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Effect of Aiolos on virtual memory T cell differentiation and function [RNA-Seq]

ABSTRACT: Virtual memory CD8+ T (TVM) cells provide rapid bystander protection during an infection despite their antigen naivety. In addition, these cells are also capable of antigen-specific response, making them an intriguing part of both the host innate and adaptive immune repertoire. While the innate and adaptive capabilities of these cells have been well characterized, much remains to be defined regarding the mechanisms governing their differentiation and function. Here, we investigate the role of the Ikaros zinc-finger (IkZF) transcription factor Aiolos in regulating CD8+ TVM generation and function. Using bulk RNA-sequencing and Assay for Transposase-Accessible Chromatin (ATAC)-sequencing, we identify differences in gene expression as well as accessibility profiles of key TVM effectors and regulators in TVM cells isolated from the spleen of control (wild-type) and Aiolos-deficient (Ikzf3-/-) mice. These studies will provide mechanistic insight into the regulation of TVM differentiation and function by Aiolos.

ORGANISM(S): Mus musculus

PROVIDER: GSE284441 | GEO | 2025/11/10

REPOSITORIES: GEO

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			Action	DRS
		Other
	GSE284441_raw_counts-TVM.csv.gz	Csv
	GSE284441_raw_counts-WT_naive.csv.gz	Csv

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Effect of Aiolos on virtual memory T cell differentiation and function [ATAC-Seq]

Project description:Virtual memory CD8+ T (TVM) cells provide rapid bystander protection during an infection despite their antigen naivety. In addition, these cells are also capable of antigen-specific response, making them an intriguing part of both the host innate and adaptive immune repertoire. While the innate and adaptive capabilities of these cells have been well characterized, much remains to be defined regarding the mechanisms governing their differentiation and function. Here, we investigate the role of the Ikaros zinc-finger (IkZF) transcription factor Aiolos in regulating CD8+ TVM generation and function. Using bulk RNA-sequencing and Assay for Transposase-Accessible Chromatin (ATAC)-sequencing, we identify differences in gene expression as well as accessibility profiles of key TVM effectors and regulators in TVM cells isolated from the spleen of control (wild-type) and Aiolos-deficient (Ikzf3-/-) mice. These studies will provide mechanistic insight into the regulation of TVM differentiation and function by Aiolos.

2025-11-10 | GSE305887 | GEO

Aiolos modulates IL-15 responsiveness of intestinal intraepithelial lymphocytes [ATAC-seq]

Project description:Intestinal intraepithelial lymphocytes (IEL) are capable of rapid innate-like responses to microenvironmental cues. While poised to activation, IEL effector functions must be stringently controlled. Aiolos is an Ikaros zinc finger (IKZF) family member encoded by Ikzf3 that promotes histone deacetylation. Here, we found that Aiolos is a crucial regulator of IEL activation. Ikzf3–/– CD8αα+ IEL expressed high levels of innate NK receptors, cytotoxic enzymes, cytokines and chemokines. Single cell RNAseq of IEL revealed that Ikzf3 deficiency mostly amplified the effector machinery of a CD8αα+ IEL subset characterized by high expression CD122, the receptor for IL-15. Furthermore, Ikzf3 deficiency increased IEL responsiveness to IL-15. Aiolos binding sites were close to those for STAT5 and RUNX transcription factors that promote IL-15 signaling and cytolytic programs, respectively; lack of Ikzf3 increased accessibility and histone acetylation of these chromatin regions. Ikzf3 deficiency increased susceptibility to colitis, demonstrating the functional relevance of Aiolos-mediated regulation of IEL effector functions.

