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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.

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Dendritic cells from patients with hyper-IgE syndrome less efficiently generate induced regulatory T cells.

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.

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.

R-spondin1 stimulates the proliferation of intestinal stem cells through the Wnt signaling pathway and protects against graft-versus-host disease.

The E3 ubiquitin ligase component FBXW7 modulates homeostasis and inhibits tumorigenesis in the murine intestine.

In glioblastoma multiforme, the most common adult primary brain tumor, the glycolytic enzyme hexokinase 2 facilitates growth and therapeutic resistance.

During CNS autoimmunity, brain endothelial cell CXCR7 internalizes CXCL12 from the perivascular space, thereby permitting leukocyte migration into the CNS parenchyma.

Conformational changes influence functional properties of circumsporozoite protein expressed on the surface of Plasmodium sporozoites.

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.

By modifying dendritic cell cytokine production, Dectin-1 suppresses Th1 differentiation in mice infected with the fungal pathogen Aspergillus fumigatus.

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.

In Special Collection: 2018 Nobel Prize Collection

A new mouse model of spontaneous autoimmune disease reveals an important role for the inhibitory co-receptor LAG-3 in suppressing autoimmunity.

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