Inhibition of ADAM17 with apratastat or TMI-1 ameliorates neutrophilia and cytokine storm in a mouse model of Covid-19-related lung injury induced by poly(I:C) and the receptor-binding domain of the SARS-CoV2 Spike protein (RBD-S).

IRF3 modulates multiple responses of IFNγ-primed macrophages to intracellular bacteria, including production of nitric oxide; meanwhile, IFNγ reciprocally inhibits IRF3, contributing to immune homeostasis.

B. pertussis is able to survive within both M1 and M2 macrophages but M2c proved to be the best suited subtype for bacterial intracellular persistence.

Demonstration that TLR-inducible Hdac7 enzymatic activity is required for inducible cytokine production in murine macrophages, whereas it instructs inducible glycolysis independently of enzyme activity.

Selection of CCR7⁺ DCs using chemically synthesized and tagged CCL19 selects a population of DC which improves anti-tumour immunity and efficacy in solid and metastatic tumour models.

TNF-a plays an important role in iNKT cell development, activation and maturation, and chronic alcohol consumption enhances iNKT cell activation and maturation through TNF-a.

Extracellular vesicle-associated miRNAs alter the immune response by inter-cellular and inter-organ communication and thereby contribute to the pathobiology of various liver diseases.

PAD4 promotes malaria immunopathology by regulating chemokine production in macrophages and enhancing recruitment of inflammatory cells.

Review on platelet extracellular vesicles (pEVs); includes a special focus on pEV's potential as predictors of and contributors to COVID-19.

Hepatic CD24⁺ iNKT cells show higher levels of proliferation, glucose metabolism and mTOR activity comparing to CD24^- iNKT cells

Review on the analysis of TFH cells during COVID-19 infection and vaccination and the role of these cells as biomarkers of neutralising antibody development.

T lymphocytes are activated and actively involved in DADA2 pathogenesis; and ligand-receptor crosstalk with monocytes likely leads to up-regulation of STAT1 and subsequently augmented responses of cells to IFN upon stimulation.