ON THE COVER
Chow et al. and Christopher et al. find that macrophages in the bone marrow control the retention and mobilization of hematopoietic stem cells. The cover image represents the network of signals received by macrophages and transmitted to other cells in the bone marrow niche. Artwork by Lewis Long (email@example.com).
See pages 251 and 261
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Brief Definitive Report
Growth differentiation factor 15 deficiency protects against atherosclerosis by attenuating CCR2-mediated macrophage chemotaxis
The TGF-β family member GDF-15 promotes lesion formation and plaque instability in atherosclerosis-prone LDLr-deficient mice.
Human immunodeficiency syndrome with loss of DCs, monocytes, and T reg cells; preservation of Langerhans cells; associated loss of BM multilymphoid progenitors; and overproduction of Flt3 ligand.
Defective IL-10 signaling in hyper-IgE syndrome results in impaired generation of tolerogenic dendritic cells and induced regulatory T cells
Dendritic cells from patients with hyper-IgE syndrome less efficiently generate induced regulatory T cells.
Expression of the G-CSF receptor in monocytic cells is sufficient to mediate hematopoietic progenitor mobilization by G-CSF in mice
Expression of the G-CSF receptor on bone marrow monocytes is sufficient to trigger HSC mobilization in response to G-CSF, in part via effects on osteoblast lineage cells.
Bone marrow CD169+ macrophages promote the retention of hematopoietic stem and progenitor cells in the mesenchymal stem cell niche
Both fast-cycling and quiescent mouse hematopoietic stem cells (HSCs) can reconstitute lifelong hematopoiesis, and HSC cycling status can fluctuate over time in steady state and accelerate upon inflammation.
The Wnt agonist R-spondin1 regulates systemic graft-versus-host disease by protecting intestinal stem cells
R-spondin1 stimulates the proliferation of intestinal stem cells through the Wnt signaling pathway and protects against graft-versus-host disease.
FBXW7 influences murine intestinal homeostasis and cancer, targeting Notch, Jun, and DEK for degradation
The E3 ubiquitin ligase component FBXW7 modulates homeostasis and inhibits tumorigenesis in the murine intestine.
Hexokinase 2 is a key mediator of aerobic glycolysis and promotes tumor growth in human glioblastoma multiforme
In glioblastoma multiforme, the most common adult primary brain tumor, the glycolytic enzyme hexokinase 2 facilitates growth and therapeutic resistance.
CXCR7 influences leukocyte entry into the CNS parenchyma by controlling abluminal CXCL12 abundance during autoimmunity
During CNS autoimmunity, brain endothelial cell CXCR7 internalizes CXCL12 from the perivascular space, thereby permitting leukocyte migration into the CNS parenchyma.
The malaria circumsporozoite protein has two functional domains, each with distinct roles as sporozoites journey from mosquito to mammalian host
Conformational changes influence functional properties of circumsporozoite protein expressed on the surface of Plasmodium sporozoites.
Homeostatic proliferation generates long-lived natural killer cells that respond against viral infection
Like memory T cells, natural killer cells that undergo homeostatic expansion in mice self-renew and retain the ability to respond to subsequent viral infection.
Dectin-1 diversifies Aspergillus fumigatus–specific T cell responses by inhibiting T helper type 1 CD4 T cell differentiation
By modifying dendritic cell cytokine production, Dectin-1 suppresses Th1 differentiation in mice infected with the fungal pathogen Aspergillus fumigatus.
Aire-dependent production of XCL1 mediates medullary accumulation of thymic dendritic cells and contributes to regulatory T cell development
Aire regulates medullary epithelial cell production of XCL1, a chemoattractant for XCR1-expressing thymic DCs whose presence in the medulla contributes to the generation of T reg cells.
A new mouse model of spontaneous autoimmune disease reveals an important role for the inhibitory co-receptor LAG-3 in suppressing autoimmunity.
Broadly cross-reactive antibodies dominate the human B cell response against 2009 pandemic H1N1 influenza virus infection