December 2012 | Volume 209, No. 13
Brief Definitive Reports
- 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.
- Sustained effector function of IL-12/15/18–preactivated NK cells against established tumors
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.
- Antibody orientation at bacterial surfaces is related to invasive infection
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.
- BCL6 positively regulates AID and germinal center gene expression via repression of miR-155
The transcriptional repressor BCL6 reduces miRNA levels in germinal center B cells to increase AID expression.
- Programmed death 1 protects from fatal circulatory failure during systemic virus infection of mice
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.