Characterization of meningeal type 2 innate lymphocytes and their response to CNS injury

Gadani, Sachin P.; Smirnov, Igor; Smith, Ashtyn T.; Overall, Christopher C.; Kipnis, Jonathan

doi:10.1084/jem.20161982

Cited by 107 publications

(135 citation statements)

References 49 publications

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“…Epithelial, endothelial, and myeloid cells in most organs express IL-25, IL-33, and TSLP, these are known to modulate ILC2 expansion in the lungs and activation in inflammation 17,19–22,36 . In the current study, we show that IL-25, IL-33, and TSLP expression increased in response to systemic inflammation caused by experimental peritonitis, and sepsis induces expansion of ILC2 in the lungs consistent with the changes in the expression of IL-25, IL-33, and TSLP.…”

Section: Discussionmentioning

confidence: 99%

Group 2 innate lymphoid cells protect lung endothelial cells from pyroptosis in sepsis

et al. 2018

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Group 2 innate lymphoid cells (ILC2) are one of three subgroups of innate lymphoid cells (ILC1, ILC2, and ILC3), and the major ILC population detected in the lungs. The function of ILC2 in the regulation of lung inflammation remains unclear. In the current study, we explored an important role of ILC2 in protecting lung endothelial cell (EC) from pyroptosis in sepsis-induced acute lung inflammation and the underlying mechanism. Using a cecal ligation and puncture (CLP) mouse sepsis model, we demonstrated that IL-33, which is released in response to sepsis, acting through its receptor ST2 mediates ILC2 expansion in the lungs. We further showed that the increased ILC2 in the lungs secrete IL-9, which in turn prevents lung EC from undergoing pyroptosis, a pro-inflammatory cell death form, by attenuating caspase-1 activation. These findings suggest a previously unidentified innate pathway that negatively regulates lung inflammation following sepsis.

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Section: Discussionmentioning

confidence: 99%

Group 2 innate lymphoid cells protect lung endothelial cells from pyroptosis in sepsis

et al. 2018

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“…Disappearance of IL‐33 producing cells (oligodendrocytes) from the lesion site have also been observed in the brain after spinal cord physical injury . This was associated with rapid release of endogenous IL‐33 in cerebrospinal fluid 1 hours postinjury followed by activation of meningeal ILC2s . IL‐33 release was very transient since the cytokine was not detected at 3 hours or at 24 hours postinjury …”

Section: Mechanisms Of Il‐33 Releasementioning

confidence: 97%

Interleukin‐33 (IL‐33): A nuclear cytokine from the IL‐1 family

Cayrol

Girard

2017

Immunological Reviews

653

588

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“…ILCs have been detected within the meningeal space and lungs. Notably, experimental spinal injury changes the gene-expression profile of these cells 152 .…”

Section: Cerebral and Extracerebral Challenges To The Innate Immune Smentioning

confidence: 99%

Innate immune responses to trauma

2018

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Trauma can affect any individual at any location and at any time over a lifespan. The disruption of macrobarriers and microbarriers induces instant activation of innate immunity. The subsequent complex response, designed to limit further damage and induce healing, also represents a major driver of complications and fatal outcome after injury. This Review aims to provide basic concepts about the posttraumatic response and is focused on the interactive events of innate immunity at frequent sites of injury: the endothelium at large, and sites within the lungs, inside and outside the brain and at the gut barrier.

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Characterization of meningeal type 2 innate lymphocytes and their response to CNS injury

Cited by 107 publications

References 49 publications

Group 2 innate lymphoid cells protect lung endothelial cells from pyroptosis in sepsis

Group 2 innate lymphoid cells protect lung endothelial cells from pyroptosis in sepsis

Interleukin‐33 (IL‐33): A nuclear cytokine from the IL‐1 family

Innate immune responses to trauma

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