-
Cover Image
Cover Image
ON THE COVER
Common house dust contains NKT cell antigens capable of promoting airway inflammation, as reported by Wingender et al. Also in this issue, Brigl et al. find that NKT cells predominantly respond to innate stimuli during bacterial infection, rather than to microbial ligands presented by CD1 molecules. The varied ways to turn on NKT cells are discussed in the context of other recent findings in a Minireview by Godfrey and Rossjohn. The cover depicts dust motes in a beam of sunlight. Artwork by Lewis Long (longdesign@earthlink.net).
See pages 1121, 1151, and 1163 - PDF Icon PDF LinkTable of Contents
- PDF Icon PDF LinkEditorial Board
Review
New ways to turn on NKT cells
Godfrey and Rossjohn discuss the varied ways to turn on NKT cells in the context of recent findings.
Brief Definitive Report
IL-23–responsive innate lymphoid cells are increased in inflammatory bowel disease
Increased numbers of innate lymphoid cells in patients with inflammatory bowel disease.
Article
Ebf1 or Pax5 haploinsufficiency synergizes with STAT5 activation to initiate acute lymphoblastic leukemia
STAT5 is abnormally activated in patients with acute lymphoblastic leukemia, and increased STAT5 activation synergizes with PAX5 and EBF1 to induce disease.
Invariant NKT cells are required for airway inflammation induced by environmental antigens
House dust contains antigens capable of activating mouse and human iNKT cells, contributing to allergen-induced airway inflammation.
Innate and cytokine-driven signals, rather than microbial antigens, dominate in natural killer T cell activation during microbial infection
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 induces an intravascular surveillance program mediated by long-lived LFA-1–ICAM-1 interactions
PLZF-expressing NKT cells establish residence at intravascular locations, failing to enter the circulation because of constitutive interactions with LFA-1 and ICAM-1.
miR-146a is a significant brake on autoimmunity, myeloproliferation, and cancer in mice
Mice lacking miR-146a exhibit exaggerated inflammatory responses, autoimmunity, and increased rate of tumorigenesis.
Hemophagocytosis causes a consumptive anemia of inflammation
IFN-γ stimulates blood-eating macrophages (hemophagocytes) by acting directly on macrophages to promote phagocytosis and uptake of blood cells.
Polyubiquitin binding to ABIN1 is required to prevent autoimmunity
The polyubiquitin-binding domain of ABIN1 limits TLR-induced MyD88 signaling to prevent spontaneous autoimmunity in mice.
Tissue plasminogen activator prevents white matter damage following stroke
Tissue plasminogen activator protects white matter from stroke-induced lesions via the EGF-like domain and independent of proteolytic activity by promoting oligodendrocyte survival.
A dynamic T cell–limited checkpoint regulates affinity-dependent B cell entry into the germinal center
Entry into the germinal center requires antigen-bearing B cells to compete for cognate T cell help at the T–B border.
Platelet activation attracts a subpopulation of effector monocytes to sites of Leishmania major infection
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 enables efficient thymic egress
Lipid phosphate phosphatase 3 in endothelial and epithelial cells promotes efficient T cell emigration from the thymus to the periphery.
T cell receptor signal strength in Treg and iNKT cell development demonstrated by a novel fluorescent reporter mouse
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.
NKAP is required for T cell maturation and acquisition of functional competency
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.
Hierarchical organization and early hematopoietic specification of the developing HSC lineage in the AGM region
A CD45-negative population of pre-HSCs develops into definitive HSCs in the AGM region of the embryo.
The Bordetella pertussis adenylate cyclase toxin binds to T cells via LFA-1 and induces its disengagement from the immune synapse
The Bordella pertussis toxin CyaA binds to LFA-1 on T cells and disrupts the immune synapse.
