Issues

Soyon Hong is a group leader at the UK Dementia Research Institute at UCL. Her lab is interested in investigating how cell types work together to maintain brain function, and how these interactions are dysregulated during neurodegenerative disease states such as Alzheimer’s disease.

Tingible body macrophages in lymph node clear apoptotic B cell debris. Gurwisz et al. and Grootveld et al. report how tingible body macrophages, originating from tissue-resident macrophages, clear apoptotic B cells in the germinal center using a “stand-hunting” strategy.

Macrophages activate a cascade to drive anti-androgen therapy resistance in the prostate bone metastasis microenvironment.

There is growing appreciation of the heterogeneity of type 2 immunity in food allergy and how type 2 cytokines from distinct cell types contribute to pathogenesis. The landscape of clinical trials in food allergy is being transformed with type 2–targeting therapeutics.

The authors use single-cell RNA-sequencing and TCR tracking to analyze blood and tumors from breast and ovarian cancer patients treated with PD-1 blockade and CDK4/6 inhibition. They find that both therapies are immunologically active and enhance T cell effector function and memory, respectively.

Mice from different genetic backgrounds have widely diverse responses to the same metabolic challenges. Only PWK/PhJ mice show significant mitochondrial dysfunction and progression to fibrotic NASH that resembles human NASH. The PWK/PhJ strain is a novel NASH mouse model.

Tingible body macrophages (TBMs) were discovered more than 100 yr ago, yet their origins and cellular dynamics were unknown. Gurwicz et al. demonstrate that TBMs arise from lymph node–resident precursors and consume germinal center B cells by highly dynamic dendrites to prevent intracellular-content dissemination.

New mechanism of macrophage-driven therapy resistance of metastatic prostate cancer with high ECM expression and SRC activation using a novel in vivo model of bone-metastatic prostate cancer.

Sun et al. found that STAT3, activated by IL-10 and IL-21, regulates the terminal differentiation of effector CD8⁺ T cells in cancer and also plays an important role in effector CD8⁺ T cells in acute infection.

Collaboration between myeloid and lymphoid lineages on hematopoiesis has not been fully elucidated. Here, we showed that during systemic infection, a unique B cell subset expressing myeloid markers emerged to enhance on-demand emergency myelopoiesis by producing IL-10.

Wade-Vallance et al. reveal that antigen- or antibody-mediated ligation of the B cell receptor on IgE plasma cells induces apoptosis. This mechanism also operates in the context of endogenous IgE regulation, highlighting its relevance to allergic disease and treatment.

Natural (n)IgM is critical for immune homeostasis and host defense. Smith et al. show that BM nIgM-secreting B-1 plasma cells require TCRαβ⁺ CD4 T cell help. Their repertoire lacks known B-1 cell specificities but instead contains public clones with oligoclonal, short Igh-CDR3 motifs.

This study characterizes the plasma cell and monoclonal antibody repertoire throughout the human colon at high resolution using matched single-cell V(D)J- and RNA-seq profiling, as well as antibody characterization of biopsies from patients with ulcerative colitis and healthy controls.

Yuling Li et al. identify selective expression of BCL6 in CCR6⁺ ILC3 among ILC family. BCL6 expression, promoted by intestinal microbiota, restrains the effector function and plasticity of CCR6⁺ ILC3.

Xue, Peng, and colleagues employed multiomics approaches including Hi-C to demonstrate that CTCF promotes cytotoxic effector differentiation through dynamic redistribution, local chromatin accessibility control, and higher-order genomic reorganization, while enclosing memory precursor–associated genes within insulated neighborhoods to restrain their activation.

Petkova et al. identify a new Ptx3-positive immune-interacting subtype of lymphatic endothelial cells, iLECs, that drive oncogenic PI3K-driven lymphatic malformations. These cells produce chemokines that recruit pro-lymphangiogenic macrophages, which in turn promote pathological lymphatic vessel growth.