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Dysregulation of the expression of HLA-DR, costimulatory molecule, and chemokine receptors on immune cells in children with autism.

Abstract：

:Autism spectrum disorder (ASD) is a heterogeneous disorder diagnosed based on the severity of abnormalities in social skills. Several studies have acknowledged the presence of abnormal immune functions among individuals diagnosed with ASD. HLA-DR (human leukocyte antigen-antigen D related) has been shown to play a significant role in several inflammatory and neurological disorders; however, the role of HLA-DR signaling in ASD has not yet been fully clarified. In this study, we investigated the role of HLA-DR signaling in children with ASD. Flow cytometric analysis, using peripheral blood mononuclear cells (PBMCs), revealed the numbers of CD4+, CD8+, CD28+, CXCR4+, and CCR7+ expressing HLA-DR cells in typically developing (TD) controls and children with ASD. We also determined the numbers of IFN-γ+, IL-21+, and Foxp3+ expressing HLA-DR cells in TD controls and in children with ASD using PBMCs. We observed mRNA and protein expression levels of HLA-DR by RT-PCR and western blotting analysis. Our results revealed that children with ASD had significantly increased numbers of HLA-DR+CD4+, HLA-DR+CD8+, CD28+HLA-DR+, HLA-DR+CXCR4+, HLA-DR+CCR7+ cells compared with TD controls. We found that children with ASD showed increased HLA-DR+IFN-γ+ and HLA-DR+IL-21+ and decreased HLA-DR+Foxp3+ expression levels compared with TD controls. Furthermore, children with ASD showed higher HLA-DR mRNA and protein expression levels compared with TD controls. These results indicated that HLA-DR could play an essential role in the immune abnormalities associated with ASD.

journal_name

Int Immunopharmacol

journal_title

International immunopharmacology

authors

Ahmad SF,Ansari MA,Nadeem A,Bakheet SA,Al-Ayadhi LY,Alotaibi MR,Alhoshani AR,Al-Hosaini KA,Attia SM

doi

10.1016/j.intimp.2018.10.027

subject

Has Abstract

pub_date

2018-12-01 00:00:00

pages

360-365

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(18)30540-X

journal_volume

65

pub_type

杂志文章

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