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Retinoic Acid Induces an IFN-Driven Inflammatory Tumour Microenvironment, Sensitizing to Immune Checkpoint TherapyWith immune checkpoint therapy (ICT) having reshaped the treatment of many cancers, the next frontier is to identify and develop novel combination therapies to improve efficacy. Previously, we and others identified beneficial immunological effects of the vitamin A derivative tretinoin on anti-tumour immunity.
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Abacavir inhibits but does not cause self-reactivity to HLA-B*57:01-restricted EBV specific T cell receptorsPre-existing pathogen-specific memory T cell responses can contribute to multiple adverse outcomes including autoimmunity and drug hypersensitivity. How the specificity of the T cell receptor (TCR) is subverted or seconded in many of these diseases remains unclear. Here, we apply abacavir hypersensitivity (AHS) as a model to address this question because the disease is linked to memory T cell responses and the HLA risk allele, HLA-B*57:01, and the initiating insult, abacavir, are known.
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Comprehensive Testing of Chemotherapy and Immune Checkpoint Blockade in Preclinical Cancer Models Identifies Additive CombinationsAntibodies that target immune checkpoints such as cytotoxic T lymphocyte antigen 4 (CTLA‐4) and the programmed cell death protein 1/ligand 1 (PD-1/PD-L1) are now a treatment option for multiple cancer types. However, as a monotherapy, objective responses only occur in a minority of patients. Chemotherapy is widely used in combination with immune checkpoint blockade (ICB). Although a variety of isolated immunostimulatory effects have been reported for several classes of chemotherapeutics, it is unclear which chemotherapeutics provide the most benefit when combined with ICB.
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Celebrating 100 years of Immunology & Cell Biology – a special focus on the field of tumor immunology in AustraliaIn this Commentary article, as part of the 100-year celebrations of the journal, we reflect on the contribution of articles published in ICB in the field of tumor immunology. A highlight is a series of interviews conducted with three Australian-based ICB authors who have contributed key papers over the years: Rajiv Khanna, Delia Nelson and Ian Frazer.
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Transcriptional rewiring in CD8+ T cells: implications for CAR-T cell therapy against solid tumoursT cells engineered to express chimeric-antigen receptors (CAR-T cells) can effectively control relapsed and refractory haematological malignancies in the clinic. However, the successes of CAR-T cell therapy have not been recapitulated in solid tumours due to a range of barriers such as immunosuppression, poor infiltration, and tumour heterogeneity.
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Activation of ERBB4 in Glioblastoma Can Contribute to Increased Tumorigenicity and Influence Therapeutic ResponseThe functional effects of increased ERBB4 activation identify ERBB4 as a potential prognostic and therapeutic target
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Most clinical anti-EGFR antibodies do not neutralize both wtEGFR and EGFRvIII activation in gliomaWe discovered a previously unknown major resistance mechanism in glioma in that most EGFR domain III-targeting antibodies do not neutralize EGFRvIII
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PI3K activation in neural stem cells drives tumorigenesis which can be ameliorated by targeting the cAMP response element binding proteinA novel mouse model for glioma demonstrating that the PI3K pathway is important for initiation of tumorigenesis
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CMV drives the expansion of highly functional memory T cells expressing NK-cell receptors in renal transplant recipientsCytomegalovirus (CMV) is a common opportunistic infection encountered in renal transplant recipients (RTRs) and may be reactivated without symptoms at any time post-transplant.
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The Cold Atmospheric Plasma Inhibits Cancer Proliferation Through Reducing Glutathione SynthesisCold atmospheric plasma (CAP) is a safe and effective alternative to radiotherapy for cancer treatment. Its anticancer effects are attributed to increased intracellular reactive oxygen species (ROS). Glutathione, a key antioxidant derived from glutamine, is critical for cell proliferation. This study investigated whether CAP-induced ROS elevation results from reduced glutamine-glutathione conversion and elucidates the underlying mechanisms.