Issues

Surface-trapped TNF-α and single-cell sequencing can identify Ag-specific TCRs.

Exogenous TCR expression in donor cells allows characterization and epitope mapping.

Btk supports autoreactive B cells through an early immune tolerance checkpoint.

Btk mediates antiapoptotic Bcl-xL expression in anergic anti-insulin B cells.

Mature autoreactive B cells do not require Btk for survival or Ag presentation.

Nimodipine alleviates EAU by regulating T cells through the p38–MAPK pathway.

Nimodipine suppresses the T cells on proliferation, activation, and differentiation.

H2-O deficiency does not predispose to organ-specific or systemic autoimmunity.

H2-O controls the establishment of a chronic γ-herpesvirus infection.

The linkage of ERAP1 with increased susceptibility to CNS autoimmunity is confirmed.

ERAP1-mediated susceptibility to CNS autoimmunity is B cell intrinsic.

The IL-10⁺ CNS immune compartment at the single-cell and protein levels is reconstructed.

CD29 expression enriches for cytotoxic CD4⁺ T cells in blood, tumor, and CMV infection.

CD29^hiCD4⁺ T cells produce more proinflammatory cytokines and granzymes.

CD29^hiCD4⁺ T cells have superior killing capacity against tumor cells in vitro.

RUNX1 reduces cell cycle and immediate early gene expression in naive B cells.

BCR stimulation triggers a switch from RUNX1 to RUNX3 binding at cell cycle genes.

Notch signaling is downregulated by RUNX1 in follicular B cells.

IRF4 is limiting for efficient production of high-affinity GCBs.

Irf4 haploinsufficiency causes suboptimal regulation of Blimp-1 expression in GCBs.

Irf4 haploinsufficient cells are competitively disadvantaged for T cell help.

CD24 and IgM cause transfer of CD24, IgM, and lipid between B cells.

Transfer of lipid and IgM is mediated by extracellular vesicles.

The transferred CD24 and IgM are functional in recipient cells.

Multiorgan inflammation with IFN signature is observed in Adar1^K948N/K948N mice.

White matter abnormalities and gliosis are detected in aged Adar1^K948N/K948N mice.

A K948N point mutation reduces ADAR1 p150–mediated RNA editing, activating MDA5.

LT-HSCs retain the potential to develop into TRMΦ but are tissue specific.

Large/small peritoneal MΦ exhibit a dual ontogeny, with yolk sac and LT-HSC origins.

Brain-resident microglia are not regenerated by fetal LT-HSCs.

Gα₁₃ plays a role in integrin-dependent neutrophil transendothelial migration.

Gα₁₃ enhances motility but did not affect directionality of neutrophil migration.

Integrin outside-in signaling mediates Gα₁₃-dependent neutrophil migration.

Zebrafish sirt7 negatively regulates antiviral responses.

Zebrafish sirt7 attenuates irf3 and irf7 phosphorylation.

Sirt7 carries out its suppressive role in antiviral responses independent of its enzymatic activity.

CgPDGFRβ bound different bacteria and interacted with CgSrc.

The activated CgSrc interacted with CgStat to induce its nuclear translocation.

CgPDGFRβ-mediated signaling induced the production of immune effectors.

IL-33 activity is mediated by cell surface ST2L and antagonized by decoy soluble ST2.

Il13^−/− mice had heightened IL-33 responses relative to WT.

IL-13 limits IL-33 activity by modulating the transmembrane and soluble forms of ST2.

Lean Il4ra^Δmyel mice have a deteriorated insulin sensitivity.

Obese Il4ra^Δmyel mice have a rather improved metabolic phenotype.

IL-13 stimulation increases CD11c expression in macrophages.

FAM177A1 is a negative regulator of IL-1β–induced signaling.

FAM177A1 inhibits TRAF6-mediated polyubiquitination.

FAM177A1 impairs TRAF6–Ubc13 interaction.

Notch signaling enhances SMAD-dependent expression of mucosal mast cell markers.

Notch signaling regulates epigenetic modification of mucosal mast cell marker genes.

Notch signaling promotes the nuclear localization of SMADs 3 and 4 in mast cells.

In vivo development of alloprimed CD8⁺ CTLs requires iNKT or CD4⁺ T cell help.

iNKTs promote the in vivo development of alloprimed CXCR3⁺CCR4⁺CD8⁺ T cells.

CXCR3⁺CCR4⁺CD8⁺ T cells are a multipotent, highly cytotoxic CD8⁺ T cell subset.

Obesity enhances tumor growth while priming macrophages for inflammatory phenotypes.

The obesity-associated hormone leptin is sufficient to enhance antitumor immunity.

Leptin reprograms macrophages to complement PD-1 blockade immunotherapy.

β₂-Adrenergic signaling impacts monocyte-derived cells rather than dendritic cells.

Propranolol improves cancer vaccine treatment of melanoma in mice.