The Experts below are selected from a list of 8538 Experts worldwide ranked by ideXlab platform
Gabrielle T. Belz - One of the best experts on this subject based on the ideXlab platform.
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single Cell rna seq identifies a pd 1 hi ilc progenitor and defines its development pathway
Nature, 2016Co-Authors: Simon Clare, Jason C H Tsang, Cui Wang, Juexuan Wang, Xi Chen, Cordelia Brandt, Leanne Kane, Lia S Campos, Gabrielle T. BelzAbstract:Innate Lymphoid Cells (ILCs) functionally resemble T lymphocytes in cytotoxicity and cytokine production but lack antigen-specific receptors, and they are important regulators of immune responses and tissue homeostasis. ILCs are generated from common Lymphoid progenitors, which are subsequently committed to Innate Lymphoid lineages in the α-Lymphoid progenitor, early Innate Lymphoid progenitor, common helper Innate Lymphoid progenitor and Innate Lymphoid Cell progenitor compartments. ILCs consist of conventional natural killer Cells and helper-like Cells (ILC1, ILC2 and ILC3). Despite recent advances, the Cellular heterogeneity, developmental trajectory and signalling dependence of ILC progenitors are not fully understood. Here, using single-Cell RNA-sequencing (scRNA-seq) of mouse bone marrow progenitors, we reveal ILC precursor subsets, delineate distinct ILC development stages and pathways, and report that high expression of programmed death 1 (PD-1hi) marked a committed ILC progenitor that was essentially identical to an Innate Lymphoid Cell progenitor. Our data defined PD-1hiIL-25Rhi as an early checkpoint in ILC2 development, which was abolished by deficiency in the zinc-finger protein Bcl11b but restored by IL-25R overexpression. Similar to T lymphocytes, PD-1 was upregulated on activated ILCs. Administration of a PD-1 antibody depleted PD-1hi ILCs and reduced cytokine levels in an influenza infection model in mice, and blocked papain-induced acute lung inflammation. These results provide a perspective for exploring PD-1 and its ligand (PD-L1) in immunotherapy, and allow effective manipulation of the immune system for disease prevention and therapy.
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type 1 Innate Lymphoid Cell biology lessons learnt from natural killer Cells
Frontiers in Immunology, 2016Co-Authors: Yuhao Jiao, Cyril Seillet, Nicholas D. Huntington, Gabrielle T. BelzAbstract:Group 1 Innate Lymphoid Cells (ILCs) comprise the natural killer (NK) Cells and ILC1s that reside within peripheral tissues. Several different ILC1 subsets have recently been characterized; however, no unique markers have been identified that uniquely define these subsets. Whether ILC1s and NK Cells are in fact distinct lineages, or alternately exhibit transitional molecular programs that allow them to adapt to different tissue niches remains an open question. NK Cells are the prototypic member of the Group 1 ILCs and have been historically assigned the functions of what now appears to be a multi-subset family that are distributed throughout the body. This raises the question of whether each of these populations mediate distinct functions during infection and tumor immunosurveillance. Here, we review the diversity of the Group 1 ILC subsets in their transcriptional regulation, localization, mobility, and receptor expression, and highlight the challenges in unraveling the individual functions of these different populations of Cells.
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bcl11b is essential for group 2 Innate Lymphoid Cell development
Journal of Experimental Medicine, 2015Co-Authors: Jennifer A Walker, Hans Reimer Rodewald, Gabrielle T. Belz, Pentao Liu, Christopher J Oliphant, Alexandros Englezakis, Simon Clare, Padraic G Fallon, Andrew N J MckenzieAbstract:Group 2 Innate Lymphoid Cells (ILC2s) are often found associated with mucosal surfaces where they contribute to protective immunity, inappropriate allergic responses, and tissue repair. Although we know they develop from a common Lymphoid progenitor in the bone marrow (BM), the specific lineage path and transcriptional regulators that are involved are only starting to emerge. After ILC2 gene expression analysis we investigated the role of Bcl11b, a factor previously linked to T Cell commitment, in ILC2 development. Using combined Bcl11b-tom and Id2-gfp reporter mice, we show that Bcl11b is expressed in ILC2 precursors in the BM and maintained in mature ILC2s. In vivo deletion of Bcl11b, by conditional tamoxifen-induced depletion or by Bcl11b(-/-) fetal liver chimera reconstitution, demonstrates that ILC2s are wholly dependent on Bcl11b for their development. Notably, in the absence of Bcl11b there is a concomitant expansion of the RORγt(+) ILC3 population, suggesting that Bcl11b may negatively regulate this lineage. Using Nippostrongylus brasiliensis infection, we reveal that the absence of Bcl11b leads to impaired worm expulsion, caused by a deficit in ILC2s, whereas Citrobacter rodentium infection is cleared efficiently. These data clearly establish Bcl11b as a new factor in the differentiation of ILC2s.
