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ILC2s directly activate anti-tumor cytotoxic CD8+ T lymphocytes by internalizing, processing, and presenting exogenous antigens

ABSTRACT: ILC2s directly activate anti-tumor cytotoxic CD8+ T lymphocytes by internalizing, processing, and presenting exogenous antigens

PROVIDER: PRJNA1010791 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25820073_1.fastq.gz	Fastqsanger.gz
	SRR25820073_2.fastq.gz	Fastqsanger.gz
	SRR25820074_1.fastq.gz	Fastqsanger.gz
	SRR25820074_2.fastq.gz	Fastqsanger.gz
	SRR25820075_1.fastq.gz	Fastqsanger.gz

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ILC2s directly activate anti-tumor cytotoxic CD8+ T lymphocytes by internalizing, processing, and presenting exogenous antigens

Project description:Type-2 innate-lymphoid cells (ILC2s) associate with both tumor promotion and inhibition. We found that ILC2s may induce anti-tumor immunity by a hitherto-unrealized mechanism: they may internalize, process, and present exogenous tumor antigen on major-histocompatibility-complex class-I (MHCI) molecules with costimulatory molecules to CD8+ T cells. This converts the T cells into cytotoxic-T-lymphocytes (CTLs). Specifically, transferring ILC2s into tumor-bearing mice inhibited tumor growth in a CD8+ T cell-dependent manner. Moreover, co-culturing human or murine CD8+ T cells with ILC2s upregulated T-cell expression of cytotoxic molecules. The resulting CTLs efficiently killed tumor cells in vitro and upon transfer into tumor-bearing mice. ILC2s were found to internalize exogenous antigens via clathrin-dependent endocytosis and to process/present them as efficiently as professional antigen-presenting cells for CD8+ T cells (type-1 conventional dendritic cells). Thus, ILC2s can present antigen to CD8+ T cells and induce their tumor-killing activity. This novel finding has promising implications for anti-tumor strategies.

2024-08-31 | GSE241945 | GEO

Expression data from naive, effector and memory-like ILC2s isolated from mouse lungs and those from effector and memory-like ILC2s isolated from mediastinal lymph node

Project description:Group 2 innate lymphoid cells (ILC2s) in the lung are stimulated by inhaled allergens. ILC2s do not directly recognize allergens but they are stimulated by cytokines including interleukin (IL)-33 released by damaged epithelium.Lung ILC2s, upon stimulation, produce T helper 2 cell-type cytokines inducing T cell independent allergic lung inflammation. We now report that lung ILC2s, upon activation by an allergen or IL-33, acquire the properties of memory cells. The activated ILC2s initially proliferate and secrete cytokines, followed by a contraction phase as they stop producing cytokines. Nevertheless, some persist long after the resolution of the inflammation and acquire intrinsic capacities to react to unrelated allergens more vigorously than naÃ¯ve ILC2s, thus mediating a severe allergic lung inflammation. Gene expression profiles of the previously activated ILC2s show a gene signature of memory T cells. These antigen non-specific memory ILC2s may explain why asthma patients are often sensitized to multiple allergens. ILC2s were isolated from mouse lungs from naive and IL-33 injected mice 4 days, 14 days and 4 months after the initial treatment. RNA was extracted from those ILC2 populations and analyzed for gene expression profiles. RNA was also extracted from ILC2s isolated from lung draining mediastinal lymph node (mLN) 4 days and 14 days after IL-33 treatment.

2016-06-30 | E-GEOD-81700 | biostudies-arrayexpress

Proteome of group 2 innate lymphoid cells (ILC2s) stimulated with IL33 and TL1A

Project description:We analyzed the total proteome of group 2 innate lymphoid cells (ILC2s) after different stimulation with interleukin-33 (IL-33), a cytokine playing a critical role in human asthma, and TL1A, a TNF-family cytokine also known to activate ILC2s. Upon combined stimulation with IL-33 plus TL1A, we show that lung ILC2s produce high amounts of IL-9 and acquire a transient ‘ILC9’ phenotype. This phenotype is characterized by simultaneous production of large amounts of type 2 cytokines (IL-5, IL-13 and IL-9), induction of the IL-2 receptor CD25 (Il2ra), and of the transcription factors IRF4, JunB and BATF, that form immune-specific complexes known to induce IL-9 expression.

