Issues

Batf3 expression by CD8 T cells critically regulates memory T cell development.

Batf3^−/− CD8 T cells undergo increased apoptosis during contraction.

Batf3^−/− CD8 T cells have an impaired recall ability but remain functional.

NRF2 promotes keratinization and replenishes epidermal thiol gradient.

NRF2-dependent antioxidative response directs allergic contact dermatitis.

NRF2 may provide critical direction to the early phases of atopic disorders.

Generation and screening of anti–SARS-CoV-2 RBD mAbs reveal a potently protective Ab.

mAb 2B04 potently neutralizes SARS-CoV-2 in vitro.

mAb 2B04 protects mice from morbidity in a murine model of SARS-CoV-2 infection.

Three of the four HLA-DOA common alleles have differential impact on DM function.

Fifty-two percent of all DOA variants tested displayed altered function.

Two DOA variants were genetically linked to the outcome of hepatitis B infection.

A recent study proposes a new process as the dominant mechanism of human/mouse SHM.

We re-examine these results by estimating the false positive rates of their approach.

We find no evidence that templated mutagenesis is a major contributor to SHM.

CLEC16A correlates to surface CLIP expression in human B-LCLs and primary B cells.

CLEC16A knockdown impairs BCR-mediated uptake of Ag into MIICs.

CLIP is abundant and not coregulated with CLEC16A in blood B cells of MS patients.

Metformin + 2-DG represses human CD4⁺ T cell IFN-γ production and cell proliferation.

Metformin + 2-DG inhibits human CD4⁺ T cell Gln uptake and metabolic reprogramming.

Metformin + 2-DG reduces MYC and HIF-1A expression in human CD4⁺ T cells.

Osteomacs are associated with endplate osteosclerosis in MCs.

Osteomacs can regulate osteogenesis through the OSM-STAT3/YAP1 signaling axis.

OSM blockade prevents endplate osteosclerosis in MCs.

Tob2 inhibits TLR-induced proinflammatory cytokine expression.

Tob2 negatively regulates TLR4-induced NF-κB and MAPK activation.

Tob2 interacts with TRAF6 and MyD88 and inhibits signaling from them.

lncRNA AW112010 expression is increased in proinflammatory T cells.

AW112010 associates with histone demethylase KDM5A.

AW112010 suppresses IL-10 expression through histone demethylation.

Mice lacking VHL in their T cells are resistant to EAE.

VHL-deficient CD4 T cells have reduced capacity for Th17 differentiation.

VHL-deficient Th17 cells have altered cellular metabolism.

Myeloid cell–intrinsic IRF5 regulates chemokine-dependent T cell migration.

Myeloid cell IRF5 regulates key checkpoints in T cell activation/differentiation.

IRF5 risk variants modulate myeloid cell–dependent T cell–conditioning outcomes.

S. aureus–infected DCs induce Vδ2⁺ cell IFN-γ secretion via cell contact and IL-12.

Vδ2⁺ IFN-γ secretion promotes reciprocal enhancement of DC activation.

Coculturing infected DCs with γδ T cells enhances CD4⁺ cell responses to S. aureus.

Developing CD11c⁺ T-bet⁺ B cells require T_FH1 cells that produce both IFN-γ and IL-21.

Obligate IFN-γ and CD40L signals are provided at distinct times following infection.

CD11c⁺ B cells lacking T-bet undergo normal differentiation but improper switching.

LLEC exhibit transcriptional characteristics common to effector and memory T cells.

LLEC undergo homeostatic proliferation but do not critically depend on IL-15.

LLEC are predominantly derived from KLRG1^hi effector cells at 12 d postinfection.

Macrophages of different cellular origins remodel chromatin differently.

DNA shape features flanking PU.1 motifs may regulate chromatin remodeling.

ILC2s are activated even after injury from respiratory viral infection is resolved.

ILC2s contribute to a chronic type 2 immune response after viral infection.

ILC2s depend on myeloid–macrophage lineage cells to drive postviral disease.

C5aR2 agonism dampens C5aR1-, C3aR-, and CMKLR1-mediated ERK signaling in macrophages.

C5aR2 agonism modulates C5aR1-, C3aR-, and LTB4R-mediated calcium mobilization.

C5aR2 activation downregulates TLRs 3, 4, 7, Mincle-, and STING-mediated cytokines.

Macrophages expressing CD122 accumulate in the uterus and maternal–fetal interface.

M-CSF and IFNs drive macrophages to express CD122.

IL-15 causes CD122⁺ macrophages to activate ERK and enhance cytokine production.

Mitochondrial catalase regulates inflammation by altering cellular metabolism.

NAD(H) levels modulate NF-κB activation in macrophages.

Zebrafish phd3 negatively regulates antiviral responses.

Zebrafish phd3 suppresses irf7 transactivity.

Phd3 suppresses irf7 transactivity independent of its enzymatic activity.

Active Gsk3 promotes hepatocyte autophagy in response to TNF-α.

Gsk3 N-terminal phosphorylation inhibits macrophage TLR activation.

COX inhibition increased Alternaria extract–induced pulmonary ILC2 responses.

COX inhibition promoted Alternaria extract–induced IL-33 release in the lung.

COX inhibition augmented rIL-33–induced pulmonary ILC2 responses.

Both radioresistant and radiosensitive cells produce Il-18bp during CpG-induced MAS.

Il-18bp behaves as Ifn-γ signature gene during CpG-induced MAS.

Elevated circulating levels of Il-18bp prevent systemic effects of Il-18 in MAS.

Single-cell/Ab resolution characterizes recall with unprecedented resolution.

Recalled IgG-SCs appear fast and, at this early stage, free of naive IgG-SCs.

Recalled IgG-SCs correlated strongly with the IgG-SCs generated during boost.