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Godfrey and Rossjohn discuss the varied ways to turn on NKT cells in the context of recent findings.

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Increased numbers of innate lymphoid cells in patients with inflammatory bowel disease.

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STAT5 is abnormally activated in patients with acute lymphoblastic leukemia, and increased STAT5 activation synergizes with PAX5 and EBF1 to induce disease.

House dust contains antigens capable of activating mouse and human iNKT cells, contributing to allergen-induced airway inflammation.

TLR-mediated signaling and the production of IL-12 by APCs, rather than recognition of microbial antigens, enables rapid iNKT cell responses to diverse microbial infections.

PLZF-expressing NKT cells establish residence at intravascular locations, failing to enter the circulation because of constitutive interactions with LFA-1 and ICAM-1.

Mice lacking miR-146a exhibit exaggerated inflammatory responses, autoimmunity, and increased rate of tumorigenesis.

IFN-γ stimulates blood-eating macrophages (hemophagocytes) by acting directly on macrophages to promote phagocytosis and uptake of blood cells.

The polyubiquitin-binding domain of ABIN1 limits TLR-induced MyD88 signaling to prevent spontaneous autoimmunity in mice.

Tissue plasminogen activator protects white matter from stroke-induced lesions via the EGF-like domain and independent of proteolytic activity by promoting oligodendrocyte survival.

Entry into the germinal center requires antigen-bearing B cells to compete for cognate T cell help at the T–B border.

Leishmania infection triggers the recruitment of Gr1+ monocytes to the site of infection via platelet-derived PDGF and subsequent CCL2 production.

Lipid phosphate phosphatase 3 in endothelial and epithelial cells promotes efficient T cell emigration from the thymus to the periphery.

Generation of a Nur77 reporter mouse is used to demonstrate TCR signal strength during thymic selection and peripheral maintenance of conventional and nonconventional T cell subsets and presents a novel tool for studying antigen receptor activation in vivo.

The transcriptional repressor NKAP drives T cell maturation after positive selection in the thymus, with NKAP deficiency resulting in functionally immature peripheral T cells that maintain the phenotype of recent thymic emigrants.

A CD45-negative population of pre-HSCs develops into definitive HSCs in the AGM region of the embryo.

The Bordella pertussis toxin CyaA binds to LFA-1 on T cells and disrupts the immune synapse.

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