ON THE COVER
Using two-photon microscopy, Tal et al. find in vivo evidence that discrete regions of immobilized CCL21 on lymphatic endothelium (white) provide docking sites for mouse CCR7+ dermal DCs (green), thus allowing recruitment and entry into the lymphatics. Although the cutaneous DCs are relatively sessile in the steady state and remain adherent to blood vessels (turquoise), they become motile and affix to the lymphatic vessels upon inflammation. Artwork by Joshua Graver (Joshuagraver@mac.com)
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Aifantis and colleagues examine the conflicting roles of Notch signaling in various cancer types.
Brief Definitive Report
In addition to other receptors, including sphingosine-1-phosphate receptor 1, cannabinoid receptor 2 positions mouse marginal zone B cells within the marginal zone and also prevents their loss to the blood.
Blocking CCL2 nitration in tumors promoted CD8+ influx and reduced tumor growth and prolonged survival in mice when combined with adoptive cell therapy.
Mice lacking all three Rb genes in the liver develop tumors resembling specific subgroups of human hepatocellular carcinomas, and Notch activity appears to suppress the growth and progression of these tumors.
Non–lineage/stage-restricted effects of a gain-of-function mutation in tyrosine phosphatase Ptpn11 (Shp2) on malignant transformation of hematopoietic cells
A common Shp2 mutation leads to myeloproliferative disease and malignant acute leukemia in stem cells and committed progenitors, associated with Shp2 maintaining chromosomal stability
Dendritic cell responsiveness to type I interferon is required for the generation of antitumor T cell responses and tumor rejection.
Host type I IFN signals are required for antitumor CD8+ T cell responses through CD8α+ dendritic cells
The generation of antitumor CD8+ T cell responses requires type I interferon responsiveness in host antigen-presenting cells
Megakaryocytes possess a functional intrinsic apoptosis pathway that must be restrained to survive and produce platelets
Deletion of Bak and Bax, the effectors of mitochondrial apoptosis, does not affect platelet production, however, loss of prosurvival Bcl-xL results in megakaryocyte apoptosis and failure of platelet shedding.
In a manner dependent on CD4 T cell help and Toll-like receptor signals, B cells lacking WASp induce autoantibody production and autoimmune disease in mice.
Sustained suppression by Foxp3+ regulatory T cells is vital for infectious transplantation tolerance
A new genetic mouse model demonstrates the necessity of Foxp3+ T reg cells for infectious tolerance.
SOCS1 is essential for regulatory T cell functions by preventing loss of Foxp3 expression as well as IFN-γ and IL-17A production
SOCS1 is required to restrict IFN-γ and IL-17 expression and maintain Foxp3 expression in and function of regulatory T cells.
Critical role of Bcl11b in suppressor function of T regulatory cells and prevention of inflammatory bowel disease
Bcl11b is required for optimal FoxP3 expression and suppressor function by regulatory T cells and for the generation of inducible regulatory T cells.
Herpes simplex virus encephalitis in a patient with complete TLR3 deficiency: TLR3 is otherwise redundant in protective immunity
A new autosomal recessive form of complete TLR3 deficiency reveals that human TLR3 is nonredundant in immunity against herpes simplex virus 1 in the central nervous system (CNS) but redundant in host defense against viruses outside the CNS.
E3 ubiquitin ligase CHIP facilitates Toll-like receptor signaling by recruiting and polyubiquitinating Src and atypical PKCζ
In mouse macrophages and dendritic cells, the CHIP E3 ubiquitin ligase is needed for transduction of signals initiated by TLR4 and TLR9 stimulation.
Airborne lipid antigens mobilize resident intravascular NKT cells to induce allergic airway inflammation
Resident intravascular NKT cells exacerbate airway hyperreactivity in mice dependent on dendritic cell co-presentation of glycolipid and peptide antigens.
Angiotensin-II–driven calcineurin activation and regulator of calcineurin-1 (Rcan-1) expression is required for pathological vascular remodeling in mice.