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Nfil3 is required for the development of all Innate Lymphoid Cell subsets
The Journal of experimental medicine, 2014Co-Authors: Cyril Seillet, Lucille C. Rankin, Joanna R. Groom, Lisa A. Mielke, Julie Tellier, Michael Chopin, Nicholas D. Huntington, Gabrielle T. Belz, Sebastian CarottaAbstract:Innate Lymphoid Cell (ILC) populations protect against infection and are essential for Lymphoid tissue formation and tissue remodeling after damage. Nfil3 is implicated in the function of adaptive immune lineages and NK Cell development, but it is not yet known if Nfil3 regulates other Innate Lymphoid lineages. Here, we identify that Nfil3 is essential for the development of Peyer’s patches and ILC2 and ILC3 subsets. Loss of Nfil3 selectively reduced Peyer’s patch formation and was accompanied by impaired recruitment and distribution of lymphocytes within the patches. ILC subsets exhibited high Nfil3 expression and genetic deletion of Nfil3 severely compromised the development of all subsets. Subsequently, Nfil3−/− mice were highly susceptible to disease when challenged with inflammatory or infectious agents. Thus, we demonstrate that Nfil3 is a key regulator of the development of ILC subsets essential for immune protection in the lung and gut.
Cyril Seillet - One of the best experts on this subject based on the ideXlab platform.
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type 1 Innate Lymphoid Cell biology lessons learnt from natural killer Cells
Frontiers in Immunology, 2016Co-Authors: Yuhao Jiao, Cyril Seillet, Nicholas D. Huntington, Gabrielle T. BelzAbstract:Group 1 Innate Lymphoid Cells (ILCs) comprise the natural killer (NK) Cells and ILC1s that reside within peripheral tissues. Several different ILC1 subsets have recently been characterized; however, no unique markers have been identified that uniquely define these subsets. Whether ILC1s and NK Cells are in fact distinct lineages, or alternately exhibit transitional molecular programs that allow them to adapt to different tissue niches remains an open question. NK Cells are the prototypic member of the Group 1 ILCs and have been historically assigned the functions of what now appears to be a multi-subset family that are distributed throughout the body. This raises the question of whether each of these populations mediate distinct functions during infection and tumor immunosurveillance. Here, we review the diversity of the Group 1 ILC subsets in their transcriptional regulation, localization, mobility, and receptor expression, and highlight the challenges in unraveling the individual functions of these different populations of Cells.
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Deciphering the Innate Lymphoid Cell Transcriptional Program
Cell reports, 2016Co-Authors: Cyril Seillet, Lisa A. Mielke, Daniela Amann-zalcenstein, Jerry Gao, Francisca F. Almeida, Wei Shi, Matthew E. Ritchie, Shalin H. Naik, Nicholas D. HuntingtonAbstract:Innate Lymphoid Cells (ILCs) are enriched at mucosal surfaces, where they provide immune surveillance. All ILC subsets develop from a common progenitor that gives rise to pre-committed progenitors for each of the ILC lineages. Currently, the temporal control of gene expression that guides the emergence of these progenitors is poorly understood. We used global transcriptional mapping to analyze gene expression in different ILC progenitors. We identified PD-1 to be specifically expressed in PLZF+ ILCp and revealed that the timing and order of expression of the transcription factors NFIL3, ID2, and TCF-1 was critical. Importantly, induction of ILC lineage commitment required only transient expression of NFIL3 prior to ID2 and TCF-1 expression. These findings highlight the importance of the temporal program that permits commitment of progenitors to the ILC lineage, and they expand our understanding of the core transcriptional program by identifying potential regulators of ILC development.
