Academic literature on the topic 'Human ILC2 function'
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Journal articles on the topic "Human ILC2 function"
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Lim, Ai Ing, Silvia Menegatti, Jacinta Bustamante, Lionel Le Bourhis, Matthieu Allez, Lars Rogge, Jean-Laurent Casanova, Hans Yssel, and James P. Di Santo. "IL-12 drives functional plasticity of human group 2 innate lymphoid cells." Journal of Experimental Medicine 213, no. 4 (March 14, 2016): 569–83. http://dx.doi.org/10.1084/jem.20151750.
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Group 2 innate lymphoid cells (ILC2) include IL-5– and IL-13–producing CRTh2+CD127+ cells that are implicated in early protective immunity at mucosal surfaces. Whereas functional plasticity has been demonstrated for both human and mouse ILC3 subsets that can reversibly give rise to IFN-γ–producing ILC1, plasticity of human or mouse ILC2 has not been shown. Here, we analyze the phenotypic and functional heterogeneity of human peripheral blood ILC2. Although subsets of human CRTh2+ ILC2 differentially express CD117 (c-kit receptor), some ILC2 surface phenotypes are unstable and can be modulated in vitro. Surprisingly, human IL-13+ ILC2 can acquire the capacity to produce IFN-γ, thereby generating plastic ILC2. ILC2 cultures demonstrated that IFN-γ+ ILC2 clones could be derived and were stably associated with increased T-BET expression. The inductive mechanism for ILC2 plasticity was mapped to the IL-12–IL-12R signaling pathway and was confirmed through analysis of patients with Mendelian susceptibility to mycobacterial disease due to IL-12Rβ1 deficiencies that failed to generate plastic ILC2. We also detected IL-13+IFN-γ+ ILC2 ex vivo in intestinal samples from Crohn’s disease patients. These results demonstrate cytokine production plasticity for human ILC2 and further suggest that environmental cues can dictate ILC phenotype and function for these tissue-resident innate effector cells.
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Surace, Laura, Jean-Marc Doisne, Carys A. Croft, Anna Thaller, Pedro Escoll, Solenne Marie, Natalia Petrosemoli, et al. "Dichotomous metabolic networks govern human ILC2 proliferation and function." Nature Immunology 22, no. 11 (October 22, 2021): 1367–74. http://dx.doi.org/10.1038/s41590-021-01043-8.
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AbstractGroup 2 innate lymphoid cells (ILC2s) represent innate homologs of type 2 helper T cells (TH2) that participate in immune defense and tissue homeostasis through production of type 2 cytokines. While T lymphocytes metabolically adapt to microenvironmental changes, knowledge of human ILC2 metabolism is limited, and its key regulators are unknown. Here, we show that circulating ‘naive’ ILC2s have an unexpected metabolic profile with a higher level of oxidative phosphorylation (OXPHOS) than natural killer (NK) cells. Accordingly, ILC2s are severely reduced in individuals with mitochondrial disease (MD) and impaired OXPHOS. Metabolomic and nutrient receptor analysis revealed ILC2 uptake of amino acids to sustain OXPHOS at steady state. Following activation with interleukin-33 (IL-33), ILC2s became highly proliferative, relying on glycolysis and mammalian target of rapamycin (mTOR) to produce IL-13 while continuing to fuel OXPHOS with amino acids to maintain cellular fitness and proliferation. Our results suggest that proliferation and function are metabolically uncoupled in human ILC2s, offering new strategies to target ILC2s in disease settings.
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Hurrell, Benjamin P., Doumet Goerges Helou, Pedram Shafiei-Jahani, Emily Diane Howard, Jacob Dean Painter, Christine Quach, and Omid Akbari. "CB2 engagement enhances group 2 innate lymphoid cell expansion and induction of airway hyperreactivity." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 109.14. http://dx.doi.org/10.4049/jimmunol.208.supp.109.14.
