August 2012 | Volume 209, No. 9
Brief Definitive Reports
- Mutually exclusive redox forms of HMGB1 promote cell recruitment or proinflammatory cytokine release
HMGB1 orchestrates leukocyte recruitment and their induction to secrete inflammatory cytokines by switching between mutually exclusive redox states.
- Smad3 binding to the foxp3 enhancer is dispensable for the development of regulatory T cells with the exception of the gut
Binding of Smad3 to the foxp3 enhancer is not required for thymic T reg cell development, but thymic involution with aging reveals the contribution of TGF-β–Smad2 signaling in gut T reg cell development.
- The coding genome of splenic marginal zone lymphoma: activation of NOTCH2 and other pathways regulating marginal zone development
Notch2 mutations represent the most frequent lesion in splenic marginal zone lymphoma.
- Heterozygous TBK1 mutations impair TLR3 immunity and underlie herpes simplex encephalitis of childhood
Two unrelated children with HSE carry distinct heterozygous mutations in the gene encoding TANK-binding kinase 1.
- Zinc finger transcription factor zDC is a negative regulator required to prevent activation of classical dendritic cells in the steady state
Conventional DCs from mice lacking zDC (also known as Zbtb46) express more MHCII and produce more VEGF in the steady state.
- IL-1β mediates chronic intestinal inflammation by promoting the accumulation of IL-17A secreting innate lymphoid cells and CD4+ Th17 cells
IL-1β promotes chronic intestinal inflammation through recruitment of granulocytes, activation of ILCs, accumulation of pathogenic T cells, and promotion of Th17 responses.
- miR-146a controls the resolution of T cell responses in mice
By suppressing expression of TRAF6 and IRAK1, miR-146a regulates NF-κB activation in T cells through a negative feedback loop and controls the resolution of T cell responses in mice.
- MyD88 inhibition amplifies dendritic cell capacity to promote pancreatic carcinogenesis via Th2 cells
MyD88 blockade exaggerates the ability of dendritic cells to promote the transition from chronic pancreatitis to pancreatic cancer.
- IL-1R–MyD88 signaling in keratinocyte transformation and carcinogenesis
Keratinocyte MyD88 is a component of an IL-1α–IL-1R autocrine loop that drives Ras-mediated transformation in vitro and contributes to skin tumor formation in vivo.