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Nfil3 is required for the development of all Innate Lymphoid Cell subsets
The Journal of experimental medicine, 2014Co-Authors: Cyril Seillet, Lucille C. Rankin, Joanna R. Groom, Lisa A. Mielke, Julie Tellier, Michael Chopin, Nicholas D. Huntington, Gabrielle T. Belz, Sebastian CarottaAbstract:Innate Lymphoid Cell (ILC) populations protect against infection and are essential for Lymphoid tissue formation and tissue remodeling after damage. Nfil3 is implicated in the function of adaptive immune lineages and NK Cell development, but it is not yet known if Nfil3 regulates other Innate Lymphoid lineages. Here, we identify that Nfil3 is essential for the development of Peyer’s patches and ILC2 and ILC3 subsets. Loss of Nfil3 selectively reduced Peyer’s patch formation and was accompanied by impaired recruitment and distribution of lymphocytes within the patches. ILC subsets exhibited high Nfil3 expression and genetic deletion of Nfil3 severely compromised the development of all subsets. Subsequently, Nfil3−/− mice were highly susceptible to disease when challenged with inflammatory or infectious agents. Thus, we demonstrate that Nfil3 is a key regulator of the development of ILC subsets essential for immune protection in the lung and gut.
Laurel A Monticelli - One of the best experts on this subject based on the ideXlab platform.
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lung Innate Lymphoid Cell composition is altered in primary graft dysfunction
American Journal of Respiratory and Critical Care Medicine, 2020Co-Authors: Laurel A Monticelli, Elia Tait D Wojno, Steven A Saenz, David Artis, Joshua M Diamond, Mary K Porteous, Edward Cantu, Jason D ChristieAbstract:Rationale: Primary graft dysfunction (PGD) is the leading cause of early morbidity and mortality after lung transplantation, but the immunologic mechanisms are poorly understood. Innate Lymphoid Cells (ILC) are a heterogeneous family of immune Cells regulating pathologic inflammation and beneficial tissue repair. However, whether changes in donor-derived lung ILC populations are associated with PGD development has never been examined.Objectives: To determine whether PGD in chronic obstructive pulmonary disease or interstitial lung disease transplant recipients is associated with alterations in ILC subset composition within the allograft.Methods: We performed a single-center cohort study of lung transplantation patients with surgical biopsies of donor tissue taken before, and immediately after, allograft reperfusion. Donor immune Cells from 18 patients were characterized phenotypically by flow cytometry for single-Cell resolution of distinct ILC subsets. Changes in the percentage of ILC subsets with reperfusion or PGD (grade 3 within 72 h) were assessed.Measurements and Main Results: Allograft reperfusion resulted in significantly decreased frequencies of natural killer Cells and a trend toward reduced ILC populations, regardless of diagnosis (interstitial lung disease or chronic obstructive pulmonary disease). Seven patients developed PGD (38.9%), and PGD development was associated with selective reduction of the ILC2 subset after reperfusion. Conversely, patients without PGD exhibited significantly higher ILC1 frequencies before reperfusion, accompanied by elevated ILC2 frequencies after allograft reperfusion.Conclusions: The composition of donor ILC subsets is altered after allograft reperfusion and is associated with PGD development, suggesting that ILCs may be involved in regulating lung injury in lung transplant recipients.
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β2 adrenergic receptor mediated negative regulation of group 2 Innate Lymphoid Cell responses
Science, 2018Co-Authors: Saya Moriyama, Jonathan R. Brestoff, Annelaure Flamar, Naomi Yudanin, Lucille C. Rankin, Christoph S N Klose, Jesper B Moeller, Laurel A MonticelliAbstract:The type 2 inflammatory response is induced by various environmental and infectious stimuli. Although recent studies identified group 2 Innate Lymphoid Cells (ILC2s) as potent sources of type 2 cytokines, the molecular pathways controlling ILC2 responses are incompletely defined. Here we demonstrate that murine ILC2s express the β 2 -adrenergic receptor (β 2 AR) and colocalize with adrenergic neurons in the intestine. β 2 AR deficiency resulted in exaggerated ILC2 responses and type 2 inflammation in intestinal and lung tissues. Conversely, β 2 AR agonist treatment was associated with impaired ILC2 responses and reduced inflammation in vivo. Mechanistically, we demonstrate that the β 2 AR pathway is a Cell-intrinsic negative regulator of ILC2 responses through inhibition of Cell proliferation and effector function. Collectively, these data provide the first evidence of a neuronal-derived regulatory circuit that limits ILC2-dependent type 2 inflammation.
