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

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

PROVIDER: PRJNA1138257 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29905024_1.fastq.gz	Fastqsanger.gz
	SRR29905024_2.fastq.gz	Fastqsanger.gz
	SRR29905025_1.fastq.gz	Fastqsanger.gz
	SRR29905025_2.fastq.gz	Fastqsanger.gz
	SRR29905026_1.fastq.gz	Fastqsanger.gz

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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

Neutrophil extracellular traps melt Peyer’s patches following stroke and myocardial infarction

Project description:Sterile tissue injury after stroke causes lymphocyte contraction in lymphoid tissues and may decrease circulating IgA-levels. Intestinal Peyer’s patches (PP) harbor large numbers of IgA+ B cell precursors and plasma cells. Whether and how tissue injury triggers PP-B cell death, thereby mediating IgA-loss, is unknown. We found decreased circulating IgA levels in stroke and myocardial infarction patients. Experimental stroke and myocardial infarction in mice phenocopied the human situation. Decreased plasma and fecal IgA were accompanied by rapid and macroscopic shrinkage of PP caused by substantial losses of PP-resident IgA+ precursors and plasma cells in mice. Tissue injury induced neutrophil activation endowed with the release of toxic neutrophil extracellular traps (NETs). Antibody-mediated or genetically- induced neutrophil loss, digestion of NETs, or inhibition of their release by the Gasdermin D blockade completely prevented lymphocyte loss and PP shrinkage. We also identified NETs in the plasma of stroke and myocardial infarction patients. Hence, tissue injury induces systemic NET-release, which might be targeted to maintain immune homeostasis at mucosal barriers.

2024-02-28 | PXD044644 | Pride

SFB-Driven Remodeling of Peyer’s Patches Enhances IgA and IgG2b Class Switching and Atypical Memory B Cell Generation

Project description:The intestinal microbiota plays a central role in shaping host mucosal immunity, but the mechanisms by which specific commensals influence B cell responses remain incompletely defined. Segmented filamentous bacteria (SFB), potent inducers of Th17 cells, have been implicated in both protective and pathogenic immune outcomes. Here, we show that SFB colonization in specific pathogen-free (SPF) mice induces a profound remodeling of Peyer’s patches (PPs), characterized by increased cellularity, germinal center (GC) formation, and robust class switching to IgA and IgG2b, but not IgG1. Using flow cytometry, bone marrow chimeras, and single-cell RNA sequencing coupled with BCR repertoire analysis, we demonstrate that SFB enhances recruitment of naïve B cells through the CXCR5-CXCL13 axis and promotes T cell-dependent expansion of both GC and memory B cells. These memory B cells exhibit hallmark features of atypical B cells (ABCs), including CD11c expression and somatic hypermutation, and arise via a GC-dependent pathway. SFB increases the number of activated CD11c+SIRPa+BST2-CD11b+ DCs in the the PP subepithelial dome (SED), and T helper 17 (Th17) and T follicular helper (Tfh) cells. Surprisingly, unlike previous reports, neither Th17 effector function (IL-17R-/-) nor Th17-to-Tfh conversion (CD4CRE-RORgtfl/fl) was essential for the observed B cell changes. Finally, we show that SFB colonization enhances clonal diversity and somatic hypermutation in IgA⁺ and IgG2b⁺ B cells qualitatively as well as quantitatively. These findings establish a mechanistic link between microbiota composition and mucosal B cell immunity, with implications for vaccine responses, mucosal homeostasis, and autoimmune susceptibility.

2026-07-01 | GSE301432 | GEO

SFB-Driven Remodeling of Peyer’s Patches Enhances IgA and IgG2b Class Switching and Atypical Memory B Cell Generation II

2026-07-01 | GSE301577 | GEO

SFB-Driven Remodeling of Peyer’s Patches Enhances IgA and IgG2b Class Switching and Atypical Memory B Cell Generation [scRNA-Seq]

2026-07-01 | GSE301871 | GEO

SFB-Driven Remodeling of Peyer’s Patches Enhances IgA and IgG2b Class Switching and Atypical Memory B Cell Generation

Project description:SFB-Driven Remodeling of Peyer’s Patches Enhances IgA and IgG2b Class Switching and Atypical Memory B Cell Generation

| PRJNA1285166 | ENA

SFB-Driven Remodeling of Peyer’s Patches Enhances IgA and IgG2b Class Switching and Atypical Memory B Cell Generation II

Project description:SFB-Driven Remodeling of Peyer’s Patches Enhances IgA and IgG2b Class Switching and Atypical Memory B Cell Generation II

| PRJNA1285479 | ENA

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.

2022-07-13 | GSE160732 | GEO

SFB-Driven Remodeling of Peyer’s Patches Enhances IgA and IgG2b Class Switching and Atypical Memory B Cell Generation [scRNA-Seq]

Project description:SFB-Driven Remodeling of Peyer’s Patches Enhances IgA and IgG2b Class Switching and Atypical Memory B Cell Generation [scRNA-Seq]

| PRJNA1287675 | ENA

Fibroblastic reticular cell lineage convergence in Peyer’s patches governs intestinal homeostasis

Project description:Fibroblastic reticular cell lineage convergence in Peyer’s patches governs intestinal homeostasis

| PRJEB39116 | ENA