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Immune system regulation and role of the human leukocyte antigen in posttraumatic stress disorder.

ABSTRACT: Posttraumatic stress disorder (PTSD) is a debilitating condition that adversely affect mental and physical health. Recent studies have increasingly explored the role of the immune system in risk for PTSD and its related symptoms. Dysregulation of the immune system may lead to central nervous system tissue damage and impair learning and memory processes. Individuals with PTSD often have comorbid inflammatory or auto-immune disorders. Evidence shows associations between PTSD and multiple genes that are involved in immune-related or inflammatory pathways. In this review, we will summarize the evidence of immune dysregulation in PTSD, outlining the contributions of distinct cell types, genes, and biological pathways. We use the Human Leukocyte Antigen (HLA) locus to illustrate the contribution of genetic variation to function in different tissues that contribute to PTSD etiology, severity, and comorbidities.

SUBMITTER: Katrinli S

PROVIDER: S-EPMC8322450 | biostudies-literature | 2021 Nov

REPOSITORIES: biostudies-literature

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Immune system regulation and role of the human leukocyte antigen in posttraumatic stress disorder.

Katrinli Seyma S Smith Alicia K AK

Neurobiology of stress 20210712

Posttraumatic stress disorder (PTSD) is a debilitating condition that adversely affect mental and physical health. Recent studies have increasingly explored the role of the immune system in risk for PTSD and its related symptoms. Dysregulation of the immune system may lead to central nervous system tissue damage and impair learning and memory processes. Individuals with PTSD often have comorbid inflammatory or auto-immune disorders. Evidence shows associations between PTSD and multiple genes tha ...[more]

PMID: 34355049

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Project description:Epigenetic marks, including DNA methylation, are modifiable molecular factors that may underlie mental disorders, especially responses to trauma, including the development of and resilience to posttraumatic stress disorder (PTSD). Previous work has identified differential DNA methylation at CpG dinucleotide sites genomewide between trauma exposed individuals with and without PTSD, suggesting a role for epigenetic potential-the capacity to epigenetically regulate behavior and physiology in response to lived experiences. The human species is characterized by an increased period of adaptive plasticity during brain development. The evolutionary history of epigenetic potential in relation to adaptive plasticity is currently unknown. Using phylogenetic methods and functional annotation analyses, we trace the evolution of over 7000 CpG dinucleotides, including 203 associated with PTSD, during the descent of humans in during mammalian evolution and characterize the biological significance of this evolution. We demonstrate that few (7%) PTSD-associated CpG sites are unique to humans, while the vast majority of sites have deep evolutionary origins: 73 and 93% were unambiguously present in the last common ancestor of humans/orangutans and humans/chimpanzees, respectively. Genes proximal to evolved PTSD-associated CpG sites revealed significant enrichment for immune function during recent human evolution and regulation of gene expression during more ancient periods of human evolution. Additionally, 765 putative transcription factor binding motifs (TFBMs) were identified that overlap with PTSD-associated CpG sites. Elucidation of the evolutionary history of PTSD-associated CpG sites may provide insights into the function and origin of epigenetic potential in trauma responses, generally, and PTSD, specifically. The human capacity to respond to trauma with stable physiologic and behavioral changes may be due to epigenetic potentials that are shared among many mammalian species.

Dataset Information

Immune system regulation and role of the human leukocyte antigen in posttraumatic stress disorder.

Publications

Immune system regulation and role of the human leukocyte antigen in posttraumatic stress disorder.

Similar Datasets

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