Issues

The Vdr is expressed in Aire⁺ medullary thymic epithelial cells.

Thymic vitamin D signaling stimulates Aire expression and Aire-dependent gene transcription.

Aire interacts with the Vdr and is a coactivator of Vdr-dependent transcription.

T-bet is required and sufficient to drive competitive liver CD4 TRM formation.

T-bet drives CD18 expression on CD4 T cells.

CD18 blockade ablated the T-bet–dependent effect of TRM formation.

HMB, a body-building supplement in humans, suppresses EAE.

HMB enhances Tregs and downregulates Th17/Th1.

HMB requires PPARβ, not PPARα, for immunomodulation and protection of EAE.

sTACI-s and sTACI-l are shed from plasmablasts by ADAM10.

sTACI-s blocks BAFF, and sTACI-l additionally blocks APRIL.

sTACI-l is the prevalent form of sTACI in human serum.

ΔSatb1 thymocytes show precocious thymic egress after positive selection.

Loss of Satb1 affects mTECs by lower expression of Tnfsf11 and Cd40lg.

Early egress and mTEC defects affect tTreg production in ΔSatb1.

The combinatorial dual-epitope DC vaccine is safe.

This vaccine regimen induced an immune response in a minority of patients.

One patient had an exceptional response and long-term survival.

3D cytotoxicity assay models can be used to evaluate T cell efficacy in solid tumors.

TEG A3 are highly tumor specific and lyse 3D tumor structures effectively in vitro.

TEG A3 are tumor specific in mixed 3D hybrid target structures.

The RNA-binding protein DDX5 regulates CD8⁺ T cell differentiation.

DDX5 represses the generation of central memory CD8⁺ T cells.

DDX5-deficient CD8⁺ T cells exhibit increased expression of central memory cell–associated genes.

SARS-CoV-2 ORF8 but not IL-17 upregulates cytokines in monocytes/macrophages.

Monocytes and macrophages infected with SARS-CoV-2 do not express IL-17RC.

ORF8 signals through MyD88.

LPS increased phagocytosis, NADPH oxidase activity, hypoxic signals, and inflammation.

NAM increased NAD and posttranslational modifications to inhibit the LPS response.

Decreased macrophage activation by NAM may reduce inflammation and pathogen clearance.

Th1 cells alter the transcriptional output of IL-6 during acute inflammation.

IL-6 and IFN-γ activities combine to steer tissue responses to inflammation.

STAT1 and STAT3 work in partnership to regulate immune outcomes.

Nlrp3-specific ASO treatment downregulates Nlrp3 expression and IL-1β release in murine CAPS.

Nlrp3-specific ASO treatment reduces systemic inflammation in murine CAPS.

PIP-CpG is a systemically administered, tumor-targeting TLR9 agonist.

PIP-CpG drives effective T cell–mediated immunity against spontaneous breast tumors.

PIP-CpG dramatically alters the innate and adaptive immune landscape of these tumors.