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Circulatory ILC2 convert and persist as part of the long-term tissue-resident pool after infection [Infection Timecourse with Vascular Labelling]

ABSTRACT: Circulating ILC2 can serve as a first line of defense against infection prior to the local expansion of lung-resident ILC2. The fate of these circulating ILC2 and their contribution to the long-term lung-resident ILC2 pool is not understood. Using reporter mice in combination with single cell RNA sequencing (scRNA-seq) and novel applications of Cellular Indexing of Transcriptomes and Epitopes sequencing (CITE-seq), we assessed vascular and parenchymal ILC2 populations during helminth infection and the fate of circulatory ILC2. These studies revealed that circulating ILC2 rapidly convert to a tissue-resident phenotype upon arrival in the lung. Once converted, former circulating ILC2 become largely indistinguishable from lung-resident ILC2 over time. Key gene expression retained by converted ILC2 at the peak of the tissue-resident ILC2 response was related to maintained IL-25-responsiveness and unique cytokine potential. These converted ILC2 accumulate, expand, and persist alongside conventional lung-resident populations even after repeated pulmonary infections. These findings reveal an important contribution of circulating ILC2 to the long-term health and maintenance of the lung-resident ILC2 population.

ORGANISM(S): Mus musculus

PROVIDER: GSE299902 | GEO | 2026/03/30

REPOSITORIES: GEO

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Circulatory ILC2 convert and persist as part of the long-term tissue-resident pool after infection [Congenic Transfer]

Project description:Circulating ILC2 can serve as a first line of defense against infection prior to the local expansion of lung-resident ILC2. The fate of these circulating ILC2 and their contribution to the long-term lung-resident ILC2 pool is not understood. Using reporter mice in combination with single cell RNA sequencing (scRNA-seq) and novel applications of Cellular Indexing of Transcriptomes and Epitopes sequencing (CITE-seq), we assessed vascular and parenchymal ILC2 populations during helminth infection and the fate of circulatory ILC2. These studies revealed that circulating ILC2 rapidly convert to a tissue-resident phenotype upon arrival in the lung. Once converted, former circulating ILC2 become largely indistinguishable from lung-resident ILC2 over time. Key gene expression retained by converted ILC2 at the peak of the tissue-resident ILC2 response was related to maintained IL-25-responsiveness and unique cytokine potential. These converted ILC2 accumulate, expand, and persist alongside conventional lung-resident populations even after repeated pulmonary infections. These findings reveal an important contribution of circulating ILC2 to the long-term health and maintenance of the lung-resident ILC2 population.

2026-03-30 | GSE299900 | GEO

Circulatory ILC2 convert and persist as part of the long-term tissue-resident pool after infection [Infection Timecourse with Vascular Labelling]

Project description:Circulatory ILC2 convert and persist as part of the long-term tissue-resident pool after infection [Infection Timecourse with Vascular Labelling]

| PRJNA1277291 | ENA

Circulatory ILC2 convert and persist as part of the long-term tissue-resident pool after infection [Congenic Transfer]

Project description:Circulatory ILC2 convert and persist as part of the long-term tissue-resident pool after infection [Congenic Transfer]

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ILC2s navigate tissue redistribution during infection using stage-specific S1P receptors [ATAC-seq]

Project description:Lymphocytes can circulate as well as take residence within tissues. The mechanisms by which circulating populations are recruited to infected tissue sites have been characterized, but the extent and molecular basis of tissue-resident cell recirculation is enigmatic. Here, we show that helminth infection- or IL-25-induced redistribution of intestinal tissue-localized group 2 innate lymphoid cells (ILC2s) requires access to the lymphatic vessel network even though secondary lymphoid structures, which are essential signal hubs for adaptive lymphocyte differentiation and dispatch, are dispensable for tissue ILC2 mobilization. IL-25 signals induce a dramatic change in epigenetic landscape of intestinal ILC2s, enabling the expression of sphingosine-1-phosphate (S1P) receptors. S1PR5 is critical for ILC2 exit from intestinal tissue to lymph, whereas S1PR1 plays a dominant role in ILC2 egress from mesenteric lymph nodes to blood circulation and then to lung, where redistributed ILC2s contribute to tissue repair. The requirement of two S1PRs is largely due to the dynamic expression of the tissue-retention marker CD69, which mediates S1PR1 internalization. This stage-specific requirement of different S1P receptors for ILC2 redistribution during infection illustrates that innate and adaptive lymphocytes share a circulatory network frame but employ specialized navigation cues for their distinct migratory requirements.