2023-10-20 | GSE220021 | GEO

Aiolos modulates IL-15 responsiveness of intestinal intraepithelial lymphocytes [scRNA-seq]

2023-10-20 | GSE220028 | GEO

Aiolos modulates IL-15 responsiveness of intestinal intraepithelial lymphocytes [CUT&RUN]

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Aiolos modulates IL-15 responsiveness of intestinal intraepithelial lymphocytes [RNA-seq]

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Virtual memory T-cells orchestrate extra-lymphoid responses conducive to resident memory

Project description:A primary immune response is typically initiated in secondary lymphoid organs. Virtual memory CD8+ T (TVM) cells are antigen-inexperienced T cells of a central-memory phenotype, acquired through self antigen-driven homeostatic proliferation. Unexpectedly, here we find that, TVM cells are composed of CCR2+ and CCR2- subsets that differentially elaborate a spectrum of effector- and memory-poised functions directly in the tissue. During a primary flu infection, TVM cells rapidly infiltrate the lung in the first day and execute early viral control. TVM cells that recognize viral antigen are retained in the tissue, clonally expand independent of secondary lymphoid organs, and preferentially give rise to tissue-resident memory cells. By orchestrating an extra-lymphoid primary response, heterogenous TVM cells bridge innate reaction and adaptive memory directly in the infected tissue.

2021-06-15 | GSE148364 | GEO

A Variant in Human AIOLOS Impairs Adaptive Immunity by Interfering with IKAROS

Project description:A missense mutation (G158R) in Aiolos, encoded by Ikzf3 gene, resulted in defective generation of B cells in mice. Pre-B cells were profoundly decreased in homozygous mutant mice. Heterozygous mutant mice showed milder B cell developmental defects, and B cells in the secondary lymphoid organs decreased. Genome-wide binding of Aiolos and Ikaros were altered in the thymus of homozygous Ikzf3 G158R mice. Our findings indicate that Aiolos-G158R hinders B cell development by interfering Ikaros' function via formation of heterodimers. A heterozygous missense variant (G159R) in AIOLOS, encoded by IKZF3 gene, resulted in impaired adaptive immunity, which predominantly manifested as profound B cell developmental defect. Genome-wide binding of wild-type AIOLOS and AIOLOS G159R mutant were examined in IKZF3 knock-out human pre-B cell line NALM-6, retrovirally transduced with doxycycline inducible wild-type AIOLOS or AIOLOS G159R. Changes in genome-wide binding and binding motif were observed for AIOLOS G159R mutant.

2021-05-01 | GSE167487 | GEO

A distinct CD8+ T cell subset derived from virtual memory T cells causes alopecia areata through innate-like cytotoxicity [scRNA-seq]

Project description:Virtual memory T (TVM) cells are a T-cell subtype that exhibit a memory phenotype without prior exposure to a foreign antigen. Although several recent studies suggest that TVM cells exert anti-viral and anti-bacterial function, pathological roles of TVM cells causing inflammatory diseases have not been studied. Here, we identified a novel CD8+ T-cell subset (CD44s-hiCD49dlo CD8+ T cells), which is originated from TVM cells and can cause a chronic inflammatory disease, alopecia areata (AA). In the skin of alopecic mice, we detected a distinct TVM-cell subpopulation characterized by superior expression of CD44 and features of tissue residency, which was transcriptionally, phenotypically, and functionally distinct from conventional CD8+ TVM cells. Mechanistically, this cell population could be induced from conventional TVM cells by IL-12, IL-15, and IL-18 stimulation. Moreover, the pathological activity of CD44s-hiCD49dlo CD8+ T cells was mediated by NKG2D-depedent innate-like cytotoxicity against target cells, which was further augmented by IL-15 stimulation and triggered the onset of disease. Collectively, our results suggest a new immunological mechanism through which TVM cells can cause chronic inflammatory disease by innate-like cytotoxicity.

2023-05-16 | GSE229581 | GEO

A distinct CD8+ T cell subset derived from virtual memory T cells causes alopecia areata through innate-like cytotoxicity [RNA-seq]

2023-05-16 | GSE229145 | GEO

A missense mutation in AIOLOS causes B cell deficiency by interfering with IKAROS

Project description:A missense mutation (G158R) in Ikzf3 gene resulted in defective generation of B cells in mice. Pre-B cells were profoundly decreased in homozygous mutant mice. Heterozygous mutant mice showed milder B cell developmental defects, and decreased B cells in the secondary lymphoid organs were observed. Ikzf3 encodes Aiolos, which makes heterodimer with Ikaros. Our findings indicate that the loss-of-function mutation in Aiolos hinders B cell development by interfering Ikaros' function via formation of heterodimers.

2022-02-16 | GSE126778 | GEO

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