Fig. 5: Schematic of potential pathogenic pathways by which genetic risk variants enriched at epigenetically active sites in T cells could lead to neuronal changes and ultimately psychiatric disorders. | Nature Communications

Fig. 5: Schematic of potential pathogenic pathways by which genetic risk variants enriched at epigenetically active sites in T cells could lead to neuronal changes and ultimately psychiatric disorders.

From: Genetic variants associated with psychiatric disorders are enriched at epigenetically active sites in lymphoid cells

Fig. 5

Infection or other stressors may induce activation of regulatory elements in T cells that are enriched for trans- or cis-diagnostic risk variants, potentially leading to atypical T cell phenotypes and downstream activation of innate immune (myeloid) cells in the periphery and CNS (light blue boxes). Atypical activation of T cells resident in the CNS, or trafficking into the meninges and brain from the periphery, could adversely affect neuronal function. Developmentally (light green box), T cells are known to control microglial pruning of neuronal synapses as part of normative brain developmental programs in childhood and adolescence. Atypical T cells, in genetically-at-risk individuals, could promote atypical microglial pruning of synapses, contributing to the formation of disconnected networks or circuits in the adult brain. CNS, central nervous system. Parts of the figure were drawn by using pictures from Servier Medical Art. Servier Medical Art by Servier is licensed under a Creative Commons Attribution 3.0 Unported License (https://creativecommons.org/licenses/by/3.0/).

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