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ILC2s navigate tissue redistribution during infection using stage-specific S1P receptors [RNA-seq]

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Tissue-specific transcriptional imprinting and heterogeneity in human innate lymphoid cells revealed by full-length single-cell RNA-sequencing

Project description:The impact of the microenvironment on innate lymphoid cell (ILC)-mediated immunity in humans remains largely unknown. Here we used full-length Smart-seq2 single-cell RNA-sequencing to unravel tissue-specific transcriptional profiles and heterogeneity of CD127+ ILCs across four human tissues. Correlation analysis identified gene modules characterizing the migratory properties of tonsil and blood ILCs, and signatures of tissue-residency, activation and modified metabolism in gut and lung ILCs. Trajectory analysis revealed potential differentiation pathways from circulating and tissue-resident naïve ILCs to a spectrum of mature ILC subsets. In the lung we identified both CRTH2+ and CRTH2- ILC2 with lung-specific signatures, which could be recapitulated by alarmin-exposure of circulating ILC2. Finally, we describe unique TCR-V(D)J-rearrangement patterns of blood ILC1-like cells, revealing a subset of potentially immature ILCs with TCR-d rearrangement. In summary, we provide publicly available data as a resource for in-depth understanding of ILC-mediated immunity in humans, with implications for disease.

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Amino acid availability acts as a metabolic rheostat to determine the magnitude of ILC2 responses - SLC7A5 and SLC7A8 KO

Project description:Group 2 innate lymphoid cells (ILC2) are functionally poised, tissue-resident lymphocytes that respond rapidly to damage and infection at mucosal barrier sites. ILC2 reside within complex microenvironments where they are subject to cues from both the diet and invading pathogens – including helminths. Emerging evidence suggests ILC2 are acutely sensitive not only to canonical activating signals, but also perturbations in nutrient availability. In the context of helminth infection, we identify amino acid availability as a nutritional cue in regulating ILC2 responses. ILC2 were found to be uniquely pre-primed to import amino acids via the large neutral amino acid transporters Slc7a5 and Slc7a8. Cell-intrinsic deletion of these transporters individually impaired ILC2 expansion, while concurrent loss of both transporters markedly impaired the proliferative and cytokine producing capacity of ILC2. Moreover, amino acid determined the magnitude of ILC2 responses in part via tuning of mTOR. These findings implicate essential amino acids as a metabolic requisite for optimal ILC2 responses within mucosal barrier tissues.

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Amino acid availability acts as a metabolic rheostat to determine the magnitude of ILC2 responses - WT ILC2

2022-12-22 | PXD038792 | Pride

Expression data from circulating and lung tissue resident memory CD4 T cell responding towards infuenza A virus infection

Project description:How tissue resident memory CD4 T cell differ from circulating memory CD4 T cells and how such differences impact functional recall responses to pathogens is unknown. We used microarrays to detail the global programme of gene expression underlying differences between sort purified circulating memory CD4 T cells from the lung and spleen, which are labelled with flourescent antibody following intravenous administration, and lung tissue resident memory CD4 T cells, which are not labelled with flourescent antibody following intravenous administration, on day 28 post influenza infection.

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Dynamic equilibrium of lung Trm dictates waning immunity after IAV infection

Project description:Lung resident memory (Trm) CD8 T cells induced by influenza A virus (IAV), are pivotal for providing heterosubtypic immunity, but are not maintained long term, causing gradual loss of protection. This contrasts sharply with long-term maintenance of Trm induced by localized infections of the skin and other tissues. Here we show that the decline in lung Trm is determined by an imbalance between apoptosis and lung recruitment/conversion to Trm of circulating memory cells. At the cellular level, circulating effector memory (Tem) rather than central memory (Tcm) cells are the precursors for conversion to lung Trm. Time-dependent changes in expression of genes critical for Trm differentiation together with enrichment of Tcm diminish the capacity of circulating memory CD8 T cells to form Trm, explaining why IAV-induced Trm are not stably maintained over time. Importantly, systemic booster immunization, through increasing the number of circulating Tem cells, induces an increase in lung Trm pool, providing a new rational for future IAV vaccines.

2016-11-18 | GSE86973 | GEO

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