Issues

p38α signaling reshapes keratinocyte gene expression during allergic dermatitis.

p63 phosphorylation by p38α is essential for epidermal MMP13 induction.

Topical p38α and MMP13 inhibitors suppress atopic dermatitis–like disease in mice.

A contact allergen, DNCB, binds proteins in a short time frame.

DNCB directly binds HSP90, which appears to contribute to contact hypersensitivity.

Inhibition of HSP90 can attenuate DNCB-induced contact hypersensitivity.

Inducible AID-knockout model shows that AID impacts the primary B cell repertoire in naive mice.

Natural Ags and microbiome may potentiate AID footprints.

CD47-expressing apoptotic cells accumulate in autoimmune valvular carditis.

CD47 blockade promotes efferocytosis and reduces inflammatory cytokine production.

CD47 blockade reduces the severity of autoimmune valvular carditis in mice.

In ESS mice, significant nuclear translocation of IL-33 occurred during the disease.

IL-33 stimulates the epithelium to play a proinflammatory and chemotactic role.

IL-33 indirectly promotes T cell differentiation in a variety of ways.

We evaluated four heterologous prime-boost HIV vaccine strategies in a clinical trial.

Three strategies, all including the HIV MVA-B vaccine, led to T cell responses.

A gene expression signature related to the HIV MVA-B vaccine was identified.

Ab repertoire can serve as a biomarker for immune status classification.

Various infections share a set of public repertoire features.

Private features can distinguish one infection from another.

Zbtb46 has a dominant role in maintaining homeostasis of dendritic cells.

Zbtb46 controls dendritic cell activation by suppressing Cd80/86 and Cd40 signals.

Zbtb46 regulates cd80/86 and cd40 expression by reprogramming epigenetic regulation.

The suppressor proteins 4E-BP1/2 regulate mTORC1 activation in CD8 T cells.

4E-BP1/2 proteins are required for CD8 T cell proliferation and differentiation.

4E-BP proteins exert translational control on mitochondrial biogenesis in CD8 T cells.

We studied the ontogeny of the Ig repertoires and microbiome in mice aged 0–8 wk.

Gut–spleen shared clones initiate in the gut and then expand to the spleen.

Diversity indices of the Ig repertoire and microbiome change in a correlated manner.

SM03 (an anti-CD22 mAb) immunomodulates B cells in autoimmunity in a novel mechanism of action.

SM03 converts cis-to-trans binding of CD22 to α2,6-linked sialic acid glycans.

SM03 induces immunomodulation and immune tolerance of B cells to autoantigens.

Asialo-glycoproteins mediate CD8⁺ T cell localization to the spleen, not the liver.

Asialo-glycoprotein–expressing effector CD8⁺ T cells are removed from the spleen.

Platelets have a minimal role in CD8⁺ T cell localization to the liver.

Peritoneal cavity B cells express T-bet following infection.

Peritoneal cavity CXCR3⁺ and CXCR3⁻ B cells are transcriptionally distinct.

T-bet⁺ MBCs dominate the peritoneal cavity B cell pool during chronic infection.

TSCs and TSC-TBs have functional IFN antiviral mechanisms.

ESCs are deficient in expressing IFN-α/β, but they can respond to IFN-α/β.

TSCs/TSC-TBs can provide IFN antiviral effect to ESCs via paracrine signaling.

Thrombin substantially modulated bacteria-induced inflammation in human whole blood.

Complement C5 and CD14 inhibition reduced the overall cytokine release significantly.

The TCA cycle intermediates citrate and succinate modulate cytokine expression.

SDH subunits exert different effects on IL-1β, IL-10, and IL-23 induction.

NAD⁺/NADH redox balance supports cytokine production through mitochondrial shuttles.

PBD-2 can actively enter cells and interacts with VASH1.

PBD-2 inhibits LPS-induced downregulation of VASH1.

PBD-2 inhibits the LPS-induced Akt/NF-κB signaling pathway via VASH1.

IFN-λ limits neutrophil-induced immunopathology during severe viral bronchiolitis.

IFN-λ signaling in neutrophils regulates ROS production.

IFN-λ signaling in neutrophils regulates PAD4-independent NETosis.

Splicing efficiency by the four proteasome subtypes depends on the peptide sequence.

Availability of the splice reactants is a factor controlling splicing efficiency.

Affinity of the C-terminal splice reactant for the primed binding site also seems key.

Hyaluronan-enriched tumor stroma supports the development of PD-L1⁺ cell clusters.

Fibroblasts and epithelial tumor cells serve as the main source of hyaluronan.

Hyal2-expressing myeloid cells contribute to the development of PD-L1⁺ macrophages.

CD4⁺ T_RM cells can initiate an antitumor immune response.

The CD4⁺ T_RM/NK cell axis shapes the TME and orchestrates antitumor immunity.

CD4⁺ T cells dominate antitumor immunity.

Constitutively activated STAT3 induces the expression of pentraxin-related protein 3 in chronic lymphocytic leukemia cells.

Pentraxin-related protein 3 attenuates spontaneous apoptosis rate of chronic lymphocytic leukemia cells.

We performed a comprehensive analysis of PSPs by mass spectrometry–based de novo sequencing.

We validated proteasome splicing–dependent HLA presentation using reactive T cells.

Murine Bc.DLFL1 lymphoma originates from an age-associated B cell subset.

BAFF-R antagonization blocks the in vivo expansion of lymphoma cells.

The extranodal growth of lymphoma cells alters their local cytokine milieu.