2012
DOI: 10.1038/nature11603
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Interleukin receptor activates a MYD88–ARNO–ARF6 cascade to disrupt vascular stability

Abstract: The innate immune response is essential for combating infectious disease. Macrophages and other cells respond to infection by releasing cytokines such as interleukin-1β (IL-1β), which in turn activate a well-described myeloid differentiation factor 88 (MYD88) -mediated, nuclear factor-κB (NF-κB) -dependent transcriptional pathway that results in inflammatory cell activation and recruitment1–4. Endothelial cells, which usually serve as a barrier to the movement of inflammatory cells out of the blood and into ti… Show more

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Cited by 151 publications
(209 citation statements)
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“…In the periphery, cytokines and chemokines released by circulating effector cells such as T cells and neutrophils are also known to affect CNS barrier homeostasis. Notably, IL-1b has been shown to modulate BBB permeability in mice and rats and to activate human ECs (7,81,82). Interestingly, we found in the present study that blocking or deleting the endothelial IL-1R1 prevents the adhesion of circulating neutrophils to the spinal cord endothelium and delays EAE onset.…”
Section: Discussionsupporting
confidence: 64%
See 1 more Smart Citation
“…In the periphery, cytokines and chemokines released by circulating effector cells such as T cells and neutrophils are also known to affect CNS barrier homeostasis. Notably, IL-1b has been shown to modulate BBB permeability in mice and rats and to activate human ECs (7,81,82). Interestingly, we found in the present study that blocking or deleting the endothelial IL-1R1 prevents the adhesion of circulating neutrophils to the spinal cord endothelium and delays EAE onset.…”
Section: Discussionsupporting
confidence: 64%
“…In the animal model of MS, experimental autoimmune encephalomyelitis (EAE), the BSCB is compromised, thereby exposing the fragile CNS environment to the immune system and its cellular arsenal. This leads to immune cell invasion, formation of demyelinated lesions, and axonal damage (4,(6)(7)(8). Early breakdown of the BSCB in EAE has been widely documented, but the precise timing and triggers of this disruption are still a matter of debate (9)(10)(11)(12).…”
mentioning
confidence: 99%
“…ARNO-Arf6 pathway to affect vascular endothelium cell-cell interactions, but Arf6 is not required for the IL-1␤-induced NF-B activation (26). We find that TLR2-dependent NF-B activation is also independent of Arf6.…”
Section: Discussionsupporting
confidence: 50%
“…Arf6 is required for TLR9 signaling via the regulation of cellular uptake of CpG oligodeoxynucleotides (ODN) (25). Arf6 also mediates interleukin-1␤ (IL-1␤) induced vascular endothelium stability (26). Both TLR9 and the IL-1␤ receptor use MyD88, but not Mal for their signal transduction (25)(26)(27).…”
mentioning
confidence: 99%
“…More recently, it has been demonstrated that interleukin 1b regulates endothelial cell permeability through Arf6 activation to allow inflammatory cells to be recruited to inflammatory sites 43 . Taken together, these reports suggest that VEGF-stimulated Arf6 pathways and functions might be revealed through the study of different model systems.…”
Section: Discussionmentioning
confidence: 99%