Interleukin 17

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Interleukin 17A is a pro-inflammatory cytokine.

In autism-spectrum disorder[edit | edit source]

Recent research has led some to believe that IL-17 may have a significant role in the development and persistence of autism through its inflammatory effects on the brain. Inspired by the observation that fever often temporarily reduces the behavioral deficits in autistic children, researchers discovered it may be the production of IL-17 during the fever state that causes these changes.[citation needed]

Though cytokines are immune-modulating agents, IL-17 was shown in one study to work like a neuro-modulator in mice with autism-like behavioral changes, having the paradoxical effects of increased risk of behavioral changes when exposed in-utero to maternal IL-17, but decreased behavioral abnormalities in adult mice.[1] The mechanism by which IL-17 seemed to create these changes was by affecting the brain region S1DZ, part of the somatosensory cortex that is likely responsible for sensing where the body is in space.

In reference to IL-17's role in the brain, one researcher from the latter study said, “What’s fascinating about this communication is the immune system directly sends its messengers to the brain, where they work as if they’re brain molecules, to change how the circuits work and how the behaviors are shaped.”[2] These findings may be significant to people with M.E. because they demonstrate the role of inflammation and immune-modulated cytokines on the central nervous system and behavior.

Further studies have demonstrated the importance of IL-17 production in response to gut bacteria in the modulation of autism as well, which may also hold clues for those who suspect their M.E. symptoms to be due to neuroinflammation and/or the result of an infection.[3][4]

Learn more[edit | edit source]

See also[edit | edit source]

References[edit | edit source]

  1. Reed, Michael Douglas; Yim, Yeong Shin; Wimmer, Ralf D.; Kim, Hyunju; Ryu, Changhyeon; Welch, Gwyneth Margaret; Andina, Matias; King, Hunter Oren; Waisman, Ari (Dec 18, 2019). "IL-17a promotes sociability in mouse models of neurodevelopmental disorders". Nature: 1–5. doi:10.1038/s41586-019-1843-6. ISSN 1476-4687. 
  2. "Study may explain how infections reduce autism symptoms". MIT News. Retrieved Jan 7, 2020. 
  3. Atladóttir, Hjördís Ósk; Thorsen, Poul; Schendel, Diana E.; Østergaard, Lars; Lemcke, Saane; Parner, Erik T. (May 3, 2010). "Association of Hospitalization for Infection in Childhood With Diagnosis of Autism Spectrum Disorders: A Danish Cohort Study". Archives of Pediatrics & Adolescent Medicine. 164 (5): 470–477. doi:10.1001/archpediatrics.2010.9. ISSN 1072-4710. 
  4. "Autism symptoms reduced nearly 50 percent two years after fecal transplant". ScienceDaily. Retrieved Jan 7, 2020. 

myalgic encephalomyelitis (ME) - A disease often marked by neurological symptoms, but fatigue is sometimes a symptom as well. Some diagnostic criteria distinguish it from chronic fatigue syndrome, while other diagnostic criteria consider it to be a synonym for chronic fatigue syndrome. A defining characteristic of ME is post-exertional malaise (PEM), or post-exertional neuroimmune exhaustion (PENE), which is a notable exacerbation of symptoms brought on by small exertions. PEM can last for days or weeks. Symptoms can include cognitive impairments, muscle pain (myalgia), trouble remaining upright (orthostatic intolerance), sleep abnormalities, and gastro-intestinal impairments, among others. An estimated 25% of those suffering from ME are housebound or bedbound. The World Health Organization (WHO) classifies ME as a neurological disease.

The information provided at this site is not intended to diagnose or treat any illness.
From MEpedia, a crowd-sourced encyclopedia of ME and CFS science and history.