Abstract
Killer-cell immunoglobulin-like receptors (KIRs) are a family of cell surface proteins found on natural killer cells, which are components of the innate immune system. KIRs recognize MHC class I proteins, mainly HLA-C and are further divided into two groups: short-tailed 2/3DS activating receptors and long-tailed 2/3DL inhibitory receptors. Based on the Barker Hypothesis, the origins of illness can be traced back to embryonic development in the uterus, and since KIR:HLA interaction figures prominently in the maternal–fetal interface, we investigated whether specific KIR:HLA combinations may be found in autism spectrum disorders (ASD) children compared with their healthy parents. This study enrolled 49 ASD children from different Israeli families, and their healthy parents. Among the parents, a higher frequency of HLA-C2 allotypes was found in the fathers, while its corresponding ligand 2DS1 was found in higher percentage in the maternal group. However, such skewing in KIR:HLA frequencies did not appear in the ASD children. Additionally, analysis of “overall activation” indicated higher activation in maternal than in paternal cohorts.
Highlights
Autism spectrum disorders (ASD) encompass a range of neurodevelopmental syndromes defined by difficulties in social communication and stereotyped behaviors [1]
The aim of our research was to genotype the killer-cell immunoglobulinlike receptor (KIR) receptors known to interact with histocompatibility leukocyte antigens (HLA) ligands in autistic children and their non-autistic parents, and to compare KIR receptor: HLA ligand frequencies between these groups
By interacting with MHC class I proteins expressed on all cell types, KIRs regulate the killing function of natural killer (NK)
Summary
Autism spectrum disorders (ASD) encompass a range of neurodevelopmental syndromes defined by difficulties in social communication and stereotyped behaviors [1]. Recent data indicate a prevalence of up to 1 in 66 children [2]. Immune system dysregulation reported in ASD patients includes differential cell fractions and reactivity, autoimmune phenomena, altered cytokine and antibody profiles, and genetic correlations [6]. These findings partially corroborate the theory that chronic neurological inflammation in fetal or newborn brain underlies the development of ASD. Subsequent dysregulation of the immune system may contribute to ASD development in genetically susceptible children
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