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Regulatory B cells expressing granzyme B (GZMB+Bregs)

ABSTRACT: Regulatory B cells expressing granzyme B (GZMB+Bregs)

PROVIDER: PRJNA931282 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23333016_1.fastq.gz	Fastqsanger.gz
	SRR23333016_2.fastq.gz	Fastqsanger.gz
	SRR23333017_1.fastq.gz	Fastqsanger.gz
	SRR23333017_2.fastq.gz	Fastqsanger.gz
	SRR23333018_1.fastq.gz	Fastqsanger.gz

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Gene expression profile at single cell level of in vitro induced regulatory B cells expressing granzyme B (GZMB+Bregs) and non-Bregs from healthy donors and kidney transplant recipients.

Project description:Regulatory B cells are considered as a very heterogenous population of different origins and functions. We used single cell RNA sequencing (scRNA-seq) to analyze the regulatory B cells expressing granzyme B (GZMB+Bregs).

2023-08-23 | GSE224460 | GEO

Gene expression profile of CD4+ CD25- T cells in coculture with regulatory B cells expressing granzyme B (GZMB+Bregs) or total B cells

Project description:Gene expression profile of CD4+ CD25- T cells in coculture with regulatory B cells expressing granzyme B (GZMB+Bregs) or total B cells

| PRJNA934570 | ENA

Gene expression profile at single cell level of in vitro induced regulatory B cells expressing granzyme B (GZMB+Bregs) and non-Bregs from healthy donors and kidney transplant recipients.

Project description:Gene expression profile at single cell level of in vitro induced regulatory B cells expressing granzyme B (GZMB+Bregs) and non-Bregs from healthy donors and kidney transplant recipients.

| PRJNA934568 | ENA

Gene expression profile of CD4+ CD25- T cells in coculture with regulatory B cells expressing granzyme B (GZMB+Bregs) or total B cells

Project description:Regulatory B cells are considered as a very heterogenous population of different origin and functions. Here, we show that Notably, Bregs induced a strong inhibition of T cell genes associated to proliferation, activation, inflammation and apoptosis compared to total B cells. We identified and validated 5 receptor/ligand interactions between Bregs and T cells.

2023-08-23 | GSE224456 | GEO

Profiling of Granzyme B Secreting B cells

Project description:B cells with regulatory functions have been described both in immune homeostasis in healthy volunteers and in different pathological conditions. Whereas Il-10 secreting B cells represent the main subset described, recently, a subset of B cells secreting granzyme B (GZMB+) was evidenced in a growing numbers of immunological contexts, autoimmunity, chronic infections and neoplasias. Until now, no phenotype has been evidenced for these GZMB+ B cells and their regulatory functions as well are still to clarify.

2020-09-27 | GSE125901 | GEO

Regulatory B cells expressing granzyme B (GZMB+Bregs)

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-08-23 | GSE224461 | GEO

Cytotoxic Granzyme C Expressing ILC1s Contribute to Antitumor Immunity and Neonatal Autoimmunity

Project description:Innate lymphocytes are integral components of the cellular immune system that coordinates host defense against a multitude of challenges and can trigger immunopathology when dysregulated. Natural killer (NK) cells and innate lymphoid cells (ILCs) are innate immune effectors postulated to functionally mirror conventional cytotoxic T lymphocytes and helper T cells, respectively. Here, we show that the cytolytic molecule granzyme C was surprisingly expressed in cells with the phenotype of type 1 ILCs (ILC1s) in mouse liver and salivary gland. Cell fate-mapping and transfer studies revealed that granzyme C-expressing innate lymphocytes could be derived from ILC progenitors and did not interconvert with NK cells, ILC2s, or ILC3s. Granzyme C defined a maturation state of ILC1s, which required the transcription factor T-bet and to a lesser extent Eomes specifically in the salivary gland for their maintenance. Furthermore, transforming growth factor-b (TGF-b) signaling promoted maintenance of granzyme C-expressing ILC1s in the salivary gland and in the tumor of a transgenic breast cancer model, and their depletion caused accelerated tumor growth. ILC1s gained granzyme C expression following interleukin-15 (IL-15) stimulation, which enabled perforin-mediated cytotoxicity. Strikingly, constitutive activation of the IL-15-regulated transcription factor Stat5 in granzyme C-fate-mapped ILC1s triggered lethal perforin-dependent autoimmunity in neonatal mice. Thus, granzyme C marks a cytotoxic effector state of ILC1s, broadening their function beyond ‘helper-like’ lymphocytes.

2022-02-18 | GSE196716 | GEO

A novel and divergent role of granzyme A and B in resistance to helminth infection

Project description:Granzyme (gzm) A and B, proteases of NK cells and T killer cells, mediate cell death, but also cleave extracellular matrices, inactivate intracellular pathogens and induce cytokines. Moreover, macrophages, T helper 2 cells, regulatory T cells, mast cells and B cells can express gzms. We recently reported gzm induction in human filarial infection. Here we show that in rodent filarial infection with Litomosoides sigmodontis worm loads were significantly reduced in gzmAxB and gzmB knock out (ko) mice, but enhanced in gzmA ko compared to wildtype (wt) mice. GzmA/B deficiency was associated with a defense-promoting Th2 cytokine and antibody shift and enhanced early inflammation gene expression, whereas gzmA deficiency was linked with alternatively activated macrophages and reduced inflammation. This suggests a novel and divergent role for gzms in helminth infection with gzmA contributing to resistance and gzmB promoting susceptibility. Keywords: knock out vs wild type

2011-07-29 | GSE17544 | GEO

Cytotoxic Granzyme C Expressing ILC1s Contribute to Antitumor Immunity and Neonatal Autoimmunity

Project description:Cytotoxic Granzyme C Expressing ILC1s Contribute to Antitumor Immunity and Neonatal Autoimmunity

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CD1d-dependent immune suppression mediated by regulatory B cells through modulations of iNKT cells

Project description:Regulatory B cells (Breg) express high levels of CD1d that presents lipid antigens to invariant natural killer T (iNKT) cells. The function of CD1d in Breg biology and iNKT cell activity during inflammation remains unclear. Here we show, using chimeric mice, cell depletion and adoptive cell transfer, that CD1d-lipid presentation by Bregs induces iNKT cells to secret IFN-γ to contribute, partially, to the down-regulation of T helper (Th)1 and Th17 adaptive immune responses for ameliorating experimental arthritis. Mice lacking CD1d-expressing B cells develop exacerbated diseases compared to wild-type mice, and fail to respond to α-galactosylceramide treatment. Absence of lipid presentation by B cells causes altered activation of iNKT cells, with disruption of regulatory pathways including those involved in metabolism and cytokine responses. Thus, we identify an IL-10-independent mechanism by which Bregs restrain excessive inflammation via lipid presentation.

2018-01-25 | E-MTAB-6381 | biostudies-arrayexpress

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