Issues

A threshold of epitope density for a self-antigen elicits IgG1, IgG2b, and IgG3.

The class-switched autoreactive Abs were induced in the absence of T cell help.

TREX1 catalytic inactivity causes self-DNA sensing and IFN-I–dependent autoimmunity.

TREX1-deficient T cells exhibit evidence of DNA sensing and IFN-α expression.

Activated TREX1–deficient T cells spontaneously produce IFN-α protein.

B cell–specific deletion of Ship2 phosphatase reduces CLL formation in a mouse model.

Ship2 inhibition reduces Akt/mTORC1/S6 signaling in murine and human CLL cells.

Ship2 supports survival of CLL cells via the key antiapoptotic protein Mcl-1.

Immunization with COBRA P1 elicits broadly HA-binding ASC.

P1 HA-elicited mAbs have different binding and functional activities.

The P1-elicited 1F8 mAb exhibits broad H1N1 binding and functional activity.

Dendritic cells recognize and mount an immune response against B. miyamotoi.

Recognition of B. miyamotoi is partially mediated by TLR2.

Dendritic cells stimulated with B. miyamotoi induce proliferation of T cells.

PRRSV infection induces SOCS1 upregulation.

PRRSV N protein upregulates SOCS1, and NLS-2 is essential for this function.

AP-1 signaling pathways are indispensable for PRRSV-induced SOCS1 expression.

BLP tolerization promotes an early PMN recruitment in the infectious site.

This early PMN influx occurs via the CXCL2-formed concentration gradient.

Blockage of PMN influx eliminates BLP tolerance–afforded protection against sepsis.

IKIP inhibits NF-κB activation.

IKIP inhibits IKKα/β phosphorylation.

IKIP protects mice against LPS-induced septic shock and DSS-induced colitis.

Annotated lncRNA 1810058I24Rik encodes a conserved mitochondrial micropeptide.

Macrophages fail to activate the Nlrp3 inflammasome in the absence of Mm47.

Genetic deletion of Mm47 in macrophages affects only Nlrp3 and not Aim2 or Nlrc4.

Fibrinogen is a specific trigger for cytolytic eosinophil degranulation.

Eosinophils adhere to and degrade fibrinogen substrates in a CD11b-dependent manner.

Fibrinogen-interacting eosinophils are more metabolically active than collagen.

LSD1 suppresses PD-1 expression following acute infection or ex vivo induction.

Blimp-1 binding to the Pdcd1 locus is required to recruit LSD1.

LSD1 is required to fully remethylate the Pdcd1 proximal promoter region.

Chkα and choline metabolism are upregulated in mouse TRAF3–deficient B cells.

Reconstitution of TRAF3 in human malignant B cells inhibits choline metabolism.

Inhibition of Chkα reverses the survival phenotype of TRAF3-deficient B cells.