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B cell residency but not T cell-independent IgA switching in the gut requires innate lymphoid cells

ABSTRACT: B cell residency but not T cell-independent IgA switching in the gut requires innate lymphoid cells

PROVIDER: PRJNA703728 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13759077.fastq.gz	Fastqsanger.gz
	SRR13759078.fastq.gz	Fastqsanger.gz
	SRR13759079.fastq.gz	Fastqsanger.gz
	SRR13759080.fastq.gz	Fastqsanger.gz

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B cell residency but not T cell-independent IgA switching in the gut requires innate lymphoid cells

Project description:Immunoglobulin A (IgA)-producing plasma cells derived from conventional B cells in the gut play an important role in maintaining the homeostasis of gut flora. Both T cell-dependent and T cell-independent IgA class switching occurs in the lymphoid structures in the gut, whose formation depends on lymphoid tissue inducers (LTis), a subset of innate lymphoid cells (ILCs). However, our knowledge on the functions of ILCs, the innate counter parts of CD4 T helper cells, in promoting IgA production is still limited. By cell adoptive transfer and utilizing a unique mouse strain, we demonstrated that the generation of IgA-producing plasma cells from B cells in the gut occurred efficiently in the absence of both T cells and ILCs and without engaging TGFβ signaling. Nevertheless, B cell recruitment and/or retention in the gut required NKp46-CCR6+ LTis. Therefore, while ILCs contribute to the accumulation of B cells in the gut through inducing lymphoid structure formation, they are not essential for the T cell-independent generation of IgA-producing plasma cells.

2021-06-28 | GSE167188 | GEO

B cell residency but not T cell-independent IgA switching in the gut requires innate lymphoid cells.

Project description:Immunoglobulin A (IgA)-producing plasma cells derived from conventional B cells in the gut play an important role in maintaining the homeostasis of gut flora. Both T cell-dependent and T cell-independent IgA class switching occurs in the lymphoid structures in the gut, whose formation depends on lymphoid tissue inducers (LTis), a subset of innate lymphoid cells (ILCs). However, our knowledge on the functions of non-LTi helper-like ILCs, the innate counter parts of CD4 T helper cells, in promoting IgA production is still limited. By cell adoptive transfer and utilizing a unique mouse strain, we demonstrated that the generation of IgA-producing plasma cells from B cells in the gut occurred efficiently in the absence of both T cells and helper-like ILCs and without engaging TGF-β signaling. Nevertheless, B cell recruitment and/or retention in the gut required functional NKp46-CCR6+ LTis. Therefore, while CCR6+ LTis contribute to the accumulation of B cells in the gut through inducing lymphoid structure formation, helper-like ILCs are not essential for the T cell-independent generation of IgA-producing plasma cells.

| S-EPMC8271577 | biostudies-literature

Chromatin remodeling in HIF-1a deficient B cell during IgA class switching [ChIP-seq]

Project description:The interconnection between metabolic programming and chromatin remodeling during IgA class switching suggest that HIF-1a-dependent glycolytic flux may control the epigenetic modification at α class switching region (Sα) in the Igh locus. To test our hypothesis, histone acetylation was analyzed by chromatin immunoprecipitation sequencing (ChIP-seq) (H3K9ac and H3K27ac) in Hif-1a deficient and control B cell during IgA class switching. Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for histone modifications H3K27ac and H3K9ac in B cell from WT and HIF-1a deficient mice.

2025-01-08 | GSE228366 | GEO

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Project description:Investigate the function HIF-1a in the regulation of B cell IgA class switching using WT and HIF-1a conditional knockout mice.

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Metabolic fitness of IgA+ plasma cells in the gut requires DOCK8

Project description:Metabolic fitness of IgA+ plasma cells in the gut requires DOCK8

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Metabolic fitness of IgA+ plasma cells in the gut requires DOCK8

Project description:DOCK8 is required for T cell-dependent gut IgA by maintaining plasma cell metabolic fitness

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Chromatin remodeling in HIF-1a deficient B cell during IgA class switching [ChIP-seq]

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Krüppel-like factor 2 controls IgA plasma cell compartmentalization and IgA responses

Project description:Krüppel-like factor 2 (KLF2) is a potent regulator of lymphocyte differentiation, activation and migration. However, its functional role in adaptive and humoral immunity remains elusive. Therefore, by using mice with a B cell-specific deletion of KLF2, we investigated plasma cell differentiation and antibody responses. We revealed that the deletion of KLF2 resulted in perturbed IgA plasma cell compartmentalization, characterized by the absence of IgA plasma cells in the bone marrow, their reductions in the spleen, the blood and the lamina propria of the colon and the small intestine, concomitant with their accumulation and retention in mesenteric lymph nodes and Peyer’s patches. Most intriguingly, secretory IgA in the intestinal lumen was almost absent, dimeric serum IgA was drastically reduced and antigen-specific IgA responses to soluble Salmonella flagellin were blunted in KLF2-deficient mice. Perturbance of IgA plasma cell localization was caused by deregulation of CCR9, Integrin chains αM, α4, β7, and sphingosine-1-phosphate receptors. Hence, KLF2 not only orchestrates the localization of IgA plasma cells by fine-tuning chemokine receptors and adhesion molecules but also controls IgA responses to Salmonella flagellin.

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Project description:To compare gene expression between CD11b+ IgA and CD11b- IgA cells in the small intestine, each cell population was isolated from the murine small intestine. Similar experiment with different sample was performed as described in Gene expression on CD11b+ IgA and CD11b- IgA cells in the small intestine #02

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Peyer’s patches are required for Bacteroides fragilis to induce protective systemic IgA

Project description:Gut-educated IgA-secreting plasma cells that disseminate beyond the mucosa and into systemic tissues can help prevent disease in several contexts. Here we show, the commensal bacteria Bacteroides fragilis (Bf), is an efficient inducer of systemic IgA responses. The generation of bone marrow IgA plasma cells and high levels of serum IgA specific to Bf requires robust intestinal colonization. Bf-specific IgA responses were severely diminished in mice lacking Peyer’s patches, but not mice lacking a cecal patch. Colonization resulted in few changes in the host transcriptional profile in the gut, suggesting a commensal relationship. High levels of Bf-specific serum IgA, but not IgG, provided protection from peritoneal abscess formation in a bowel perforation model of Bf dissemination. These findings demonstrate a critical role for bacterial colonization and Peyer’s patches in the induction of robust systemic IgA responses that confer protection from bacterial dissemination originating from the gut.

2024-07-25 | GSE272717 | GEO

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