead cell-derived antigens for cross-presentation and the induction of effective CD8+ T cell immune responses. Here, we show that this process is regulated by E3 ubiquitin ligase RNF41 and define a new ubiquitin-mediated mechanism for regulation of Clec9A, reflecting the unique properties of Clec9A as a receptor specialized for delivery of antigens for cross-presentation. We reveal RNF41 is a negative regulator of Clec9A and the cross-presentation of dead cell-derived antigens by mouse dendritic cells. Intriguingly, RNF41 regulates the downstream fate of Clec9A by directly binding and ubiquitinating the extracellular domains of Clec9A. At steady-state, RNF41 ubiquitination of Clec9A facilitates interactions with ER-associated proteins and degradation machinery to control Clec9A levels. However, Clec9A interactions are altered following dead cell uptake to favor antigen presentation. These findings provide important insights into antigen cross-presentation and have implications for development of approaches to modulate immune responses.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2050-084X
Relation: https://elifesciences.org/articles/63452; https://doaj.org/toc/2050-084X
DOI: 10.7554/eLife.63452
Access URL: https://doaj.org/article/ce7301ac4e2c47ffba46b495f1882e5b
Accession Number: edsdoj.7301ac4e2c47ffba46b495f1882e5b
Database: Directory of Open Access Journals