Participating Experts: Stefani Spranger, PhD (MIT) and Santiago Zelenay, PhD (Cancer Research UK)
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Explore/download the Cell-Intrinsic Innate Immunity Signaling Pathway Diagram: cst-science.com/mz55z2
While targeting T cells has proven to be a technically successful treatment protocol for most cancer immunotherapies, only a fraction of cancer patients respond to these interventions. Of late there has been a surge of interest in investigating the relatively underexplored innate immune system as a possible tool for therapeutic intervention. Innate immune effector cells, including natural killer cells, macrophages, and dendritic cells, have been shown to interact with cancers and inhibit their progression. Dissecting the molecular details of these interactions will aid in identifying cancer-derived intrinsic factors that can be exploited to be develop effective immunotherapy regimens. In this webinar recording, the speakers provide examples of how innate immunity pathways are involved in fighting cancer, and how these pathways might be co-opted to generate new treatments.
Table of Contents:
0:43 Welcome and overview
2:56 Santiago Zelenay speaker profile
3:32 Manipulating inflammation to raise cancer immunogenicity
5:07 How tumors evade immune responses: a longstanding question
6:48 Dual role of inflammation in cancer
8:50 Mutant Braf-driven melanoma cells from progressively growing tumours in WT mice
9:42 Innate immune cells are essential for initiating adaptive immunity
10:48 Conditioned medium from Braf(V600E) melanoma cells has profound modulatory effects on dendritic cells
13:25 Braf(V600E) melanoma cells produce PGE2 via COX-2 and COX-1
14:49 COX-dependent melanoma growth through evasion of immunity
20:04 Manipulating inflammation to raise cancer immunogenicity
20:46 Cyclooxygenase-inhibition synergizes with PD-1 blockade
23:23 A COX-2 dependent inflammatory signature is conserved in human cancers
24:52 Conclusions and implications
26:38 Stephani Spranger speaker profile
27:27 The relationship between Batf3-DC and anti-tumor T-cell responses
25:54 CD8+ T cell inflammation is associated with an increased response to checkpoint blockade therapy
29:31 Anti-PD-1 therapy appears to be preferentially effective in T cell-inflamed tumors
31:00 Identification of pathways differentially activated between T cell-inflamed and non-T cell-inflamed patients
32:50 Genetically engineered mouse tumors lack T cell infiltration
34:40 CTLA-4/PD-L1 checkpoint blockade fails to control beta-catenin-expressing tumors
34:41 Non-T cell-inflamed tumors have reduced numbers of Batf3-DC
37:13 Lack of CD103+ DC is associated with reduced priming of tumor-specific T cells
38:19 CD103+ DC are essential for T cell priming
40:24 Tumors lacking Batf-3 DC show reduced 2C T cell numbers
45:00 Are Batf3-DC within the tumor required for recruitment of effector T cells?
46:40 CD103+ DC are essential for effector T cell recruitment and T cell priming
48:01 Questions and Answers
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