Heme induces programmed necrosis on macrophages through autocrine TNF and ROS production

TL;DR: The results demonstrate that heme can modulate adaptive immunity (at least humoral immunity) by the mode of double concentration-thresholds.

TL;DR: In this article , it was shown that a Ca2+ concentration of at least 1.5 mM during in vitro stimulation is needed for optimal cytokine production by conventional αβ T cells.

TL;DR: Emerging concepts on how iron influences and determines myeloid cell polarization in the context of its uptake, storage, and metabolism are reviewed, including in conditions such as multiple sclerosis, sickle cell disease, and tumors.

TL;DR: In this article , the authors hypothesize that when incubated in the presence of high heme concentration, macrophages display concomitant and distinct types of cell death, including necroptosis and a yet to be identified type of cell deaths.

TL;DR: This review will focus on the JNK group of MAP kinases, which are characterized by the sequence TEY and the two stress-activatedMAP kinases: p38 with the sequence TGY, and the c-Jun NH2-terminal kinases (JNK) with the sequences TPY.

TL;DR: The findings suggest that RIP3 controls programmed necrosis by initiating the pronecrotic kinase cascade, and that this is necessary for the inflammatory response against virus infections.

TL;DR: Evidence now reveals that necrosis can also occur in a regulated manner, and necroptosis participates in the pathogenesis of diseases, including ischaemic injury, neurodegeneration and viral infection, thereby representing an attractive target for the avoidance of unwarranted cell death.

TL;DR: Data indicate RIP3 as the determinant for cellular necrosis in response to TNF-alpha family of death-inducing cytokines.