Issues

C/EBPδ is elevated in mouse and human AGN.

IL-17–induced C/EBPδ promotes expression of renal-damaging genes.

Cebpd^−/− and Il17ra^−/− mice are refractory to AGN and exhibit fibrosis in renal injury.

Intraislet Tregs have a uniquely dysfunctional phenotype compared to periphery Tregs.

Augmenting Nrp1 specifically on Tregs causes a delay or prevention of diabetes onset within the NOD model.

Transcriptional analysis showed that Nrp1⁺ and Nrp1⁻ Tregs exhibit significant differences regardless of tissue site.

Lactate is crucial for cytosolic mtDNA to induce IFN-I responses.

Lactate promotes lactylation of cGAS, thereby inhibiting its ubiquitination.

Targeting lactate alleviates disease development in humanized SLE chimeras.

Neutralizing anti–IFN-α and IFN-β Abs were cloned from PBMCs.

This study identified two pairs of natural mAbs capable of neutralizing IFN-α or IFN-β.

The identified mAbs have potential usage for therapeutic strategies.

IL-9-secreting T cells in chronic inflammation are polyfunctional.

Activin A promotes a polyfunctional Th cell phenotype.

Activin A–primed Th cells promote robust allergic airway inflammation.

Calcitriol suppresses IL-4 and IL-13 production in murine and human Th2 cells in vitro.

Calcitriol regulates Th2 phenotype by modulating the expression of Gata3 and Gfi1.

Ecr, key enhancer of Il4 and Il13, is essential for calcitriol-mediated regulation.

Vaccination with O-mannans induces trained immunity by innate lymphocytes.

O-mannan vaccination protects mice heterologously against C. albicans infection.

Trained immunity by innate lymphocytes requires neutrophils for protection.

Neutrophils swarm Cmv5^s marginal zones early and die, bringing oxidative stress.

Neutrophil clusters and spreading virus surround highly infected SIGNR1⁺ MZMs.

Macrophage loss mirrors spatial and temporal appearance of Cmv5^s tissue damage.

Inflammasome activation in renal mononuclear phagocytes activates profibrotic ILC3.

Inflammasome-derived IL-1β and the type 3 immunity cytokine IL-23 expand renal ILC3.

IL-23 inhibition reduced ILC3–phagocyte cross-talk and reduced kidney fibrosis.

The structure of W6/32 in complex with HLA-I definitively maps the epitope.

W6/32 directly blocks LILR and indirectly blocks KIR and TCR binding to HLA-I.

Colonic Tregs bifurcate into two functionally distinct activation trajectories.

Microbiota shifts colonic Tregs to enhanced PD-1⁻ CXCR3⁺ suppressive phenotype.

Microbiota-induced IL-10^high CXCR3⁺ Treg accumulates at the onset of inflammation.

CD4 T cells mediate type1 and cytotoxic immune response during lung allograft rejection.

Increased cytotoxic CD4⁺NKG7⁺ T cells in IL-10KO mice during ACR.

IL-10 regulates alloeffector CD4 T cells.

IV anti-CD45.2 label lasts for 3 days and tracks leukocyte migration to tissue.

There is continuous innate and adaptive leukocyte migration in a model of lung cancer.

Blocking or preventing systemic Treg recruitment results in tumor burden reduction.