Issues
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Cover Image
Cover Image
The tumor microenvironment (TME) plays an important role in shaping antitumor immunity. Attalla and Boucher et al. find that expression of a human epidermal growth factor receptor splice variant (HER2Δ16) associates with poor outcome in patients with breast cancer. HER2Δ16+ tumors from transgenic mice that express the splice variant in mammary epithelium had low immune infiltration and an altered cytokine profile compared to higher infiltrated tumors from transgenic mice expressing the wild-type form of HER2. Expression of ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1) on the cell surface of HER2Δ16+ tumors promotes the immune-cold phenotype, and the data highlight its potential therapeutic targeting in aggressive HER2+ breast cancer to promote an immune-hot TME. Read more in this issue on page 1184. Original image from Fig. 2A. Artwork by Corey R. Long - PDF Icon PDF LinkTable of Contents
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Journal Archive
Cancer Immunology Research (2013-Present)
(ISSN 2326-6066) Published monthly since 2013.Cancer Immunity (2001-2013; volumes 1-13)
(EISSN 1424-9634) Published periodically from 2001-2013.Table of Contents
What We're Reading
In the Spotlight
Review
Research Articles
Aerobic Exercise Alters the Melanoma Microenvironment and Modulates ERK5 S496 Phosphorylation
The mechanisms underlying exercise-induced changes in the tumor microenvironment are incompletely understood. The authors demonstrate that aerobic exercise alters intratumoral T- and myeloid-cell function and that ERK5 S496 phosphorylation is key in exercise-dependent changes in these immune cells.
HER2Δ16 Engages ENPP1 to Promote an Immune-Cold Microenvironment in Breast Cancer
The authors study the impact of wild-type or variant HER2 on the TIME using new mouse models. Surface ENPP1 on HER2Δ16 tumor cells promotes an immune-cold environment, highlighting a potential target to convert immune-cold tumors into immune-hot tumors.
Enhancing CAR T-cell Therapy Using Fab-Based Constitutively Heterodimeric Cytokine Receptors
The authors characterize a library of engineered chimeric cytokine receptors (CCR) in the context of CAR T-cell therapy. These CCRs hold the potential for tailoring cytokine signaling to the type of adoptive cell therapy being developed.
AXL Inhibition Improves the Antitumor Activity of Chimeric Antigen Receptor T Cells
Many factors reduce the efficacy of CAR T-cell therapy. The authors show AXL inhibition can skew CAR T cells to a Th1 phenotype and can selectively target M2-like cells, leading to improved CAR T-cell responses in preclinical models.
A Bispecific γδ T-cell Engager Targeting EGFR Activates a Potent Vγ9Vδ2 T cell–Mediated Immune Response against EGFR-Expressing Tumors
Vγ9Vδ2 T cells have antitumor activity. The authors show EGFR-Vδ2 bispecific T-cell engagers direct Vγ9Vδ2 T-cell reactivity to EGFR-expressing tumor cells in vitro, in vivo, and ex vivo providing rationale for testing them clinically against EGFR-expressing malignancies.
Host Interactions with Engineered T-cell Micropharmacies
Adoptive T-cell therapy is efficacious against some cancers but there are many barriers to success in solid tumors. The authors show the Synthetic Enzyme-Armed KillER (SEAKER) drug-delivery platform can overcome some of these challenges in immunocompetent hosts.
Clec4A4 Acts as a Negative Immune Checkpoint Regulator to Suppress Antitumor Immunity
The authors show that murine Clec4A4 and human CLEC4A on conventional dendritic cells are negative immune checkpoint regulators that impair antitumor immune responses, suggesting hCLEC4A as a potential target for immune checkpoint blockade tumor immunotherapy.
CCRL2 Expression by Specialized Lung Capillary Endothelial Cells Controls NK-cell Homing in Lung Cancer
The study indicates that selective expression and regulation of CCRL2 by alveolar capillary endothelial cell subsets represents an underestimated homing signal for the migration of NK cells to the lung, which has implications for tumor immunotherapy.
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