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arginase 1 is an Innate Lymphoid Cell intrinsic metabolic checkpoint controlling type 2 inflammation
Nature Immunology, 2016Co-Authors: Laurel A Monticelli, Elia Tait D Wojno, Steven A Saenz, Michael D Buck, Annelaure Flamar, Naomi Yudanin, Lisa C Osborne, Matthew R Hepworth, Sara V Tran, Hans Reimer RodewaldAbstract:Group 2 Innate Lymphoid Cells (ILC2s) regulate tissue inflammation and repair after activation by Cell-extrinsic factors such as host-derived cytokines. However, the Cell-intrinsic metabolic pathways that control ILC2 function are undefined. Here we demonstrate that expression of the enzyme arginase-1 (Arg1) during acute or chronic lung inflammation is a conserved trait of mouse and human ILC2s. Deletion of mouse ILC-intrinsic Arg1 abrogated type 2 lung inflammation by restraining ILC2 proliferation and dampening cytokine production. Mechanistically, inhibition of Arg1 enzymatic activity disrupted multiple components of ILC2 metabolic programming by altering arginine catabolism, impairing polyamine biosynthesis and reducing aerobic glycolysis. These data identify Arg1 as a key regulator of ILC2 bioenergetics that controls proliferative capacity and proinflammatory functions promoting type 2 inflammation.
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basophils promote Innate Lymphoid Cell responses in inflamed skin
Journal of Immunology, 2014Co-Authors: Kelvin Wang, Mark C Siracusa, Laurel A Monticelli, Elia Tait D Wojno, Thomas C Fung, Steven A Saenz, Mario Noti, Jonathan R. Brestoff, Masato Kubo, David ArtisAbstract:Type 2 inflammation underlies allergic diseases such as atopic dermatitis, which is characterized by the accumulation of basophils and group 2 Innate Lymphoid Cells (ILC2s) in inflamed skin lesions. Although murine studies have demonstrated that cutaneous basophil and ILC2 responses are dependent on thymic stromal lymphopoietin, whether these Cell populations interact to regulate the development of cutaneous type 2 inflammation is poorly defined. In this study, we identify that basophils and ILC2s significantly accumulate in inflamed human and murine skin and form clusters not observed in control skin. We demonstrate that murine basophil responses precede ILC2 responses and that basophils are the dominant IL-4–enhanced GFP-expressing Cell type in inflamed skin. Furthermore, basophils and IL-4 were necessary for the optimal accumulation of ILC2s and induction of atopic dermatitis–like disease. We show that ILC2s express IL-4Rα and proliferate in an IL-4–dependent manner. Additionally, basophil-derived IL-4 was required for cutaneous ILC2 responses in vivo and directly regulated ILC2 proliferation ex vivo. Collectively, these data reveal a previously unrecognized role for basophil-derived IL-4 in promoting ILC2 responses during cutaneous inflammation.
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t Cell factor 1 is required for group 2 Innate Lymphoid Cell generation
Immunity, 2013Co-Authors: Qi Yang, Laurel A Monticelli, Steven A Saenz, Gregory F Sonnenberg, Anthony W S Chi, Jiangbo Tang, Maria Elena De Obaldia, Will Bailis, Jerrod L Bryson, Kristin ToscanoAbstract:Summary Group 2 Innate Lymphoid Cells (ILC2) are Innate lymphocytes that confer protective type 2 immunity during helminth infection and are also involved in allergic airway inflammation. Here we report that ILC2 development required T Cell factor 1 (TCF-1, the product of the Tcf7 gene), a transcription factor also implicated in T Cell lineage specification. Tcf7 −/− mice lack ILC2, and were unable to mount ILC2-mediated Innate type 2 immune responses. Forced expression of TCF-1 in bone marrow progenitors partially bypassed the requirement for Notch signaling in the generation of ILC2 in vivo. TCF-1 acted through both GATA-3-dependent and GATA-3-independent pathways to promote the generation of ILC2. These results are reminiscent of the critical roles of TCF-1 in early T Cell development. Hence, transcription factors that underlie early steps of T Cell development are also implicated in the development of Innate Lymphoid Cells.
Yajen Chang - One of the best experts on this subject based on the ideXlab platform.
