ArticleNeurochemical research2018
IL-35 is a Protective Immunomodulator in Brain Ischemic Injury in Mice.
Article in Neurochemical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Regulatory T cells in intracerebral hemorrhage: mechanisms of immunomodulation and therapeutic potential.Frontiers in immunology · 2026Review
- Interleukins in Epilepsy: Friend or Foe.Neuroscience bulletin · 2024Review
- Regulatory T lymphocytes as a therapy for ischemic stroke.Seminars in immunopathology · 2023Review
- Didymin Alleviates Cerebral Ischemia-Reperfusion Injury by Activating the PPAR Signaling Pathway.Yonsei medical journal · 2022Article
- Interleukin-35 attenuates blood-brain barrier dysfunction caused by cerebral ischemia-reperfusion injury through inhibiting brain endothelial cell injury.Annals of translational medicine · 2022Article
- Interleukin-35 exhibits protective effects in a rat model of hypoxic-ischemic encephalopathy through the inhibition of microglia-mediated inflammation.Translational pediatrics · 2022Article
- Interleukin-35 from Interleukin-4-Stimulated Macrophages Alleviates Oxygen Glucose Deprivation/Re-oxygenation-Induced Neuronal Cell Death via the Wnt/β-Catenin Signaling Pathway.Neurotoxicity research · 2022Article
- Interleukin-22 Plays a Protective Role by Regulating the JAK2-STAT3 Pathway to Improve Inflammation, Oxidative Stress, and Neuronal Apoptosis following Cerebral Ischemia-Reperfusion Injury.Mediators of inflammation · 2021Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IL-35 has been identified as a novel anti-inflammatory cytokine that belongs to the IL-12 cytokine family and has been verified to play a protective role in autoimmune diseases. In this study, we investigated the protective effects of IL-35 on cerebral ischemia/reperfusion (I/R) injury in a middle cerebral artery occlusion mouse model. We determined that the expression of IL-35 was initially decreased and subsequently increased in I/R injury. Moreover, IL-35 (i.c.v.) pre- and posttreatment significantly reduced the infarct volume and improved neurological deficits after 45 min of ischemia and 24 h of reperfusion. Importantly, IL-35 treatment improved neurological function recovery, particularly in balance ability, at 14 days after treatment. Finally, our results showed that IL-35 treatment reduced the expression of IL-6 and IL-1β, which are confirmed proinflammatory cytokines, thus indicating that these cytokines have both been linked to the anti-inflammatory mechanisms of IL-35. Therefore, IL-35 may be a key immune mediator in brain ischemic injury and appears to have promising potential for clinical trials.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.