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Aifantis and colleagues examine the conflicting roles of Notch signaling in various cancer types.

Schaer et al. discuss mechanisms of immune evasions by tumors, including the recent finding that CCL2 nitrosylation prevents T cell infiltration into tumors.

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.

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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.

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.

The generation of antitumor CD8+ T cell responses requires type I interferon responsiveness in host antigen-presenting cells

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.

A new genetic mouse model demonstrates the necessity of Foxp3+ T reg cells for infectious tolerance.

SOCS1 is required to restrict IFN-γ and IL-17 expression and maintain Foxp3 expression in and function of regulatory T cells.

Bcl11b is required for optimal FoxP3 expression and suppressor function by regulatory T cells and for the generation of inducible regulatory T cells.

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.

In mouse macrophages and dendritic cells, the CHIP E3 ubiquitin ligase is needed for transduction of signals initiated by TLR4 and TLR9 stimulation.

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.

Dermal DC mobilization requires docking to CCL21 on lymphatic endothelium

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