2024-03-05 | PXD041987 | Pride

Identification of human cytotoxic ILC3s

Project description:Human ILCs are classically categorized into five subsets; cytotoxic CD127-CD94+ NK cells and non-cytotoxic CD127+CD94-, ILC1s, ILC2s, ILC3s and LTi cells. Here, we identify a novel subset within the CD127+ ILC population, characterized by the expression of the cytotoxic marker CD94. These CD94+ ILCs strongly resemble conventional ILC3s in terms of phenotype, transcriptome and cytokine production, but are highly cytotoxic. IL-15 was unable to induce differentiation of CD94+ ILCs towards mature NK cells. Instead, CD94+ ILCs retained RORγt, CD127 and CD200R expression and produced IL-22 in response to IL-15. Culturing non-cytotoxic CD127+ ILC1s or ILC3s with IL-12 induced upregulation of CD94 and cytotoxic activity, effects that were not observed with IL-15 stimulation. Thus, human helper ILCs can acquire a cytotoxic program without differentiating into NK cells.

2020-09-14 | GSE147231 | GEO

Dendritic Cells Compare the Similarity of Endogenous and Exogenous Antigens

Project description:Here we demonstrate by the use of extensive controls and stringent statistical analysis that dendritic cells differentially regulate hundreds of different genes based upon sequence similarity of endogenously- and exogenously-loaded antigens and in a T-cell independent fashion. When endogenously and exogenously-derived antigens are identical, dendritic cells upregulate many different components of the Th-1 response, favoring the priming of CD8+ effectors and promulgating cellular immunity. Keywords: Loading methodology comparison

2007-04-12 | GSE7247 | GEO

Antigens expressed by breast cancer cells undergoing EMT stimulate cytotoxic CD8+ T cell immunity

Project description:Antigens expressed by breast cancer cells undergoing EMT stimulate cytotoxic CD8+ T cell immunity

| PRJNA875919 | ENA

Transcriptomal comparison between group 2 innate lymphoid cells (ILC2s) in the murine small intestine (SI-ILC2s) and those in white adipose tissue (WAT-ILC2s)

Project description:Transcriptomal comparison between group 2 innate lymphoid cells (ILC2s) in the murine small intestine (SI-ILC2s) and those in white adipose tissue (WAT-ILC2s).

2019-07-02 | GSE130530 | GEO

Identification of antigen-presenting cell-T cell interactions driving immune responses to food

Project description:The intestinal immune system must concomitantly tolerate food and commensals and protect against pathogens. Antigen-presenting cells (APCs) orchestrate these immune responses by presenting luminal antigens to CD4+ T cells and inducing their differentiation into regulatory (pTreg) or inflammatory (Th) subsets. Here, we used LIPSTIC to identify APCs that presented dietary antigens under tolerizing and inflammatory conditions. We show that helminth infections disrupted tolerance proportionally to the reduction in ratio between tolerogenic, including migratory cDC1s and Rorγt+ APCs, and inflammatory APCs, represented primarily by cDC2 subsets. However, the inflammatory subset of cDC2s expanded by helminth infection did not present dietary antigens, thus avoiding diet-specific TH2 cell differentiation. Our data uncover cellular mechanisms by which tolerance to food is induced and can be disrupted by infection.

2024-12-19 | GSE281286 | GEO

Human CD127 negative ILC2s show immunological memory.

Project description:Group 2 Innate Lymphoid Cells (ILC2s) are key players in type 2 immunity and contribute to maintaining homeostasis and responding to inflammation. ILC2s are implicated in the development of type 2 inflammation-mediated chronic disorders like asthma. While memory ILC2s have been identified in mouse, it is unknown whether human ILC2s can acquire immunological memory. Here, we demonstrate the persistence of CD45RO, a marker previously linked to inflammatory ILC2s, in resting ILC2s that have undergone prior activation. A high proportion of these cells concurrently reduce the expression of the canonical ILC marker CD127 in a tissue specific manner. Through isolation and in vitro stimulation of CD127- CD45RO+ ILC2s, we observed an augmented ability to proliferate and produce cytokines. CD127- CD45RO+ ILC2s are found in both healthy and inflamed tissues and display a gene signature of cell activation. Our findings suggest that human ILC2s can acquire innate immune memory and warrants a revision of the current strategies to identify human ILC2s.

2024-05-20 | GSE267098 | GEO

Microarray transcription of murine lung and uterine group 2 innate lymphoid cells (ILC2s) cultured in vitro with or without 17beta-estradiol (estrogen, E2)

Project description:This experiment sought to determine whether estrogen could directly activate changes in gene transcription in lung and uterine ILC2s, whether such changes differed between lung and uterine ILC2s, and compared baseline gene expression between ILC2s from those organs. ILC2s, defined as lineage (CD3e, CD14, CD16/32 and B220) negative, CD25 positive and CD44 high lymphocytes, were sorted by flow cytometry from 8-12 week old BALB/c mice and cultured overnight in RPMI 1640 with 10% charcoal/dextran treated calf serum in the absence or presence of 100 ng/ml estrogen. RNA was extracted from the cells after culture.

2017-10-17 | E-MTAB-5789 | biostudies-arrayexpress

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