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The TAM receptor kinases Axl and Mer are critical for microglial recognition and clearance of accumulating amyloid in transgenic models of Alzheimer’s disease.
HIV-1 infection of CD4+ T cells triggers the interaction of the mitochondrial proteins NLRX1 and FASTKD5 to promote oxidative phosphorylation, leading to increased viral replication. It has now been shown that this process can be blocked by metformin.
The eradication of pathogens and establishment of immunological memory depend on the generation of both effector and long-lived memory cells within specialized immune niches. Whole-organ imaging demonstrates that, during viral infection, the fate of CD8+ T cells in lymph nodes is coupled to chemotactic signals controlling their distribution within different microanatomical sites.
In the colonic environment, sustained Wnt–β-catenin activation in regulatory T cells promotes epigenetic rewiring toward proinflammatory RORγt+ Treg cells, whose expansion parallels the disease progression from inflammatory bowel disease (IBD) to manifest colorectal cancer (CRC).
Long-term pathogen and tumor control as well as checkpoint immunotherapies rely on ‘stem-like’ CD8+ T cells. New results uncover BACH2 as a key regulator of this subpopulation and solve an important piece of the puzzle.
Brain tumors respire more oxygen, causing a hypoxic microenvironment that impairs innate γδ T cell–mediated antitumor activity. Reducing oxygen consumption by brain tumors or inhibiting hypoxia-inducible factor-1α in γδ T cells reinvigorates γδ T cell tumor-killing activity, leading to prolonged survival in brain-tumor-bearing mice.
The transition of Sub-Saharan Africans from rural settings and traditional plant-rich diets to urban settings and calorie-dense Westernized diets has led to specific shifts in serum metabolites and activates a heightened proinflammatory state in immune cells.
New research demonstrates that γδ T cells recognize Plasmodium-infected erythrocytes via interaction of the T cell antigen receptor with the phosphoantigen sensor BTN3A1 and subsequently destroy infected cells through either cytotoxic molecule secretion or antibody-dependent phagocytosis.
IRGM1 is recognized as a master regulator of type I interferon responses against pathogens, while also protecting against autoimmune diseases. It has now been shown that IRGM1 controls autoinflammatory responses by modulating mitophagy flux.
An investigation of the molecular processes of mitochondrial reprogramming and metabolic stress in antigen-experienced T cells within tumor microenvironments reveals mechanisms responsible for T cell exhaustion and dysfunction and facilitates the development of new strategies for tumor immunotherapy.
Single-cell-sequencing techniques enable the decades-old T helper subset dogma to be re-examined in an unsupervised manner, bringing nuance to the definition of known subsets while simultaneously identifying interesting new cell states.
Following internalization of an actin-bearing ligand, the C-type lectin receptor DNGR-1 promotes phagosome rupture, allowing antigens to access the cytosol and be processed through the MHC-I pathway.
