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The mechanistic characterization of NF-κB transcription inhibition by anthracyclines opens new possibilities for improved cancer chemotherapy and the treatment of inflammation-driven conditions.

A signal for inflammatory cell death is induced by the disruption of cellular metabolism.

The experimental methods that are routinely used to disperse mycobacterial aggregates markedly impact macrophage infection outcomes, which should be taken into account to appropriately interpret host-pathogen interactions studies.

A novel pathway of emergency myelopoiesis is induced by repetitive virus stimulation at peripheral barrier sites which bypasses the requirement of conventional pathways and expands myeloid infiltration in tissues.

Blockage of CXCL10/CXCR3 signaling between murine pancreatic precancerous lesion cells and inflammatory macrophages generates a tumor-promoting microenvironment.

A family of engineered immune receptors trigger internalization of cancer cells and antigen-coated targets.

Endotoxemia recruits fast-acting anti-inflammatory innate myeloid progenitors from bone marrow into regional lymphatics through release of pre-formed Ccl19 secondary to NF-κB-independent, Traf6/IκB kinase-dependent signaling.

The IL-4/IL-4Rα axis directory promotes pathological angiogenesis through communications with bone marrow cells leading to neovascular age-related macular degeneration.

Decay rate of mRNAs encoding inflammatory regulators is controlled by the balance between AU-rich element-mediated deadenylation and cytoplasmic polyadenylation element-mediated polyadenylation.

Experiments including cell and animal models investigate the molecular mechanisms underlying the regulation of homeostasis and function of monocytes.