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Brief Definitive Report

Homozygous missense mutations in POLE1 caused an inherited disorder characterized by facial dysmorphism, immunodeficiency, livedo, and short stature.

The transcription factor T-bet drives the differentiation of NKp46-expressing IL-22–producing innate lymphoid cells

RAGE is required for LPA-mediated vascular signaling and tumorigenesis


NK cells treated with a cocktail of IL-12, IL-15, and IL-18 persist with sustained effector function in vivo and enhance tumor immunotherapy.

Bacterial surface proteins switch the orientation of IgG binding depending on the antibody concentration of their environment.

The colitis-associated glycome mediates CD4+ T cell expansion and contributes to the exacerbation of T cell–mediated intestinal inflammation.

Pest resistance molecules, α-amylase/trypsin inhibitors from wheat, activate innate immune cells through engagement of TLR4 to elicit inflammatory responses in the intestine.

E2F transcription factors regulate expression of RAE-1 family NKG2D ligands in cancer cells and normal proliferating cells to promote wound healing and immune recognition.

A PI3K- and Akt-independent pathway mediated by mTORC1 regulates expression of HIF1 in CD8+ T cells and is required to sustain glucose metabolism and regulate cell trafficking.

The transcriptional repressor BCL6 reduces miRNA levels in germinal center B cells to increase AID expression.

Bcl11a regulates development of lymphoid cells in adult mice in part by inhibiting expression of p53.

The PD-1–PD-L1 pathway inhibits perforin-mediated killing of PD-L1+ vascular endothelial cells by CD8+ T cells, thereby limiting vascular damage during systemic LCMV infection.

To be added


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