Brief Definitive Report
Polymerase ε1 mutation in a human syndrome with facial dysmorphism, immunodeficiency, livedo, and short stature (“FILS syndrome”)
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.
Inducible colitis-associated glycome capable of stimulating the proliferation of memory CD4+ T cells
The colitis-associated glycome mediates CD4+ T cell expansion and contributes to the exacerbation of T cell–mediated intestinal inflammation.
Wheat amylase trypsin inhibitors drive intestinal inflammation via activation of toll-like receptor 4
Pest resistance molecules, α-amylase/trypsin inhibitors from wheat, activate innate immune cells through engagement of TLR4 to elicit inflammatory responses in the intestine.
RAE-1 ligands for the NKG2D receptor are regulated by E2F transcription factors, which control cell cycle entry
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.
PDK1 regulation of mTOR and hypoxia-inducible factor 1 integrate metabolism and migration of CD8+ T cells
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.
Epidermal ADAM17 maintains the skin barrier by regulating EGFR ligand-dependent terminal keratinocyte differentiation