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Abstract Cannabinoids modulate the activation of immune cells and physiological processes in the lungs. Group 2 innate lymphoid cells (ILC2)s are central players in type-2 asthma, but how cannabinoids modulate ILC2 activation remains to be elucidated. Using a combination of cannabinoid receptor (CB)2 KO mice, a CB2 antagonist and agonist, we here provide evidence that CB2 signaling in ILC2s is important for the development of ILC2-driven airway inflammation in both mice and human. We show that both naïve and activated murine pulmonary ILC2s express CB2. CB2 signaling did not affect ILC2 homeostasis at steady state, but strikingly stimulated ILC2 proliferation and function upon activation using various models of airway inflammation including IL-33, IL-25 and Alternaria alternata. As a result, ILC2s lacking CB2 induced lower lung inflammation, as we made similar observations using a CB2 antagonist. Conversely, CB2 agonism remarkably exacerbated ILC2-driven airway hyperreactivity and lung inflammation. Mechanistically, transcriptomic and protein analysis revealed that CB2 signaling induced CREB phosphorylation in ILC2s. Human ILC2s expressed CB2, as CB2 antagonism and agonism showed opposing effects on ILC2 effector function and development of airway hyperreactivity in humanized mice. Collectively, our results define CB2 signaling in ILC2s as an important modulator of airway inflammation. Furthermore, our findings highlight the stimulatory capacity of cannabinoids on ILC2s and offer new therapeutic avenues, including the use of substances or pathways able to modulate CB2 and capable of alleviating lung function in patients with lung inflammation.
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Maazi, Hadi, Homayon Banie, German Aleman, Gavin Lewis, Nisheel Patel, Bowen Wang, Pejman Soroosh, and Omid Akbari. "Toll-like receptor-7-mediated activation of pDCs suppresses the ILC2-mediated airway hyperreactivity and inflammation through type-I interferon." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 53.7. http://dx.doi.org/10.4049/jimmunol.198.supp.53.7.
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Abstract Type 2 innate lymphoid cells (ILC2s) are newly identified subset of immune cells that play important roles in the pathogenesis of allergic diseases and asthma. The regulatory mechanisms that control the function and homeostasis of ILC2s are incompletely understood. Plasmacytoid dendritic cells (pDCs) have been previously associated with maintaining respiratory tolerance. To identify a novel mechanism for alleviating ILC2-mediated asthma we investigated impact of pDCs on ILC2s and ILC2-mediated airway hyperreactivity and inflammation. We investigated human and murine ILC2s and used clinically relevant allergen, Alternaria Alternata, as well as IL-33, to activate ILC2s in several mouse models including BDCA-2-DTR transgenic and Interferon alpha receptor-1 deficient mice. We found that activation of pDCS by a Toll-like receptor-7 agonist, R848, suppresses ILC2-mediated AHR and airway inflammation and that depletion of pDCs reverses this suppression. Moreover, we found that pDCs suppress cytokine production and proliferation of ILC2s through the production of interferon alpha. Transcriptome analysis of both human and murine ILC2s confirms the activation of regulatory pathways in ILC2s by interferon alpha. In addition, activation of pDCs alleviates airway hyperreactivity and inflammation by suppressing ILC2’s function and survival. Our findings reveal a novel regulatory pathway in ILC2-mediated pulmonary inflammation with important clinical implications.
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Hurrell, Benjamin P., Lauriane Galle-Treger, Pedram Shafiei Jahani, Emily Howard, Doumet Georges Helou, Homayon Banie, Pejman Soroosh, and Omid Akbari. "TNFR2 signaling enhances ILC2 survival, function and induction of airway hyperreactivity." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 60.5. http://dx.doi.org/10.4049/jimmunol.204.supp.60.5.
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Abstract Group 2 innate lymphoid cells (ILC2s) can initiate pathologic inflammation in allergic asthma by secreting copious amounts of type-2 cytokines, promoting lung eosinophilia and airway hyperreactivity (AHR), a cardinal feature of asthma. We discovered that the TNF/TNFR2 axis is a central immune checkpoint in murine and human ILC2s. TNFa is a pleiotropic proinflammatory cytokine which is elevated in the airways of patients with severe asthma, signaling through two main receptors with opposing functions: TNFR1 and TNFR2. We found that murine ILC2s selectively express and induce TNFR2 upon IL-33 activation, whereas they fail to express – or induce – TNFR1. Strikingly, blocking the TNF/TNFR2 axis inhibits ILC2 survival, cytokine production, ILC2-dependent AHR and airway eosinophilia. The mechanism of action of TNFR2 in ILC2s is through utilizing non-canonical NFkB pathway as a NFkB inducing kinase (NIK) inhibitor blocks the costimulatory effects of TNFa both in vitro and in vivo. Similarly, human ILC2s selectively express TNFR2 and using the model of humanized mice that our laboratory recently developed, we show that TNFR2 engagement in human ILC2s enhances survival and activation, ultimately promoting AHR through a NIK-dependent pathway. These findings highlight the role of the TNF/TNFR2 axis in pulmonary ILC2s, suggesting that targeting TNFR2 or relevant signaling represents a novel strategy for treating patients with ILC2-dependent asthma.
