Maternal immune activation (MIA) can cause neurodevelopmental disorders, but the underlying mechanisms are incompletely understood. In this issue of Immunity, Bian et al. show that MIA triggers decidual NK cells to secrete granzyme B, which crosses the…
Somatic mutations in hematopoietic stem cells can lead to clonal hematopoiesis of indeterminate potential (CHIP), a frequent condition associated with many age-related diseases including solid cancer. In the New England Journal of Medicine, Pich et al….
Cytotoxic antibodies have become an essential tool to remove unwanted cells in patients with cancer, infection, and autoimmunity. Wöhner and Nimmerjahn summarize recent insights into how antibody-dependent cellular cytotoxicity (ADCC) reactions proceed…
Red blood cells (RBCs) undergo pathological cell death in hemolytic diseases. In a recent issue of Cell, Chen et al. reveal a mode of programmed cell death, spectosis, in which complement activation initiates (mini)NLRP3-caspase-8 complexes, culminatin…
The regulation of myeloid cell responses can determine tumor outcomes. In this issue of Immunity, Blidner et al. report that galectin-1 triggers both immunoregulatory and pro-angiogenic circuits in myeloid cells, promoting tumor growth via a VEGF-depen…
Evolutionary medicine integrates principles of evolutionary biology to understand and treat human diseases. As a classical example, positive selection of the sickle hemoglobin mutation, which confers a survival advantage against malaria in heterozygous…
To limit hyperactive T helper (Th)1-driven pathology, it is crucial that this T cell population contracts upon pathogen clearance. In this issue of Immunity, Rahman et al. define a complement-C5-mediated lipid-class-switch mechanism that regulates Th1 …
Metabolic reprogramming is a hallmark of cancer. Liu et al. demonstrate that in hepatocellular carcinoma, inflammatory macrophage-driven efflux of N1-acetylspermidine operates in a charge-dependent manner to polarize CCL1+ macrophages, which in turn re…
The pathways regulating Th1 cell contraction are not well understood. Rahman et al. demonstrate that complement receptor C5aR2 controls T cell-intrinsic prostanoid metabolism as an integral component of Th1 cell contraction. Faulty C5aR2-prostanoid rew…
Polyclonal Mycobacterium tuberculosis-specific antibody-mediated effector functions correlate with improved infection in humans; however, the precise antibody specificities and functions that contribute to this control remain undefined. Grace et al. em…
