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In caspase 8-deficient mouse T cells, necroptosis occurs via a Ripk3- and Ripk1-dependent pathway independent of autophagy and programmed necrosis.

TLR3, TLR7, and TLR9 are cleaved in the same step-wise manner in all immune cell types examined.

Compared with T-ALL diagnosis samples, samples obtained at relapse or after xenograft into immunodeficient mice exhibit additional genomic lesions in oncogenes and/or tumor suppressor genes; these lesions contribute to leukemia-initiating activity.

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miR-451 represses expression of Myc and acts as a tumor suppressor in murine and human T cell acute lymphoblastic leukemia.

In the mouse stomach epithelium, Notch signaling influences homeostasis and tumorigenesis in a cell type– and context-specific manner.

GATA4 loss as a result of promoter hypermethylation or somatic mutation promotes growth and chemotherapy resistance of human astrocytomas.

As revealed by the first crystal structure of a natural cytotoxicity receptor bound to its ligand, NKp30 engages B7-H6 in a manner structurally distinct from that of other CD28 family members.

Granulocyte colony-stimulating factor and its receptor are needed for skeletal muscle development and injury-induced regeneration in mice.

iNKT cell and pDC cross talk prevents type 1 diabetes by inducing T reg cells in the pancreatic lymph node during viral infection.

Virus-specific cytotoxic CD8+ T cells are in cell cycle as they transit from lymphoid tissues to sites of infection.

Prostaglandin E2 inhibits the expression of retinal dehydrogenase, thus inhibiting retinoic acid production and the priming of gut-tropic T cells by dendritic cells.

Zinc enhances TCR signaling in part by inhibiting Shp-1 recruitment to the TCR synapse.

IKKa associates with the il17a locus and is required in T cells for Th17-mediated CNS inflammation in vivo.

Blocking HVEM–LIGHT interactions on T cells reduces the persistence of antigen-specific memory T cell populations after secondary expansion through decreased Akt activity and loss of Bcl-2 expression.

The expression of the new Ly108 isoform H1 weakens lupus-like disease of C57BL/6.Sle1b mice.

Mouse B cells lacking NFATc1 exhibit defective proliferation, survival, isotype class switching, cytokine production, and T cell help.

The sympathetic nervous system regulates bone mass accrual by signaling via CREB and ATF4 in osteoblasts to promote proliferation and RANKL production, respectively.

IL-4Rα expression on airway smooth muscle cells is sufficient for the development of airway hyperresponsiveness.

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