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Jowett, G. M., E. Read, M. D. Norman, P. A. Arevalo, M. Vilà González, L. Roberts, L. Vallier, et al. "OP13 Mucosal organoids capture Innate Lymphoid Cells (ILC) tissue-specific development and reveal that Inflammatory Bowel Disease-associated ILC modulate intestinal remodelling." Journal of Crohn's and Colitis 15, Supplement_1 (May 1, 2021): S013—S014. http://dx.doi.org/10.1093/ecco-jcc/jjab075.012.
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Abstract Background Innate Lymphoid Cells (ILC) develop from Common Lymphoid Precursors in the bone marrow, and ILC precursors (ILCP) migrate to mucosa where they mature, promote homeostasis, and provide a potent, antigen-non-specific sources of cytokines. Deciphering what local stimuli drive the final stages of ILCP maturation in these tissues remains a pressing question, as ILC frequencies can become dysregulated during chronic infection and inflammatory diseases. For example, Type-1 innate lymphoid cells (ILC1) are enriched in the mucosa of patients with active inflammatory bowel disease (IBD) and the impact of this accumulation remains elusive. Methods Here, we develop and use co-cultures of both murine and human iPSC-derived gut and lung organoids with ILCP and with mature ILC isolated from IBD patients’ intestinal biopsies. Results Harnessing these versatile models, we demonstrate that epithelial cells provide a complex niche capable of supporting the final maturation of all helper-like ILC1, ILC2, and ILC3. Notably, organoid identity was sufficient to robustly recapitulate tissue-specific ILC imprints and frequencies, even in the absence of microbial stimuli, other cell types, or cytokine supplementation. In addition, we show that that ILC1 drive expansion of the epithelial stem cell crypt through p38γ phosphorylation, driving a potentially pathological proliferative feedback loop between β-catenin and Cd44v6. We harnessed this model to elucidate that this phenotype was unexpectedly regulated by ILC1-derived TGFβ1. We further show that human gut ILC1 also secrete TGFβ1, and drive CD44v6 expression in both HIO epithelium and mesenchyme. As TGFβ1 is a master regulator of fibrosis, the leading indicator for surgery in IBD, we next characterised the ability of ILC1 to regulate matrix remodelling using a functionalized, synthetic hydrogel system. We show that ILC1 drive both matrix stiffening and degradation, which we posit occurs through a balance of MMP9 degradation and TGFβ1-induced fibronectin deposition. Conclusion Taken together, our work provides unprecedented insight into in situ ILC maturation, which we show to be driven by epithelial signals, and into ILC function. We also report that intestinal ILC1 modulate epithelial and matrix remodelling, which may drive either wound healing in homeostasis, but may tip toward pathology when enriched in IBD. Moreover, our work introduces a modular organoid platform, which provides exquisite control over both environmental stimuli and host genetics, making it a powerful tool for dissecting the interactions between complex mucosal tissues and rare cell subtypes in development and disease.
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Galle, Lauriane, Ishwarya Sankaranarayanan, Benjamin P. Hurrell, Emily Howard, Richard Lo, Hadi Maazi, Gavin Lewis, et al. "Costimulation of type-2 innate lymphoid cells by GITR promotes effector function and ameliorates type 2 diabetes." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 122.10. http://dx.doi.org/10.4049/jimmunol.202.supp.122.10.
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Abstract Metabolic syndrome is characterized by disturbances in glucose homeostasis and the development of low-grade systemic inflammation, which increase the risk to develop type-2 diabetes mellitus (T2DM). Type-2 innate lymphoid cells (ILC2s) are a recently discovered immune population secreting Th2-cytokines. While previous studies show how ILC2s can play a critical role in the regulation of metabolic homeostasis in the adipose tissue, a therapeutic target capable of modulating ILC2 activation has yet to be identified. We found that GITR, a member of the TNF superfamily, is expressed on murine adipose tissue ILC2s and its engagement on activated ILC2s induces Th2-cytokine secretion. Moreover, we showed that GITR engagement on ILC2s improves glucose homeostasis resulting in both protection against insulin-resistance onset and amelioration of established insulin-resistance. Our adoptive transfer studies demonstrated that this protective effect is dependent on ILC2-derived Th2-cytokines, particularly IL-13. Transcriptome analysis demonstrated that GITR agonist activates the NF-κB signaling pathway and inhibits ILC2 apoptosis, altogether favoring ILC2 survival and activation. Finally, we also found that GITR is expressed on human adipose tissue resident ILC2s and GITR engagement robustly induces Th2-cytokine. Together, these results highlight the critical role of GITR as a novel therapeutic molecule against T2DM and its fundamental role as an immune checkpoint for activated ILC2s.
