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Cytokine release syndrome (CRS) and neurotoxicity limit the application of CAR T cell therapies in the clinic. In this issue, Bondanza and colleagues (p. 739) recapitulate key features of CRS in a mouse model and identify a causative role of monocyte-derived IL-1 in these adverse events, both of which can be blocked by IL-1 inhibition. In a related study, Sadelain and colleagues (p. 731) show that macrophages mediate CRS and develop a strategy to prevent CRS by expressing IL-1 inhibitor in CAR T cells. Cliona Rooney discusses both studies in a News & Views (p. 705). The cover depicts an activated monocyte producing IL-1 and IL-6.
With the ongoing demand for assisted reproduction, the need and ability to study the fundamentals of human reproduction at a cellular level have never been greater. At this juncture, we join other Nature Research Journals in formalizing our ethical guidelines for papers in this growing field.
A metastatic hormone receptor–positive breast cancer, usually resistant to immunotherapy, is successfully treated with tumor-infiltrating lymphocytes enriched for neoantigen reactivity, underscoring the broad potential of this immunotherapeutic approach.
Complete leukemic responses to chimeric antigen receptor–modified T cells are invariably accompanied by severe toxicity. Recently developed animal models allow mechanistic dissection and prevention of toxicity without loss of therapeutic benefit.
Genetic risk scores in schizophrenia are influenced by pregnancy complications that compromise the placenta, enhancing association of genes involved in metabolism and cellular stress with schizophrenia risk.
A large retrospective study involving 62,565 Danish men shows that those who have been overweight in childhood have a lower risk of having type 2 diabetes in adulthood if they had remission of overweight before 13 years of age.
Adoptive T cell therapy induced complete and durable remission in a patient with refractory metastatic breast cancer, providing proof of principle for this approach in breast cancer therapy.
An exploratory randomized controlled clinical trial of renal cell carcinoma identifies molecular patterns distinguishing responders to immune checkpoint blockade alone or combined with angiogenesis inhibitor versus angiogenesis inhibitor alone.
Interactions between the MLL3 histone methyltransferase and the BAP1–UTX complex set the level of histone H3K27 methylation and suggest a new therapy for MLL3-mutant cancer.
Accumulation of zinc in muscle cells resulting from transcriptional upregulation of metal transporter ZIP14 causes muscle atrophy and promotes cachexia in metastatic cancer.
Loss of sympathetic nerve innervention of the bone marrow contributes to the aging of hematopoietic stem cells, which can be rejuvenated using an adrenergic receptor agonist.
In a mouse model of intellectual disability, the chromatin remodeling protein ATR-X is shown to bind to G-quadruplex DNA structures and modulate target gene expression, which can be pharmacologically targeted to restore neuronal and cognitive phenotypes in these animals.
Inhibition of immune cell–derived acetylcholine synthesis or of its signaling via CHRNA2 in beige adipocytes reduces thermogenesis and exacerbates diet-induced obesity, suggesting a new mode of immuno–fat communication in energy metabolism.
Excess anti-Müllerian hormone during pregnancy results in polycystic ovary syndrome-like phenotypes in female offspring, possibly explaining its pathogenesis as well as suggesting a possible therapy.
An integrated resource of (epi)genomic features in annotated chronic lymphocytic leukemia (CLL) primary samples uncovers subgroup-specific regulatory alterations associated with clinical behavior.