July 2012 | Volume 209, No. 8
- Self-renewal of thymocytes in the absence of competitive precursor replenishment
Thomas Boehm discusses recent findings on sustained thymocyte development in the absence of replenishing hematopoietic progenitors.
Brief Definitive Reports
- Thymocytes may persist and differentiate without any input from bone marrow progenitors
New thymus transplant experiments reveal that in the absence of competing bone marrow progenitors, existing thymocytes can self-renew, guaranteeing thymus cellularity and the rapid reconstitution of the peripheral T cell pools.
- A specific role for TLR1 in protective TH17 immunity during mucosal infection
TLR1/TLR2 complexes are required for induction of IL-6 and IL-23 to generate protective TH17-mediated immunity and IgA production after oral but not systemic Yersinia enterocolitica infection.
- Familial transmission rather than defective innate immunity shapes the distinct intestinal microbiota of TLR-deficient mice
Differences between TLR-deficient mouse colonies occur from extended husbandry in isolation that are communicated to offspring by maternal transmission.
- Hematopoietic stem cell development requires transient Wnt/β-catenin activity
Deletion of β-catenin from mouse embryonic endothelium, but not embryonic hematopoietic cells, prevents hematopoietic differentiation; thus Wnt/β-catenin signaling is needed for emergence but not maintenance of HSCs.
- Broad neutralization by a combination of antibodies recognizing the CD4 binding site and a new conformational epitope on the HIV-1 envelope protein
A new method is used to isolate neutralizing antibodies recognizing a new epitope on the cell surface–expressed, but not soluble, HIV-1 spike.
- Apoptotic cells suppress mast cell inflammatory responses via the CD300a immunoreceptor
After cecal ligation and puncture, mice lacking the phosphatidylserine receptor CD300a on mast cells show more neutrophil recruitment to the peritoneal cavity, improved bacterial clearance, and extended survival.
- Interleukin-1α controls allergic sensitization to inhaled house dust mite via the epithelial release of GM-CSF and IL-33
IL-1α promotes a cascade of cytokine production from epithelial cells culminating in Th2 immunity to house dust mite allergens.