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Kovats, Susan, Sean Turner, Anna Karlik, Reegan Miller, Erola Ainsua-Enrich, and Sapana Kadel. "Androgen receptor activity underlies sex differences in lung-resident ILC2 functional responses during influenza virus infection." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 85.4. http://dx.doi.org/10.4049/jimmunol.204.supp.85.4.
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Abstract Lung-resident group 2 innate lymphoid cells (ILC2s) produce type 2 cytokines and facilitate tissue repair in response to alarmins such as IL-33 released during respiratory virus infection, but they also may be functionally suppressed by type 1 cytokines. Lung ILC2s express notably high levels of intracellular androgen receptor (AR) compared to ILC1s, T and B cells. To test the hypothesis that females and males show differential ILC2 responses in influenza virus (IAV) infection, we analyzed the numbers and functional responses of lung ILCs in IAV infected mice. On days 3–10 post-infection, lungs of female mice contained greater numbers of ILC2s and ILC1s compared to males. However, the female ILC2s were preferentially suppressed at the peak of infection, with a dampened type 2 program manifest as attenuated proliferation, decreased IL-5 and amphiregulin production, reduced expression of GATA-3 and IL-33R and increased surface IFNGR. IFNG levels in the lung were comparable between sexes at day 7 post-infection, suggesting intrinsic differences in ILC2 responses to interferons. Indeed, naïve female ILC2s showed higher expression of IFNGR and higher phospho-STAT1 levels following stimulation by IFNG. ILC2s in naive male mice with lymphocyte-restricted AR deficiency displayed levels of IFNGR comparable to female mice, suggesting AR activity underlies sex differences in intrinsic IFNGR expression. Early life orchiectomy revealed that endogenous androgens decreased ILC2 numbers but protected males from suppression of ILC2s in IAV infection. Taken together, our data show that AR activity preserves canonical ILC2 function in males during IAV infection and may help to explain the documented human gender differences in immunity to IAV.
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Valdez, Yanet, Stephen K. Kyei, Grace F. T. Poon, Fumio Takei, Carrie Peters, Steve M. Woodside, Allen C. Eaves, and Terry E. Thomas. "Fast and efficient enrichment of functional ILC2 from human whole blood." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 209.16. http://dx.doi.org/10.4049/jimmunol.196.supp.209.16.
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Abstract Group 2 innate lymphoid cells (ILC2) are a functionally distinct subset of recently identified immune cells with important roles in type-2 immunopathologies such as allergies, asthma, helminth infections and other metabolic diseases. Studying these rare cells is challenging due to a lack of specific surface markers, and currently multicolor flow cytometric analysis and cell sorting are the only methods to characterize and isolate ILC2s. However, the scarcity of these cells makes flow cytometry time-consuming, expensive and often results in low purities and recoveries. Thus, better approaches for effective identification and isolation are essential to further understanding of ILC2 biology and function. We have developed a rapid and efficient method for enrichment of human ILC2 from whole blood. In brief, non-ILC2 cells in whole blood were crosslinked to red blood cells already present in the sample using RosetteSep™. The sample was then layered over Lymphoprep in a SepMate™ tube, spun at 1200 x g for 10 minutes (min), and the untouched, desired cells simply poured off. Cells were washed once and were then ready for subsequent analysis. Starting with only 0.01 – 0.07% in whole blood, ILC2 were enriched 350 ± 220 fold to 8.2 ± 6.8% in 35 min (means ± SD, n=17). Subsequent cell sorting from these pre-enriched samples was faster and yielded higher purity ILC2 than sorting from non-enriched controls (n=3, p<0.05 paired t test). Sorted ILC2, both pre-enriched and non-enriched controls, were cultured and stimulated, and secreted similar high levels of IL-13 as assessed by ELISA, indicating that these cells are functional. In summary, ILC2 pre-enrichment improves sorting efficiency, increases ILC2 purity, and maintains ILC2 functionality.
