Immune cells in cancer

This study shows that human airway macrophages reprogram their metabolism in response to IFN-γ, leading to glycolysis-dependent functional plasticity that differs from monocyte-derived macrophages.

The paper identifies HTR2B on MDSCs as a target to enhance immune checkpoint inhibitors in breast-to-brain metastasis using clozapine and anti-PD-1 therapy.

This study shows that the cell of origin in lung adenocarcinoma affects the immunosuppressive state of the tumor microenvironment, with AT1-derived tumors showing an anti-tumor immune profile and AT2-derived tumors showing immunosuppressive features.

This study uses scRNA-seq to analyze how chemotherapy remodels the immune landscape and metabolic state in lung adenocarcinoma, identifying changes in macrophage subtypes and immune responses.

This study identifies IL-8 as a key factor instructing macrophage identity in glioblastoma, showing IL-8 is necessary for generating CD32+ M_IL-8 macrophages in tumors contacting the lateral ventricle.

This study uses single-cell RNA sequencing to show hypofractionated radiotherapy recruits CCL8high macrophages, reprograms them to an immunosuppressive state, and enhances tumor growth, which can be counteracted by CCL inhibitor Bindarit.

This study identifies granulocyte-derived lipids loaded on HDLs as essential for IL-4-induced M2 macrophage activation and oxidative phosphorylation.

This study compares agent-based and equation-based models of macrophage polarization to understand their activation dynamics under pro- and anti-inflammatory stimuli.

This study shows that AGuIX nanoparticles and their combination with ionizing radiation induce proinflammatory reprogramming of tumor-associated macrophages via AMPK-dependent mitochondrial fragmentation.

This study identifies hysteresis genes in macrophage polarization and shows that AP-1 and CTCF regulate chromatin state changes during de/repolarization.

This paper develops a vascularized tumor model to study TAM recruitment and evaluates a multispecific antibody's effect on monocyte migration and TAM repolarization.

This study identifies distinct TNF-dependent aging signatures in monocyte subpopulations, showing that aging affects their transcriptional regulation differently.

The paper uses ensemble-based genome-scale modeling to predict metabolic differences between M1 and M2 macrophage subtypes in colorectal cancer and identifies metabolic perturbations that shift M2 metabolism toward M1.

This study identifies Cystatin C as a glucocorticoid-responsive factor that recruits Trem2+ macrophages and predicts immunotherapy failure in cancer.

The paper refines a gene signature for identifying TAM polarization in CRC using single-cell RNA-seq and transfer learning, validated across multiple datasets.

The paper identifies a 338-gene signature of macrophage reactivity and tolerance that predicts disease outcomes across diverse conditions and species.

The paper identifies two neutrophil subtypes in cancer using single-cell RNA sequencing, showing their conservation across species and tumor types, and links them to immunosuppressive pathways.

This study shows that gremlin 1 promotes M2-like polarization of macrophages in response to Th2 cytokines.

The paper develops an agent-based model to simulate monocyte differentiation into nurse-like cells in chronic lymphocytic leukemia and identifies patient-specific macrophage phenotypes linked to cancer survival.

This study compares proliferation and tolerance in tissue-resident and recruited macrophages using single-cell RNA sequencing, finding that proliferative capacity differs between cell types.

This study identifies biological processes and molecules differentiating M1 and M2 macrophages using RNA-seq data from mouse samples.

The paper identifies three regulatory factors that shift macrophage polarization from M1 to M2 and increase susceptibility to S. aureus infection.

The paper develops a computational model of macrophage signaling to predict activation responses to cytokine combinations, revealing a second axis of activation distinct from the M1-M2 polarization.

The paper builds a Boolean model to simulate macrophage polarization in an in-vitro chronic lymphocytic leukaemia model, revealing the formation of tumour-associated macrophages.

This study maps the distribution of macrophages in mouse mammary glands across developmental stages using 3D imaging, revealing stage-specific variations and sexual dimorphism.