Author Correction: A conserved dendritic-cell regulatory program limits antitumour immunity

Maier, Bárbara; Leader, Andrew M.; Chen, Steven T; Tung, Navpreet; Chang, Christie; LeBérichel, Jessica; Chudnovskiy, Aleksey; Maskey, Shrisha; Walker, Laura; Finnigan, John P.; Kirkling, Margaret E.; Reizis, Boris; Ghosh, Sourav; D’Amore, Natalie Roy; Bhardwaj, Nina; Rothlin, Carla V.; Wolf, Andrea; Flores, Raja M.; Marron, Thomas U.; Rahman, Adeeb; Kenigsberg, Ephraim; Brown, Brian D.; Mérad, Miriam

doi:10.1038/s41586-020-2326-5

Cited by 13 publications

(23 citation statements)

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“…Interestingly, ligand-receptor pairs analysis indicated that the LAMP3 + DCs are the subset that would interact with Tex cells and T regs . This LAMP3 population seems to correspond to mregDCs, a DC cluster annotated in human lung cancer as a population involved in tumor antigen uptake and expressing immunoregulatory molecules (78,79).…”

Section: All Types Of T Cells (Including Treg Exhausted T Cells [Tex]mentioning

confidence: 99%

Hepatocellular Carcinoma Immune Landscape and the Potential of Immunotherapies

et al. 2021

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Hepatocellular carcinoma (HCC) is the most common liver tumor and among the deadliest cancers worldwide. Advanced HCC overall survival is meager and has not improved over the last decade despite approval of several tyrosine kinase inhibitors (TKi) for first and second-line treatments. The recent approval of immune checkpoint inhibitors (ICI) has revolutionized HCC palliative care. Unfortunately, the majority of HCC patients fail to respond to these therapies. Here, we elaborate on the immune landscapes of the normal and cirrhotic livers and of the unique HCC tumor microenvironment. We describe the molecular and immunological classifications of HCC, discuss the role of specific immune cell subsets in this cancer, with a focus on myeloid cells and pathways in anti-tumor immunity, tumor promotion and immune evasion. We also describe the challenges and opportunities of immunotherapies in HCC and discuss new avenues based on harnessing the anti-tumor activity of myeloid, NK and γδ T cells, vaccines, chimeric antigen receptors (CAR)-T or -NK cells, oncolytic viruses, and combination therapies.

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Section: All Types Of T Cells (Including Treg Exhausted T Cells [Tex]mentioning

confidence: 99%

Hepatocellular Carcinoma Immune Landscape and the Potential of Immunotherapies

et al. 2021

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“…Large amounts of dendritic cells (DCs) can be seen infiltrating tumour cells and mature DCs can be found mostly within the tumour cell area, with a few of them in the s u r r o u n d i n g s t r o m a ( 1 3 9 ) . L A M P 3 + D C s e xh i b it immunosuppressive properties and interact with exhausted T cells, Tregs, and proliferating T cells via CD28/B7 binding and IL-15 signaling in multiple tumours (140,141). M1-polarised tumour-associated macrophages (TAMs) can be found in both tumour cell areas and in the stroma, while M2-polarised macrophages are often found in the stroma when present in high density (139).…”

Section: Other Cell Populations In Npc Timementioning

confidence: 99%

Epstein–Barr Virus Epithelial Cancers—A Comprehensive Understanding to Drive Novel Therapies

et al. 2021

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Epstein–Barr virus (EBV) is a ubiquitous oncovirus associated with specific epithelial and lymphoid cancers. Among the epithelial cancers, nasopharyngeal carcinoma (NPC), lymphoepithelioma-like carcinoma (LELC), and EBV-associated gastric cancers (EBVaGC) are the most common. The role of EBV in the pathogenesis of NPC and in the modulation of its tumour immune microenvironment (TIME) has been increasingly well described. Much less is known about the pathogenesis and tumour–microenvironment interactions in other EBV-associated epithelial cancers. Despite the expression of EBV-related viral oncoproteins and a generally immune-inflamed cancer subtype, EBV-associated epithelial cancers have limited systemic therapeutic options beyond conventional chemotherapy. Immune checkpoint inhibitors are effective only in a minority of these patients and even less efficacious with molecular targeting drugs. Here, we examine the key similarities and differences of NPC, LELC, and EBVaGC and comprehensively describe the clinical, pathological, and molecular characteristics of these cancers. A deeper comparative understanding of these EBV-driven cancers can potentially uncover targets in the tumour, TIME, and stroma, which may guide future drug development and cast light on resistance to immunotherapy.