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regulation of type 2 Innate Lymphoid Cell dependent airway hyperreactivity by butyrate
The Journal of Allergy and Clinical Immunology, 2018Co-Authors: Christina Liping Thio, Poyu Chi, Alan Chuanying Lai, Yajen ChangAbstract:Background Allergic asthma is characterized by airway hyperreactivity (AHR) and inflammation driven by aberrant T H 2 responses. Type 2 Innate Lymphoid Cells (ILC2s) are a critical source of the T H 2 cytokines IL-5 and IL-13, which promote acute asthma exacerbation. Short-chain fatty acids (SCFAs) have been shown to attenuate T Cell–mediated allergic airway inflammation. However, their role in regulation of ILC2-driven AHR and lung inflammation remains unknown. Objective We investigated the immunomodulatory role of SCFAs in regulation of ILC2-induced AHR and airway inflammation and delineated the mechanism involved. Methods We assessed the role of SCFAs in regulating survival, proliferation, and cytokine production in lung sorted ILC2s. The SCFA butyrate was administered through drinking water or intranasally in BALB/c mice to evaluate its role in the ILC2-driven inflammatory response in IL-33 and Alternaria alternata models of allergic inflammation. We further confirmed our findings in human ILC2s. Results We show that butyrate, but not acetate or propionate, inhibited IL-13 and IL-5 production by murine ILC2s. Systemic and local administration of butyrate significantly ameliorated ILC2-driven AHR and airway inflammation. We further demonstrate that butyrate inhibited ILC2 proliferation and GATA3 expression but did not induce Cell apoptosis, likely through histone deacetylase (HDAC) inhibition, because trichostatin A, a pan-HDAC inhibitor, exerted similar effects on ILC2s. Importantly, cotreatment with trichostatin A and butyrate did not result in an additive effect. Finally, we show that butyrate reduces cytokine production in human ILC2s. Conclusion Our findings identify butyrate as a critical regulator of ILC2 proliferation and function through its HDAC inhibitory activity and can serve as a potential therapeutic target for asthma.
David Artis - One of the best experts on this subject based on the ideXlab platform.
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lung Innate Lymphoid Cell composition is altered in primary graft dysfunction
American Journal of Respiratory and Critical Care Medicine, 2020Co-Authors: Laurel A Monticelli, Elia Tait D Wojno, Steven A Saenz, David Artis, Joshua M Diamond, Mary K Porteous, Edward Cantu, Jason D ChristieAbstract:Rationale: Primary graft dysfunction (PGD) is the leading cause of early morbidity and mortality after lung transplantation, but the immunologic mechanisms are poorly understood. Innate Lymphoid Cells (ILC) are a heterogeneous family of immune Cells regulating pathologic inflammation and beneficial tissue repair. However, whether changes in donor-derived lung ILC populations are associated with PGD development has never been examined.Objectives: To determine whether PGD in chronic obstructive pulmonary disease or interstitial lung disease transplant recipients is associated with alterations in ILC subset composition within the allograft.Methods: We performed a single-center cohort study of lung transplantation patients with surgical biopsies of donor tissue taken before, and immediately after, allograft reperfusion. Donor immune Cells from 18 patients were characterized phenotypically by flow cytometry for single-Cell resolution of distinct ILC subsets. Changes in the percentage of ILC subsets with reperfusion or PGD (grade 3 within 72 h) were assessed.Measurements and Main Results: Allograft reperfusion resulted in significantly decreased frequencies of natural killer Cells and a trend toward reduced ILC populations, regardless of diagnosis (interstitial lung disease or chronic obstructive pulmonary disease). Seven patients developed PGD (38.9%), and PGD development was associated with selective reduction of the ILC2 subset after reperfusion. Conversely, patients without PGD exhibited significantly higher ILC1 frequencies before reperfusion, accompanied by elevated ILC2 frequencies after allograft reperfusion.Conclusions: The composition of donor ILC subsets is altered after allograft reperfusion and is associated with PGD development, suggesting that ILCs may be involved in regulating lung injury in lung transplant recipients.
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emerging concepts and future challenges in Innate Lymphoid Cell biology
Journal of Experimental Medicine, 2016Co-Authors: Elia Tait D Wojno, David ArtisAbstract:Innate Lymphoid Cells (ILCs) are Innate immune Cells that are ubiquitously distributed in Lymphoid and nonLymphoid tissues and enriched at mucosal and barrier surfaces. Three major ILC subsets are recognized in mice and humans. Each of these subsets interacts with Innate and adaptive immune Cells and integrates cues from the epithelium, the microbiota, and pathogens to regulate inflammation, immunity, tissue repair, and metabolic homeostasis. Although intense study has elucidated many aspects of ILC development, phenotype, and function, numerous challenges remain in the field of ILC biology. In particular, recent work has highlighted key new questions regarding how these Cells communicate with their environment and other Cell types during health and disease. This review summarizes new findings in this rapidly developing field that showcase the critical role ILCs play in directing immune responses through their ability to interact with a variety of hematopoietic and nonhematopoietic Cells. In addition, we define remaining challenges and emerging questions facing the field. Finally, this review discusses the potential application of basic studies of ILC biology to the development of new treatments for human patients with inflammatory and infectious diseases in which ILCs play a role.
