Archives

  • 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • br Acknowledgements br Introduction Autism is a neurodevelop

    2020-07-30


    Acknowledgements
    Introduction Autism is a neurodevelopmental disorder, and in which its main diagnostic symptoms are unfamiliar common social interactions, with intense deficiencies in social cognition in several cases (Chevallier et al., 2012, Constantino, 2011). Improper understanding of social signs and unsuitable reactions in social settings, which are intellectualized as a reduced theory of mind, mentalization, or mind blindness are features of the diagnostic symptoms of autism (Frith and Frith, 2012, Lombardo and Baron-Cohen, 2011). Current epidemiologic studies have indicated that autism is diagnosed in approximately 1% of children (Kogan et al., 2009). However, little is known about the etiology and underlying neuropathology of autism, and there are no clear biological markers for this and other related disorders. Evidence of immune dysfunction has been observed in numerous individuals with autism, with a marked activation of microglia, increased levels of proinflammatory cytokines in the mlck sale tissue, plasma, and peripheral blood mononuclear cell (PBMC) cultures (Ashwood et al., 2008, Enstrom et al., 2010). Chemokines are classified based on the position of the conserved cysteine residues as C, CC, CXC, and CX3C subfamilies. The CC and CXC chemokines are implicated as mediators of both central nervous system (CNS) and inflammatory development (Babcock and Owens, 2003, Bajetto et al., 2002). They are potential central therapeutic targets in numerous inflammatory and autoimmune disorders because of their critical role in cell recruitment and activation during inflammation. Chemokine receptors are highly expressed on naive T cells, which play a very important role in the recirculation of lymphocytes during the development of immune responses (Unsoeld et al., 2004). They have been shown to act as functional mediators of neuroinflammatory disorders (Karpus et al., 2003). Furthermore, high levels of chemokine receptors have been found in neurons of the hippocampus and other brain regions (Van der Meer et al., 2000). A previous study showed that chemokine receptors were implicated in neuroinflammation, neural damage, and astrocyte proliferation (Louboutin et al., 2011). A possible role for chemokine receptors has been suggested in numerous behavioral impairments in individuals diagnosed with autism (Ashwood et al., 2011). The levels of chemokine receptors in autism were found to be higher in the astrocytes of the anterior cingulate gyrus, which was also noted in the cerebellum and brain tissue (Vargas et al., 2005). The expression of the mRNA transcripts of chemokine receptors was elevated in the temporal cortex of individuals with autism (Garbett et al., 2008). The migration of activated T cells into the CNS is regulated by chemokine receptors and mediated by adhesion molecules (Engelhardt and Ransohoff, 2012, Holman et al., 2011). Furthermore, the constitutive expression of chemokine receptors in the choroid plexus is proposed to act as a gateway for T cells to penetrate the uninflamed CNS (Axtell and Steinman, 2009).