AccScience Publishing / AN / Volume 2 / Issue 2 / DOI: 10.36922/an.391
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Understanding the link between immunosuppressant and natural killer cell in the progression of autism: The role of natural killer cell and mammalian target of rapamycin in autistic brain

Piyush Anandand1 Shamsher Singh1*
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1 Neuropharmacology Division, Department of Pharmacology, ISF College of Pharmacy, Moga, 142001, Punjab, India
Advanced Neurology 2023, 2(2), 391 https://doi.org/10.36922/an.391
Submitted: 23 February 2023 | Accepted: 2 May 2023 | Published: 19 May 2023
© 2023 by the Author(s). This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution 4.0 International License ( https://creativecommons.org/licenses/by/4.0/ )
Abstract

Natural killer cell plays a major role in the pathogenesis of neurodevelopmental disorder including autism spectrum disorder (ASD). ASD is a neurodevelopmental disorder that is associated with symptoms that reduce the quality of life of affected individuals such as social interaction deficit, cognitive impairment, intellectual disabilities, restricted, and repetitive behavioral patterns. This disorder begins in early childhood and continues throughout adulthood. ASD pathogenesis is associated with alteration in natural killer (NK) cells as well as mammalian target of rapamycin signaling functioning that leads to altered physiological processes during development. Here, we review literature highlighting the role of immunosuppressants especially rapamycin and azathioprine and their impact on treating the neurodevelopmental disorder and mechanism by which these drugs may act to ameliorate the autistic symptoms. Furthermore, this review discusses reports highlighting the role of NK cells and familial adenomatous polyposis gene in the etiology of ASD. This review suggests that further investigative work on these drugs could be vital in the management of ASD.

Keywords
Natural Killer cell
Rapamycin
Azathioprine
Immune response
Mammalian target of rapamycin
Funding
None.
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The authors declare no financial or other conflicts of interest.
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