常规樹突細胞1型（cDC1）對於誘導保護性CD8 + T細胞對瘤和病毒抗原的反應至關重要。在許多情況下，cDC1通過內吞垂死的腫瘤或病毒感染細胞的物質來接觸這些抗原。cDC1如何提取死細胞相關的抗原並以與MHC I類分子結合的肽形式進行交差呈現至CD8 + T細胞，目前尚不清楚。 在這裡，我們回顧了樹突細胞天然殺手群體受體-1 (DNGR-1；又稱CLEC9A)的生物學，這是一種高度表達在cDC1上起著關鍵作用的C型植物血凝素受體。我們突出了最近的進展，支持DNGR-1信號在促進包含死細胞殘骸的貪婪或內嗑細胞器的誘導性破裂中發揮作用，從而使死細胞相關的抗原可以進入cDC1的內源性MHC I處理及呈現機制中。我們進一步回顧了DNGR-1如何檢測死細胞，以及受體在抗病毒和抗腫瘤免疫中的功能。最後，我們強調了DNGR-1研究如何開啟交差呈現的新視角，其中一些可能在癌症免疫治療和防範病毒疾病的疫苗接種中得到應用。 版權所有©2023年Elsevier Ltd.。版權所有。

Conventional dendritic cells type 1 (cDC1) are critical for inducing protective CD8+ T cell responses to tumour and viral antigens. In many instances, cDC1 access those antigens in the form of material internalised from dying tumour or virally-infected cells. How cDC1 extract dead cell-associated antigens and cross-present them in the form of peptides bound to MHC class I molecules to CD8+ T cells remains unclear. Here we review the biology of dendritic cell natural killer group receptor-1 (DNGR-1; also known as CLEC9A), a C-type lectin receptor highly expressed on cDC1 that plays a key role in this process. We highlight recent advances that support a function for DNGR-1 signalling in promoting inducible rupture of phagocytic or endocytic compartments containing dead cell debris, thereby making dead cell-associated antigens accessible to the endogenous MHC class I processing and presentation machinery of cDC1. We further review how DNGR-1 detects dead cells, as well as the functions of the receptor in anti-viral and anti-tumour immunity. Finally, we highlight how the study of DNGR-1 has opened new perspectives into cross-presentation, some of which may have applications in immunotherapy of cancer and vaccination against viral diseases.Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.