Similar Datasets
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
2013-04-01 | E-GEOD-37225 | biostudies-arrayexpress
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
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.
2013-04-01 | GSE37225 | GEO
Project description:Immunoglobulin A (IgA) most predominant antibody isotype at mucosal surfaces and is regulated by both T cell-dependent (TD) and independent (TI) mechanisms. In the TD pathway, T follicular helper (TFH) cells provide help to B cells to generate high-affinity antibodies. T follicular regulatory (TFR) cells fine-tune antibody responses, but precisely how these cellsregulate microbiota-directed IgA at mucosal sites has been unclear. Here, we used a TFR-deficient mouse model (Foxp3Cre Bcl6fl/fl; Bcl6FC) in which the gut microbiota develops in the absence of TFR cells, while the broader regulatory T cell compartment remains intact. While Bcl6FC mice showed similar levels of IgA-coated commensal bacteria to wild-type mice in the naïve state, following oral immunization, Bcl6FC mice exhibited a durable increase in IgA-coated commensal bacteria in feces and small intestine, without changes in overall community composition or epithelial barrier permeability. IgA-seq analysis of Bcl6FC mice revealed an increased diversity of IgA-coated taxa, both in naïve and orally immunized mice. IgA coating index analysis, a measure of IgA affinity, identified higher IgA binding to multiple taxa in Bcl6C mice compared to control mice. Consistent with these findings, sera from immunized Bcl6FC mice showed increased IgA binding to Alloprevotella and Klebsiella species but not to E. coli or Group A/B Streptococcus compared to control mice. B cell receptor repertoire sequencing demonstrated divergent patterns of somatic hypermutation (SMH) for IgA and IgG, where TFR cells repressed IgA SMH but enhanced IgG somatic hypermutation. Mechanistically, suppression of commensal-directed IgA required TFR-derived IL-10 but was independent of CTLA-4. IL-10 directly inhibited TGF-β-driven IgA class switching of B cells in vitro. Together, our data identify TFR cells as critical gatekeepers of mucosal IgA responses, constraining commensal-specific IgA responses through a novel IL-10-dependent pathway. Our findings haveimportant implications for regulation of the microbiome by TFR cells and IgA.
2026-04-15 | GSE320270 | GEO
Project description:In order to provide information on the peptide sequence of the IgA glycopeptides, a proteomics analysis was run on LC-MS/MS data of N-glycosidase F-digested IgA samples, in which the N-glycans had been released. The samples included IgA (isolated) from: 1) the saliva samples from two healthy donors, 2) a pooled-plasma standard from a minimum of 20 human donors (VisuCon-F Frozen Normal Control Plasma; Affinity Biologicals, Ancaster, Canada), 3) 10 μg of a human plasma-derived IgA standard (Lee Biosolutions, Maryland Heights, MO), and 4) a human colostrum-derived SIgA standard (Athens Research and Technology, Athens, GA).
2018-11-09 | PXD011228 | Pride
Project description:This SuperSeries is composed of the following subset Series: GSE35487: Expression data from human with IgA nephropathy (IgAN) [HG-U133A] GSE35488: Expression data from human with IgA nephropathy (IgAN) [HG-U133A_ENTREZG_10] Refer to individual Series
2012-02-02 | E-GEOD-35489 | biostudies-arrayexpress
Project description:This study identifies immune transcript signatures that may predict IgAV nephritis in skin biopsies and distinguish IgA-IRGN from IgAN and IgAV in kidney biopsies
2023-08-08 | GSE220100 | GEO
Project description:Targeted transcriptional analysis of IgA vasculitis, IgA nephropathy, and IgA dominant infection related glomerulonephritis
| PRJNA908803 | ENA