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“…The chemokine receptor XCR1 was established to be a specific marker for cDC1s. It is exclusively expressed on both human and mouse cDC1s (12, 13,[22][23][24]. XCR1 mediates chemotaxis of cDC1s towards CD8 + T cells and NK cells, because they are the main producers of the ligand of XCR1, XC chemokine ligand 1 (XCL1), the ligand of XCR1 (12, 23).…”

Section: Cdc1s Phenotypic Characterizationmentioning

confidence: 99%

“…Depletion of cDC1s, for example using Batf3 knockouts, results in loss of cross-presentation. Mice lacking cDC1s have less tumor-specific CD8 + T cells hence an impaired anti-tumor response (24,(26)(27)(28)(29). Of note, depletion of cDC1s leads, besides to diminished cross-presentation also to loss of other functions mediated by cDC1s like attracting CD8 + T cells via XCL1-XCR1 interactions as well as less IL-12 and IFN-b since it is produced by cDC1s upon TLR-3 triggering.…”

Section: Cdc1s Activate T Cells Via Cross-presentationmentioning

confidence: 99%

“…Of note, depletion of cDC1s leads, besides to diminished cross-presentation also to loss of other functions mediated by cDC1s like attracting CD8 + T cells via XCL1-XCR1 interactions as well as less IL-12 and IFN-b since it is produced by cDC1s upon TLR-3 triggering. These processes also enhance anti-tumor responses and are less efficient upon depletion of cDC1s (6,24).…”

Section: Cdc1s Activate T Cells Via Cross-presentationmentioning

confidence: 99%

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Harnessing the cDC1-NK Cross-Talk in the Tumor Microenvironment to Battle Cancer

et al. 2021

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Immunotherapeutic approaches have revolutionized the treatment of several diseases such as cancer. The main goal of immunotherapy for cancer is to modulate the anti-tumor immune responses by favoring the recognition and destruction of tumor cells. Recently, a better understanding of the suppressive effect of the tumor microenvironment (TME) on immune cells, indicates that restoring the suppressive effect of the TME is crucial for an efficient immunotherapy. Natural killer (NK) cells and dendritic cells (DCs) are cell types that are currently administered to cancer patients. NK cells are used because of their ability to kill tumor cells directly via cytotoxic granzymes. DCs are employed to enhance anti-tumor T cell responses based on their ability to present antigens and induce tumor-antigen specific CD8+ T cell responses. In preclinical models, a particular DC subset, conventional type 1 DCs (cDC1s) is shown to be specialized in cross-presenting extracellular antigens to CD8+ T cells. This feature makes them a promising DC subset for cancer treatment. Within the TME, cDC1s show a bidirectional cross-talk with NK cells, resulting in a higher cDC1 recruitment, differentiation, and maturation as well as activation and stimulation of NK cells. Consequently, the presence of cDC1s and NK cells within the TME might be of utmost importance for the success of immunotherapy. In this review, we discuss the function of cDC1s and NK cells, their bidirectional cross-talk and potential strategies that could improve cancer immunotherapy.

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Author Correction: A conserved dendritic-cell regulatory program limits antitumour immunity

Cited by 13 publications

References 0 publications

Hepatocellular Carcinoma Immune Landscape and the Potential of Immunotherapies

Hepatocellular Carcinoma Immune Landscape and the Potential of Immunotherapies

Epstein–Barr Virus Epithelial Cancers—A Comprehensive Understanding to Drive Novel Therapies

Harnessing the cDC1-NK Cross-Talk in the Tumor Microenvironment to Battle Cancer

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