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CD163 macrophages suppress CD8 and NK cells through CD163 mediated HLA-E (H2-T23)

ABSTRACT: CD163 macrophages suppress CD8 and NK cells through CD163 mediated HLA-E (H2-T23)

PROVIDER: PRJNA1236370 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32701054_1.fastq.gz	Fastqsanger.gz
	SRR32701054_2.fastq.gz	Fastqsanger.gz
	SRR32701055_1.fastq.gz	Fastqsanger.gz
	SRR32701055_2.fastq.gz	Fastqsanger.gz
	SRR32701056_1.fastq.gz	Fastqsanger.gz

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CD163 macrophages suppress CD8 and NK cells through CD163 mediated HLA-E (H2-T23)

Project description:CD163 macrophages, which can be identified in different tissues of individuals such as the colon and tumor tissues, possessed markedly immunosuppressive functions on immune cells, especially effective cells such as CD8 cells. However, the mechanism(s) by which CD163 macrophages inhibit immune responses remains to be illusive. Using single cell-sequence techniques, we identified CD163+ macrophage subset in the colon tissues. Meanwhile, we also characterized CD163+ macrophage associated immune cell populations and subpopulations in mouse colon tissues. Deletion of CD163+ macrophage subset could markedly increase the proportions of CD8 and NK cells. Mechanistically, CD163+ macrophage subpopulations can inhibit the proliferation of CD8 and NK cells through inhibitory molecules CD94/NKG2a (KLRD1/KLRC1 in mice) and their ligand HLA-E /H2-T23 (Human/mice) on the surface of CD163+ macrophages. Importantly, CD163 in macrophages could promote the expression of HLA-E/H2-T23 expression through inducing the expression of signal peptide peptidase (SPP), offering a target for immunotherapy in CD8 and NK cells associated immunosuppressive diseases such as tumor. Taken together, we demonstrate that CD163+macrophage subpopulation plays a critical role in suppressing CD8 and NK cells through CD163 mediated HLA-E/H2-T23.

2025-03-20 | GSE292042 | GEO

Fusarium vanettenii strain:T23

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6 small intestinal macrophage subsets (CD4–Tim4–CD163–, CD4+Tim4–CD163–, CD4+Tim4+CD163–, CD4–Tim4–CD163+, CD4+Tim4–CD163+, CD4+Tim4+CD163+ ) from adult male C57BL/6J mice

Project description:6 small intestinal macrophage subsets (CD4–Tim4–CD163–, CD4+Tim4–CD163–, CD4+Tim4+CD163–, CD4–Tim4–CD163+, CD4+Tim4–CD163+, CD4+Tim4+CD163+ ) from adult male C57BL/6J mice

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Single-cell RNA sequencing reveals the transcriptional landscape and heterogeneity of macrophages in intestinal tissue of WT and CD163+ macrophage-deficient mice.

Project description:CD163 macrophages, which markedly accumulated in inflammation and tumor tissues possessed markedly immunosuppressive functions on immune cells, especially effective cells such as CD8 cells. However, the mechanism of CD163 macrophages in regulating immune responses remains to be illusive. Using single cell-sequence techniques, we identified CD163 macrophage subset in the colon tissues. Meanwhile, we also characterized CD163 macrophage associated immune cell populations and subpopulations in mouse colon tissues. We found that CD163+ macrophage subset in the colon was related to gut microbiota. Deletion of CD163+ macrophage subset could markedly increase the proportions of the immune cell subsets such as CD8 and NK cells. Mechanistically, gut microbiota mediated CD163+ macrophage subpopulations can down-regulate CD8 and NK cells through inhibitory molecules CD94/NKG2a (Kird1/Kirc1 in mice) and their ligand HLA-E /QA-1 (Human/mice) on the surface of CD163+ macrophages.

2025-02-14 | GSE289171 | GEO

Pseudomonas fulva strain:T23

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Sphingomonas sp. H2 strain:H2 | isolate:H2

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Fusarium vanettenii strain:T23

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6 small intestinal macrophage subsets (CD4–Tim4–CD163–, CD4+Tim4–CD163–, CD4+Tim4+CD163–, CD4–Tim4–CD163+, CD4+Tim4–CD163+, CD4+Tim4+CD163+ ) from adult male C57BL/6J mice

Project description:To better determine functional heterogenity of small intestinal macrophages, 6 subsets of were sorted for RNA sequencing based on expression of CD4, Tim4, and CD163

2023-08-18 | GSE232645 | GEO

Altererythrobacter sp. H2 strain:H2

Project description:Altererythrobacter sp. H2 strain:H2 Genome sequencing

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Senataxin and RNase H2 act redundantly to suppress genome instability during class switch recombination

Project description:Class switch recombination generates antibody distinct isotypes critical to a robust adaptive immune system and defects are associated with auto-immune disorders and lymphomagenesis. Transcription is required during class switch to recruit the cytidine deaminase AID—an essential step for the formation of DNA doublestrand breaks—and strongly induces the formation of R loops within the immunoglobulin heavy chain locus. However, the impact of R loops on double-strand break formation and repair during class switch recombination remains unclear. Here we report that cells lacking two enzymes involved in R loop removal— Senataxin and RNase H2—exhibit increased R loop formation and genome instability at the immunoglobulin heavy chain locus without impacting class switch recombination efficiency, transcriptional activity, or AID recruitment. Senataxin and RNase H2-deficient cells also exhibit increased insertion mutations at switch junctions, a hallmark of alternative end joining. Importantly, these phenotypes were not observed in cells lacking Senataxin or RNase H2B alone. We propose that Senataxin acts redundantly with RNase H2 to mediate timely R loop removal, promoting efficient repair while suppressing AID-dependent genome instability and insertional mutagenesis.

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