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Maazi, Hadi, Nisheel Patel, Ishwarya Sankaranarayanan, Diamanda Riagas, Pejman Soroosh, Gordon Freeman, Arlene Sharpe, and Omid Akbari. "ICOS: ICOS-ligand interaction is essential for ILC2 function and survival (HYP2P.322)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 53.3. http://dx.doi.org/10.4049/jimmunol.194.supp.53.3.
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Abstract Type 2 Innate lymphoid cells (ILC2s) are a newly identified subset of immune cells that play important roles in the pathogenesis of allergic asthma by producing large amounts of IL-5 and IL-13. ILC2 lack lineage markers but express CD45, IL-2Rα, IL-33R and IL-7Rα. All murine ILC2s and a significant portion of human ILC2s express Inducible T-cell COStimulator (ICOS) that is essential for T cell activation and function, however, the role of ICOS in ILC2s remains unknown. We investigated the role of ICOS in the function and survival of murine and human ILC2s using ICOS-/- and RAG2-/- and humanized mice in different experimental setups. We found that:1) ICOS-/- mice show lower IL-33-induced airway hyperreactivity (AHR) and eosinophilia than wild type (WT) mice. 2) Survival and the number of ILC2s is substantially lower in ICOS-/- than WT mice. 3) Blocking anti-ICOS antibody reduces survival and the number of ILC2s in WT mice. 4) Ex vivo stimulated ICOS-/- ILC2s show impaired IL-5 and IL-13 production compared to WT ILC2s. 5) Human peripheral ILC2s express ICOS and blocking ICOS:ICOS-Ligand interaction impairs their IL-5 and IL-13 production in vitro and IL-33 induced AHR and eosinophilia in humanized mice. 6) Human and murine ILC2s express ICOS-Ligand. 7) ICOS signaling modulates STAT5 pathway. Our results indicate that ICOS is required for the optimal function and survival of ILC2s and can be a novel therapeutic target in patients with ILC2-mediated asthma and lung inflammation.
Dissertations / Theses on the topic "Human ILC2 function"
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Durost, Philip A. "Evaluation of IL2 and HLA on the Homeostasis and Function of Human CD4 and CD8 T Cells." eScholarship@UMMS, 2009. http://escholarship.umassmed.edu/gsbs_diss/936.
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Homeostasis of human T cells is regulated by many factors that control proliferation, differentiation of effector cells and generation of memory. Our current knowledge of the mechanisms controlling human T cell homeostasis in vivo is based on experiments in small animal models. However many differences exist between immune systems of mice and humans, including cell composition, function, and gene expression. Humanized mouse models have shown great value in the study of human immunobiology. I have used novel humanized mouse models to examine the role of human MHC (HLA) and human IL2 in CD8 T cell and CD4 regulatory T cell (Treg) homeostasis. To study human CD8 T cells I engrafted CD8 T cells from healthy donor PBMC into NOD-scid IL2rgnull (NSG) mice that lacked expression of murine MHC and that expressed HLA-A2. My data demonstrate that CD8 T cell survival and effector function required the presence of HLA-A2, helper function from human CD4 T cells and exogenous human IL2. To study human Treg homeostasis I used NSG mice engrafted with human fetal thymus and hematopoietic stem cells (BLT model). NSG-BLT mice support the growth of human thymic tissue and enable the efficient development of HLA-restricted Treg and conventional T cells. Using an AAV vector to express human IL2, I demonstrated that functional human Treg but not conventional T cells increased in number in NSG-BLT mice and that this coincided with increases in activated human NK cells. Overall my research has revealed that HLA and human IL2 have an essential role in human T cell survival and function in vivo.
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Durost, Philip A. "Evaluation of IL2 and HLA on the Homeostasis and Function of Human CD4 and CD8 T Cells." eScholarship@UMMS, 2017. https://escholarship.umassmed.edu/gsbs_diss/936.
