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CD4+ T cells contribute to neurodgeneration in Lewy Body dementia

ABSTRACT: CD4+ T cells contribute to neurodgeneration in Lewy Body dementia

PROVIDER: PRJNA675845 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13041537.fastq.gz	Fastqsanger.gz
	SRR13041538.fastq.gz	Fastqsanger.gz
	SRR13041539.fastq.gz	Fastqsanger.gz
	SRR13041540.fastq.gz	Fastqsanger.gz
	SRR13041541.fastq.gz	Fastqsanger.gz

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CD4+ T cells contribute to neurodgeneration in Lewy Body dementia

Project description:Recent studies indicate a role of the adaptive immune system in Lewy body dementia (LBD). However, the mechanisms regulating T cell brain homing in LBD remain unknown. Here, we demonstrate interaction of T cells with Lewy bodies and with dopaminergic neurons in post-mortem LBD brains. Single cell RNA sequencing of cerebrospinal fluid (CSF) cells identified upregulated expression of C-X-C Motif Chemokine Receptor 4 (CXCR4) in CD4+ T cells in LBD. CSF protein levels of the CXCR4 ligand, C-X-C Motif Chemokine Ligand 12 (CXCL12) were associated with neuroaxonal damage in LBD. Finally, we demonstrate clonal expansion and upregulated Interleukin 17A by CD4+ T cells stimulated with phosphorylated α-synuclein. Cumulatively, these results indicate CXCR4-CXCL12 signaling as a mechanistic target for inhibiting pathological T cell trafficking in LBD.

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CD4+ T cells contribute to neurodegeneration in Lewy body dementia [CSF_and_PBMCs_Healthy and LBD]

Project description:CD4+ T cells contribute to neurodegeneration in Lewy body dementia [CSF_and_PBMCs_Healthy and LBD]

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CD4+ T cells contribute to neurodegeneration in Lewy body dementia [CSF_and_PBMCs_Healthy and LBD]

Project description:Recent studies indicate that the adaptive immune system plays a role in Lewy body dementia (LBD). However, the mechanism regulating T cell brain homing in LBD is unknown. Here, we observed T cells adjacent to Lewy bodies and dopaminergic neurons in post-mortem LBD brains. Single-cell RNA sequencing of cerebrospinal fluid (CSF) identified upregulated expression of C-X-C Motif Chemokine Receptor 4 (CXCR4) in CD4+ T cells in LBD. CSF protein levels of the CXCR4 ligand, C-X-C Motif Chemokine Ligand 12 (CXCL12) were associated with neuroaxonal damage in LBD. Furthermore, we observed clonal expansion and upregulated Interleukin 17A expression by CD4+ T cells stimulated with a phosphorylated α-synuclein epitope. Thus, CXCR4-CXCL12 signaling may represent a mechanistic target for inhibiting pathological interleukin-17-producing T cell trafficking in LBD.

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Lewy body dementia promotion by air pollutants

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Project description:Evidence links air pollution to dementia, yet its role in Lewy body dementia (LBD) remains unclear. Here we show in a cohort of 56.5 million individuals across the U.S. that PM2.5 exposure significantly raises LBD risk. Mechanistically, we find PM2.5 exposure leads to brain atrophy in wild-type mice, an effect not seen in α-synuclein (αSyn)-deficient mice. PM2.5 exposure generates a highly pathogenic αSyn strain, PM-PFF, with enhanced proteinase K-resistance and neurotoxicity, resembling αSyn LBD strains. PM2.5 samples from China, the U.S., and Europe consistently induce proteinase-resistant αSyn strains and in vivo pathology. Transcriptomic analyses reveal shared responses between PM2.5-exposed mice and LBD patients, underscoring PM2.5’s role in LBD and the stresses the need for interventions to reduce air pollution and its associated neurological disease burden.

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