Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ACCESS DATA

Json Xml

Similar Datasets

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: Not available

| S-EPMC8271577 | biostudies-literature

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

2024-01-10 | GSE198847 | GEO

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

Gene expression on CD11b+ IgA and CD11b- IgA cells in the small intestine #01

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

Microbiota regulate the ability of lung dendritic cells to induce IgA class switch recombination and generate protective GI immune responses

Project description:Analyses of gene expression between CD103+ lung DCs, CD24+ lung DCs and CD64+ lung macrophages in Specific pathogen free (SPF) and germ free (GF) mice. Hypothesis tested was that the IgA class switching function of lung DCs is regulated by genes differentially expressed in GF mice compared to SPF mice. Results obtained provide important insights into the mechanisms of IgA induction by lung DCs

2015-11-13 | GSE74969 | GEO

IGA-BARIA

Project description:IGA-BARIA

| PRJEB47045 | ENA

Gut-Resident IL10+CX3CR1hi Macrophages Induce Tertiary Lymphoid Structures and IgA Response in Situ

Project description:Gut resident IL10+CX3CR1hi macrophages drive development of mucosal tertiary lymphoid structures that serve as ectopic site of the IgA response to enteric infection.

2020-04-17 | GSE121471 | GEO

Runx3 programs CD8+ T cell residency in non-lymphoid tissues and tumours

Project description:Runx3 programs CD8+ T cell residency in non-lymphoid tissues and tumours

| PRJNA419960 | ENA

IgA deglycosylation to identify glycosylation sites

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data