Full textAbstract:
Homeostasis of human T cells is regulated by many factors that control proliferation, differentiation of effector cells and generation of memory. Our current knowledge of the mechanisms controlling human T cell homeostasis in vivo is based on experiments in small animal models. However many differences exist between immune systems of mice and humans, including cell composition, function, and gene expression. Humanized mouse models have shown great value in the study of human immunobiology. I have used novel humanized mouse models to examine the role of human MHC (HLA) and human IL2 in CD8 T cell and CD4 regulatory T cell (Treg) homeostasis. To study human CD8 T cells I engrafted CD8 T cells from healthy donor PBMC into NOD-scid IL2rgnull (NSG) mice that lacked expression of murine MHC and that expressed HLA-A2. My data demonstrate that CD8 T cell survival and effector function required the presence of HLA-A2, helper function from human CD4 T cells and exogenous human IL2. To study human Treg homeostasis I used NSG mice engrafted with human fetal thymus and hematopoietic stem cells (BLT model). NSG-BLT mice support the growth of human thymic tissue and enable the efficient development of HLA-restricted Treg and conventional T cells. Using an AAV vector to express human IL2, I demonstrated that functional human Treg but not conventional T cells increased in number in NSG-BLT mice and that this coincided with increases in activated human NK cells. Overall my research has revealed that HLA and human IL2 have an essential role in human T cell survival and function in vivo.
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Sáez, Borderias Andrea. "Regulation of natural killer and cd4+T cell function by NKG2 C-type lectin-like receptors." Doctoral thesis, Universitat Pompeu Fabra, 2009. http://hdl.handle.net/10803/7133.
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This work is centered on the study of the NKG2 C-type lectin-like receptors on NK and CD4+T cells. We provide evidence supporting that CD4+T cells specific for Human Cytomegalovirus (HCMV) may express different NK cell receptors, and demonstrate that the C-type lectin-like receptor NKG2D is expressed on cytotoxic CD4+T cells with an effector/memory phenotype, enhancing their TCR-dependent proliferation and cytokine production. A second part of the work is centered on the study of the CD94/NKG2 receptors on NK cells. We show that NKG2A can be induced on NKG2C+ NK cells upon activation with rIL-12 or when cocultured with HCMV-infected dendritic cells, and that NKG2A expression inhibits the response of NKG2C+NK clones against HLA-E-expressing targets, providing a potential regulatory feedback mechanism to control cell activation. Altogether, our results support that expression of NKG2 C-type lectin like receptors may be shaped during the course of viral infections, providing mechanisms to finely regulate both NK and CD4+T cell functions.Aquesta tesi es centra en l'estudi dels receptors lectina de tipus C NKG2 en cèl·lules Natural Killer i T CD4+. Demostrem que les cèl·lules T CD4+ específiques pel Cytomegalovirus Humà poden expressar diferents receptors NK, i que el receptor lectina tipus C NKG2D s'expressa en cèl·lules citotòxiques i de memòria, potenciant la proliferació i secreció de citocines depenent del TCR. La segona part d'aquesta tesi es centra en l'estudi de l'expressió dels receptors CD94/NKG2 en cèl·lules NK. Mostrem com l'expressió de CD94/NKG2A s'indueix en cèl·lules CD94/NKG2C+ estimulades amb IL-12 o cultivades amb cèl·lules dendrítiques infectades pel Cytomegalovirus Humà, i que l'expressió de CD94/NKG2A inhibeix la resposta de clons NK CD94/NKG2C+ envers dianes HLA-E+, constituint un possible mecanisme de feedback negatiu per controlar l'activació cel·lular. En resum, els nostres resultats demostren que l'expressió dels receptors lectina tipus C NKG2 pot ser modificada durant les infeccions víriques consitutint un possible mecanisme per regular la resposta tant de cèl·lules NK com T CD4+.
Book chapters on the topic "Human ILC2 function"
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Scala, G., F. Alfinito, G. Morrone, M. Tamburrini, G. D’Alessio, C. I. Pastore, F. Ferrara, and S. Venuta. "HUMAN INTERLEUKIN 1 (ILI) AND INTERLEUKIN 2 (IL2) CAN FUNCTION AS AUTOCRINE GROWTH FACTORS FOR SOME NEOPLASTIC HUMAN LYMPHOID CELLS." In Human Tumor Markers, edited by F. Cimino, G. D. Birkmayer, J. V. Klavins, E. Pimentel, and F. Salvatore, 599–610. Berlin, Boston: De Gruyter, 1987. http://dx.doi.org/10.1515/9783110846515-043.
Full textConference papers on the topic "Human ILC2 function"
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Loibner, Hans, Manfred Schuster, Evelyne Janzek, Stefan Stranner, Bernhard Peball, Susanne Wiederkum, Oliver Mutschlechner, Nikolai Siebert, and Holger Lode. "Abstract 2858: Binding characteristics of the immunocytokine hu14.18-IL2 and induction of human effector functions as anticipated mode of action." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-2858.
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