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T cell activation is ‘digital’: exhaustive single-cell analysis shows that only the proportion of cells that cross the activation threshold is reduced when the affinity of the TCR for its ligand is reduced.
In response to epithelial DNA damage, tissue-resident γδ T cells initiate and shape a tumor-protective IgE response that requires CD4+ T cells and immune effector cells expressing the high-affinity IgE receptor FcεRI.
Co-stimulatory second signals delivered through TLRs or CD40 rescue antigen-stimulated B cells from metabolic dysfunction and apoptosis. This identifies a critical time-limited window during which B cells integrate sequential signals to successfully initiate humoral immunity.
What keeps memory T cells functionally silent in the absence of infection is unclear. New data reveal the existence of a deterministic halt in the protein-synthesis machinery of memory T cells and expose the discriminatory functions of a family of RNA-binding proteins.
Plasmacytoid dendritic cells (pDCs) are type I interferon–producing cells with antigen-presenting potential. pDC populations are composed of transcriptionally and functionally heterogeneous cellular subsets with distinct hematopoietic precursor origin.
The cytokine IL-17F constrains the growth of immunoregulatory Clostridium cluster XIVa species and represents a potential therapeutic target for the treatment of inflammatory bowel disease.
Tumor-associated natural killer cells have elevated expression of the checkpoint inhibitory receptor TIGIT. Monoclonal antibody–mediated blockade targeting TIGIT unleashes the anti-tumor activity of both natural killer cells and T cells in preclinical mouse models and efficiently delays tumor growth.
Naive T cells migrate rapidly through the lymph node. A high-resolution look at the chemokine receptor CCR7 and integrin LFA-1 reveals that T cells remain highly responsive to their microenvironment via instantaneous tuning of chemokine-regulated actin flow and integrin-regulated adhesion.
Human affinity-matured antibodies to Klebsiella pneumoniae lipopolysaccharide O-antigen have different patterns of glycan fine specificity without being polyreactive. These antibodies might constitute an important mechanism for homeostatic control of the intestinal microbiome.
The metabolic master regulator mTORC1 is shown to promote alternative macrophage activation via Semaphorin 6D reverse signaling and reprogramming of lipid metabolism.
γδ T cells accumulate with age in adipose tissue and produce the cytokine IL-17, which controls the homeostasis of regulatory T cells and adaptive thermogenesis. Thus, maintenance of core body temperature unexpectedly relies on these adipose tissue–resident γδ17 T cells.
Myeloid cells exhibit different inflammatory phenotypes after brain injury, yet the relative mechanistic roles for these diverse cell types in post-traumatic tissue damage and repair remain controversial.
Evasion of the immune system and global activation of the immune system are hallmarks of human immunodeficiency virus (HIV) infection. Studies reveal that macrophages might be responsible for HIV-associated pathogenesis via resistance to killing and induction of chronic inflammation.
The role of the transcription factor c-Maf varies in different CD4+ T cell subsets and can be associated with either pro-inflammatory activity or anti-inflammatory activity, depending on the cell context.
The activating natural killer cell receptor NKG2C can specifically recognize peptides derived from the cytomegalovirus protein UL40 in the context of HLA-E. This drives the expansion of a population of adaptive NKG2C+ natural killer cells.
Autoreactive T cells exclusively recognize the roof of the binding groove of the antigen-presenting molecule CD1c after it has caved in on short headless self lipids.
SWAP-70 and DEF6 prevent the cytokine IL-21–induced transcription factor IRF5 from binding to DNA and recruiting the transcription factor T-bet and thereby diminish the activation of age-associated B cells.
Systemic exposure to dietary and microbial components induces long-lasting epigenetic and metabolic changes in myeloid precursor cells, which results in enhanced proinflammatory and anti-microbial responses of mononuclear phagocytes after challenge with related or unrelated stimuli.
IL-33 is a mediator of allergic inflammation and is localized in mucosal tissues to respond rapidly to environmental insults. These include allergens themselves, which can directly activate IL-33 through their intrinsic proteolytic activity.
