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Transcriptome analysis of HSPCs and T cells from aplastic anemia (AA) and healthy donors

ABSTRACT: Transcriptome analysis of HSPCs and T cells from aplastic anemia (AA) and healthy donors

PROVIDER: PRJNA607953 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11112400_1.fastq.gz	Fastqsanger.gz
	SRR11112400_2.fastq.gz	Fastqsanger.gz
	SRR11112500_1.fastq.gz	Fastqsanger.gz
	SRR11112500_2.fastq.gz	Fastqsanger.gz
	SRR11131600.fastq.gz	Fastqsanger.gz

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Project description:Immune aplastic anemia (AA) is a life-threatening bone marrow (BM) failure disorder driven by an autoimmune T cell attack against the hematopoietic stem and progenitor cells (HSPCs). However, the autoantigen targets and the role of other immune cells are unknown. Here, by combining scRNA+TCRαβ-seq, TCRβ-seq, flow cytometry and plasma cytokine profiling of >250 patients with AA, >250 patients with other hematological disorders and >1,000 healthy controls, we identify NK cells and CD8+ TEMRA cells expressing NK receptors with AA-associated TCRB-seq motifs as the most dysregulated immune cell populations in AA BM. Functional co-culture experiments with scRNA-TCRαβ-seq readout utilizing primary HSPCs and immune cells (in total 55 conditions) provide evidence that NK cells alone cannot kill HSPCs, but sensitize them to CD8+ T cell mediated killing. Furthermore, HSPCs induce strong activation of T cell clones with CD8+ TEMRA NK-like phenotype and AA-associated TCR motifs. To conclude, our results reveal convergent evolution of innate and adaptive immune cells in AA, where NK cells support CD8+ T cell mediated autoimmunity.

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