Issues

CCL18 is an endogenous agonist of the human CCR8 receptor.

Conditioning therapies before transplantation induce the release of uric acid, which triggers the NLRP3 inflammasome and IL-1β production contributing to graft-versus-host disease.

Using a novel physiological knock-in model, direct evidence for self-antigen–induced TCR editing is not observed, but rather autoreactive cells are exclusively eliminated by negative selection.

CD4⁺ T cells regulate their own activity during toxoplasma infection by driving a glucocorticoid response, which results in feedback inhibition of Th1 cytokine production.

Inhibition of epidermal growth factor receptor during viral infection augments IRF1-dependent IFN-λ production and decreases viral titers.

Inactivation of the stromal p110α isoform of PI3K increases vascular density, reduces vessel size, and alters pericyte coverage, which results in enhanced tumor hypoxia and necrosis to reduce tumor growth.

The co-repressor Strawberry notch homolog 2 regulates DC-STAMP expression and osteoclast fusion, and its absence results in osteopetrosis.

Retinoic acid is required to maintain pre-DC–derived CD11b⁺CD8α⁻Esam^high dendritic cells (DCs) in the spleen and CD11b⁺CD103⁺ DCs in the gut.

Alveolar macrophages differentiate from fetal monocytes in a GM-CSF–dependent fashion and colonize the alveolar space within a few days after birth.

VEGF dampens the expression of microRNA-1, which drives inflammation in part via increasing the expression of Mpl.

Targeted deletion of CD103⁺CD11b⁺ LP DCs results in reduced LP Th17 cells at steady state, but has no impact on Citrobacter infection or the composition of the intestinal microbiota.

Using a new mouse model, the specific deletion of monocytes and macrophages reveals that, although not required to initiate immunity to Citrobacter rodentium, they contribute to the adaptive response via IL-12 secretion to induced IFN-γ⁺ Th1 polarization.

X-box–binding protein 1 suppresses tumor formation in the gut by regulating Ire1α and Stat3-mediated regenerative responses in the epithelium as a consequence of ER stress.

p53 induction regulates NK cell recruitment via CCL2, leading to NKG2D-dependent elimination of senescent tumors.

Toxoplasma gondii secretes a novel dense granule protein, GRA24, that traffics from the vacuole to the host cell nucleus where it prolongs p38a activation and correlates with proinflammatory cytokine production.

IFN-γ produced by CD8⁺ cytotoxic T cells acts on neurons to induce Stat1-associated loss of dendrites and synapses in a mouse model of viral encephalitis.

Epidermal IL-15Rα, shed by keratinocytes upon stimulation with inflammatory cytokines, counteracts IL-15–induced proliferation of IL-17–producing T cells to dampen psoriatic skin disease.

T cells from RA patients are hypoglycolytic due to insufficient induction of the glycolytic activator PFKFB3, resulting in impaired autophagy and reduced ROS production.

Targeting antigen to B cells and dendritic cells via direct conjugation to anti-CD180 antibody promotes robust antigen-specific antibody responses in the absence of adjuvant.