Abstract
Dendritic cells (DCs) efficiently process and present antigens to T cells, and by integrating environmental signals, link innate and adaptive immunity. DCs also control the balance between tolerance and immunity, and are required for T-cell mediated anti-tumor immunity. One subset of classical DCs, cDC1, are particularly important for eliciting CD8 T cells that can kill tumor cells. cDC1s are superior in antigen cross-presentation, a process of presenting exogenous antigens on MHC class I to activate CD8+ T cells. Tumor-associated cDC1s can transport tumor antigen to the draining lymph node and cross-present tumor antigens, resulting in priming and activation of cytotoxic T cells. Although cross-presenting cDC1s are critical for eliciting anti-tumor T cell responses, the role and importance of other DC subsets in anti-tumor immunity is not as well-characterized. Recent literature in other contexts suggests that critical crosstalk between DC subsets can significantly alter biological outcomes, and these DC interactions likely also contribute significantly to tumor-specific immune responses. Therefore, antigen presentation by cDC1s may be necessary but not sufficient for maximal immune responses against cancer. Here, we discuss recent advances in the understanding of DC subset interactions to maximize anti-tumor immunity, and propose that such interactions should be considered for the development of better DC-targeted immunotherapies.
Highlights
The interaction between various myeloid and lymphoid cell populations is crucial to initiate and orchestrate a robust anti-tumor response
We mainly focus on this latter scenario of non-synchronous activation events by cDC1s and cDC2s and the reorganization of plasmacytoid DCs (pDCs) to the sites of CTL priming to describe the crosstalk between Dendritic cells (DCs) subsets and propose an integrated model of multi-DC subsets, multi-cell type interactions in achieving full-strength CTL responses in anti-tumor immunity
These observations underscore the pivotal role of the crosstalk between DC subsets in maximizing immune response against cell-associated antigens
Summary
The interaction between various myeloid and lymphoid cell populations is crucial to initiate and orchestrate a robust anti-tumor response. As a result of more recent deep-phenotyping, DCs are recognized to be a heterogenous population comprising several subsets distinguished by their development, phenotypic differences, localization, and functional specialization [2,3,4,5,6]. This functional specialization of each subset allows DCs to initiate distinct immune responses in different immunological contexts [7]. We review literature supporting the hypothesis that, one DC subset, conventional DC1(cDC1), has been shown to be crucial for anti-tumor immunity, multiple DC subsets, and interactions with other cells are needed for maximal responses
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