|کد مقاله||کد نشریه||سال انتشار||مقاله انگلیسی||ترجمه فارسی||نسخه تمام متن|
|5666746||1591541||2017||3 صفحه PDF||سفارش دهید||دانلود کنید|
- Abnormal immune activation has been noted in autism (ASD).
- There is little clarity how environmental factors may foment ASD immunophenotypes.
- Environmental exposure to N2O has been proposed as etiological factor in autism.
- N2O targeting of opioidergic and cholinergic activity may impact immunophenotypes.
Abnormal immune activation, particularly of a humoral nature, has consistently been described in the etiopathogenesis of autism spectrum disorders (ASD). In this journal, Mead and Ashwood (2015) reviewed immune abnormalities in autism and linked them to severity of classic autistic symptoms. However, there remains a lack of clarity as to how environmental risk factors in ASD may contribute to such immunophenotypes. The evidence presented herein highlights these immune deficits of a humoral nature in ASD. Moreover, aligned with prior research showing a link between chronic air pollution and suppression of humoral immunity, the author of this commentary has proposed that environmental exposure to pervasive air pollutants, particularly nitrous oxide (N2O), may target several anti-inflammatory biomarkers, including alpha 7 nicotinic acetylcholine receptor (Î±7nAChR) inhibition and stimulation of kappa opioid receptor (KOR) activity. Given that these physiological targets, in particular, may promote the oft-noted humoral immunophenotypes in ASD, including B cell survival and muted antibody responses, this correspondence supports an existing line of evidence that air pollution, and particularly exposure to environmental N2O, may be an important etiological risk factor in ASD.
Journal: Immunology Letters - Volume 185, May 2017, Pages 90-92