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basophils promote Innate Lymphoid Cell responses in inflamed skin
Journal of Immunology, 2014Co-Authors: Kelvin Wang, Mark C Siracusa, Laurel A Monticelli, Elia Tait D Wojno, Thomas C Fung, Steven A Saenz, Mario Noti, Jonathan R. Brestoff, Masato Kubo, David ArtisAbstract:Type 2 inflammation underlies allergic diseases such as atopic dermatitis, which is characterized by the accumulation of basophils and group 2 Innate Lymphoid Cells (ILC2s) in inflamed skin lesions. Although murine studies have demonstrated that cutaneous basophil and ILC2 responses are dependent on thymic stromal lymphopoietin, whether these Cell populations interact to regulate the development of cutaneous type 2 inflammation is poorly defined. In this study, we identify that basophils and ILC2s significantly accumulate in inflamed human and murine skin and form clusters not observed in control skin. We demonstrate that murine basophil responses precede ILC2 responses and that basophils are the dominant IL-4–enhanced GFP-expressing Cell type in inflamed skin. Furthermore, basophils and IL-4 were necessary for the optimal accumulation of ILC2s and induction of atopic dermatitis–like disease. We show that ILC2s express IL-4Rα and proliferate in an IL-4–dependent manner. Additionally, basophil-derived IL-4 was required for cutaneous ILC2 responses in vivo and directly regulated ILC2 proliferation ex vivo. Collectively, these data reveal a previously unrecognized role for basophil-derived IL-4 in promoting ILC2 responses during cutaneous inflammation.
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tslp elicits il 33 independent Innate Lymphoid Cell responses to promote skin inflammation
Science Translational Medicine, 2013Co-Authors: Brian S Kim, Mark C Siracusa, Laurel A Monticelli, Steven A Saenz, Mario Noti, Matthew R Hepworth, Gregory F Sonnenberg, Abby S Van Voorhees, Michael R Comeau, David ArtisAbstract:Innate Lymphoid Cells (ILCs) are a recently identified family of heterogeneous immune Cells that can be divided into three groups based on their differential developmental requirements and expression of effector cytokines. Among these, group 2 ILCs produce the type 2 cytokines interleukin-5 (IL-5) and IL-13 and promote type 2 inflammation in the lung and intestine. However, whether group 2 ILCs reside in the skin and contribute to skin inflammation has not been characterized. We identify a population of skin-resident group 2 ILCs present in healthy human skin that are enriched in lesional human skin from atopic dermatitis (AD) patients. Group 2 ILCs were also found in normal murine skin and were critical for the development of inflammation in a murine model of AD-like disease. Remarkably, in contrast to group 2 ILC responses in the intestine and lung, which are critically regulated by IL-33 and IL-25, group 2 ILC responses in the skin and skin-draining lymph nodes were independent of these canonical cytokines but were critically dependent on thymic stromal lymphopoietin (TSLP). Collectively, these results demonstrate an essential role for IL-33- and IL-25-independent group 2 ILCs in promoting skin inflammation.
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Innate Lymphoid Cell interactions with microbiota implications for intestinal health and disease
Immunity, 2012Co-Authors: Gregory F Sonnenberg, David ArtisAbstract:The mammalian intestine harbors trillions of beneficial commensal bacteria that are essential for the development of the immune system and for maintenance of physiologic processes in multiple organs. However, numerous chronic infectious, inflammatory, and metabolic diseases in humans have been associated with alterations in the composition or localization of commensal bacteria that result in dysregulated host-commensal bacteria relationships. The mammalian immune system plays an essential role in regulating the acquisition, composition, and localization of commensal bacteria in the intestine. Emerging research has implicated Innate Lymphoid Cells (ILCs) as a critical immune Cell population that orchestrates some of these host-commensal bacteria relationships that can impact immunity, inflammation, and tissue homeostasis in the intestine. This review will discuss reciprocal interactions between intestinal commensal bacteria and ILCs in the context of health and disease.