Harnessing natural killer cell effector function against cancer

Blunt, Matthew D; Khakoo, Salim I

doi:10.1093/immadv/ltad031

Cited by 5 publications

(2 citation statements)

References 121 publications

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“…59,60 NK cells can also initiate apoptosis in target cells by expressing FasL and TRAIL, which engage death receptors. 56 NK cells can recruit and activate DCs, macrophages and T cells by secreting chemokines and cytokines, thereby promoting antitumour immunity. [61][62][63][64][65] T cells, the primary adaptive immune cells, can be classified into CD8+ and CD4+ T cells based on their surface markers.…”

Section: Immune Cellsmentioning

confidence: 99%

“…Inhibitory receptors, such as NKG2A and inhibitory killer cell immunoglobulin-like receptors (KIRs), can suppress the cytotoxic activity of NK cells. 56 The upregulation of HLA-E in cancer cells suppresses NK cell activation through NKG2A. 57 The interaction of NK cells with HLA class I molecules regulates their overall function by modulating the amount of releasable granzyme B, which is essential for cytotoxic activity.…”

Section: Immune Cellsmentioning

confidence: 99%

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B‐cell performance in chemotherapy: Unravelling the mystery of B‐cell therapeutic potential

Li,

Lin,

Gao

et al. 2024

Clinical & Translational Med

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Background and main bodyThe anti‐tumour and tumour‐promoting roles of B cells in the tumour microenvironment (TME) have gained considerable attention in recent years. As essential orchestrators of humoral immunity, B cells potentially play a crucial role in anti‐tumour therapies. Chemotherapy, a mainstay in cancer treatment, influences the proliferation and function of diverse B‐cell subsets and their crosstalk with the TME. Modulating B‐cell function by targeting B cells or their associated cells may enhance chemotherapy efficacy, presenting a promising avenue for future targeted therapy investigations.ConclusionThis review explores the intricate interplay between chemotherapy and B cells, underscoring the pivotal role of B cells in chemotherapy treatment. We summarise promising B‐cell‐related therapeutic targets, illustrating the immense potential of B cells in anti‐tumour therapy. Our work lays a theoretical foundation for harnessing B cells in chemotherapy and combination strategies for cancer treatment.Key points Chemotherapy can inhibit B‐cell proliferation and alter subset distributions and functions, including factor secretion, receptor signalling, and costimulation. Chemotherapy can modulate complex B‐cell–T‐cell interactions with variable effects on anti‐tumour immunity. Targeting B‐cell surface markers or signalling improves chemotherapy responses, blocks immune evasion and inhibits tumour growth. Critical knowledge gaps remain regarding B‐cell interactions in TME, B‐cell chemoresistance mechanisms, TLS biology, heterogeneity, spatial distributions, chemotherapy drug selection and B‐cell targets that future studies should address.

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Section: Immune Cellsmentioning

confidence: 99%

Section: Immune Cellsmentioning

confidence: 99%

B‐cell performance in chemotherapy: Unravelling the mystery of B‐cell therapeutic potential

Li,

Lin,

Gao

et al. 2024

Clinical & Translational Med

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NKG2A genetic deletion promotes human primary NK cell anti-tumor responses better than an anti-NKG2A monoclonal antibody

Gong,

Germeraad,

Zhang

et al. 2024

Molecular Therapy

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Cellular and transcriptional profiles of peripheral blood mononuclear cells pre-vaccination predict immune response to preventative MUC1 vaccine

Yuan,

McKeague,

Raghu

et al. 2024

Preprint

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A single arm trial (NCT007773097) and a double-blind, placebo controlled randomized trial (NCT02134925) were conducted in individuals with a history of advanced colonic adenoma to test the safety and immunogenicity of the MUC1 tumor antigen vaccine and its potential to prevent new adenomas. These were the first two trials of a non-viral cancer vaccine administered in the absence of cancer. The vaccine was safe and strongly immunogenic in 43% (NCT007773097) and 25% (NCT02134925) of participants. The lack of response in a significant number of participants suggested, for the first time, that even in a premalignant setting, the immune system may have already been exposed to some level of suppression previously reported only in cancer. Single-cell RNA-sequencing (scRNA-seq) on banked pre-vaccination peripheral blood mononuclear cells (PBMCs) from 16 immune responders and 16 non-responders identified specific cell types, genes, and pathways of a productive vaccine response. Responders had a significantly higher percentage of CD4+ naive T cells pre-vaccination, but a significantly lower percentage of CD8+ T effector memory (TEM) cells and CD16+ monocytes. Differential gene expression (DGE) and transcription factor inference analysis showed a higher level of expression of T cell activation genes, such as Fos and Jun, in CD4+ naive T cells, and pathway analysis showed enriched signaling activity in responders. Furthermore, Bayesian network analysis suggested that these genes were mechanistically connected to response. Our analyses identified several immune mechanisms and candidate biomarkers to be further validated as predictors of immune responses to a preventative cancer vaccine that could facilitate selection of individuals likely to benefit from a vaccine or be used to improve vaccine responses.

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Harnessing natural killer cell effector function against cancer

Cited by 5 publications

References 121 publications

B‐cell performance in chemotherapy: Unravelling the mystery of B‐cell therapeutic potential

B‐cell performance in chemotherapy: Unravelling the mystery of B‐cell therapeutic potential

NKG2A genetic deletion promotes human primary NK cell anti-tumor responses better than an anti-NKG2A monoclonal antibody

Cellular and transcriptional profiles of peripheral blood mononuclear cells pre-vaccination predict immune response to preventative MUC1 vaccine

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