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Intestinal type 2 inflammation reprograms mesenteric adipose tissue and permanently alters its resident immune cell niche

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE157314 | GEO | 2022/08/18

REPOSITORIES: GEO

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Intestinal type 2 inflammation reprograms mesenteric adipose tissue and permanently alters its resident immune cell niche [2022_RNA_2]

Project description:In addition to adipocytes, adipose tissue (AT) is populated by mesenchymal stem cells (MSC) in stages of commitment to the adipocyte lineage, and immune cells which support homeostatic tissue function. How MSC and immune cells interact during infection is poorly understood. We found that during intestinal nematode infection, MSC in gut-associated AT (mFAT) exhibit a bias away from commitment to the adipocyte lineage towards a pluripotent progenitor state. During this time, MSC became metabolically active, and began secreting the alarmins IL-33 and TSLP, and extracellular matrix collagens. In parallel, mFAT became irreversibly populated by Th2 resident memory (Th2RM) cells, which make the tissue modulatory cytokines amphiregulin and TGFβ1. Secretion of these cytokines, and Th2RM activation and maintenance, was driven by IL-33 and TSLP and in turn MSC activation was induced by amphiregulin and TGFβ1. Our findings link Th2RM cells to reversible mFAT remodeling during intestinal infection and underscore the reciprocal dependence of stroma and resident immune cells for lasting tissue immunity.

2022-10-13 | GSE215137 | GEO

Intestinal type 2 inflammation reprograms mesenteric adipose tissue and permanently alters its resident immune cell niche [2022_RNA_1]

2022-10-13 | GSE215136 | GEO

Intestinal type 2 inflammation reprograms mesenteric adipose tissue and permanently alters its resident immune cell niche [bulk RNA]

2022-08-18 | GSE157312 | GEO

Intestinal type 2 inflammation reprograms mesenteric adipose tissue and permanently alters its resident immune cell niche [single-cell RNA-seq]

2022-04-15 | GSE157313 | GEO

Intestinal type 2 inflammation reprograms mesenteric adipose tissue and permanently alters its resident immune cell niche

Project description:Intestinal type 2 inflammation reprograms mesenteric adipose tissue and permanently alters its resident immune cell niche

| PRJNA660810 | ENA

Intestinal type 2 inflammation reprograms mesenteric adipose tissue and permanently alters its resident immune cell niche [2022_RNA_2]

Project description:Intestinal type 2 inflammation reprograms mesenteric adipose tissue and permanently alters its resident immune cell niche [2022_RNA_2]

| PRJNA888984 | ENA

Intestinal type 2 inflammation reprograms mesenteric adipose tissue and permanently alters its resident immune cell niche [2022_RNA_1]

Project description:Intestinal type 2 inflammation reprograms mesenteric adipose tissue and permanently alters its resident immune cell niche [2022_RNA_1]

| PRJNA888985 | ENA

Intestinal type 2 inflammation reprograms mesenteric adipose tissue and permanently alters its resident immune cell niche [bulk RNA]

Project description:Intestinal type 2 inflammation reprograms mesenteric adipose tissue and permanently alters its resident immune cell niche [bulk RNA]

| PRJNA660813 | ENA

Intestinal type 2 inflammation reprograms mesenteric adipose tissue and permanently alters its resident immune cell niche [single-cell RNA-seq]

Project description:Intestinal type 2 inflammation reprograms mesenteric adipose tissue and permanently alters its resident immune cell niche [single-cell RNA-seq]

| PRJNA660812 | ENA

Chronic Inflammation Permanently Reshapes Tissue-Resident Immunity in Celiac Disease.

Project description:Tissue-resident lymphocytes play a key role in immune surveillance, but it remains unclear how these inherently stable cell populations respond to chronic inflammation. In the setting of celiac disease (CeD), where exposure to dietary antigen can be controlled, gluten-induced inflammation triggered a profound depletion of naturally occurring Vγ4+/Vδ1+ intraepithelial lymphocytes (IELs) with innate cytolytic properties and specificity for the butyrophilin-like (BTNL) molecules BTNL3/BTNL8. Creation of a new niche with reduced expression of BTNL8 and loss of Vγ4+/Vδ1+ IELs was accompanied by the expansion of gluten-sensitive, interferon-γ-producing Vδ1+ IELs bearing T cell receptors (TCRs) with a shared non-germline-encoded motif that failed to recognize BTNL3/BTNL8. Exclusion of dietary gluten restored BTNL8 expression but was insufficient to reconstitute the physiological Vγ4+/Vδ1+ subset among TCRγδ+ IELs. Collectively, these data show that chronic inflammation permanently reconfigures the tissue-resident TCRγδ+ IEL compartment in CeD. VIDEO ABSTRACT.

| S-EPMC6667191 | biostudies-literature

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