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• W2951733935 abstract "Innate lymphoid cells (ILCs) represent a heterogeneous family of lymphocytes that includes, in addition to classic cytotoxic natural killer (NK) cells, the more recently described noncytotoxic ILC populations. We have previously shown that human NK cells are able to recognize dendritic cells (DCs) through the NKp30 receptor, a member of the natural cytotoxicity receptor family, and that this recognition results in the activation of NK cells1Ferlazzo G. Tsang M.L. Moretta L. Melioli G. Steinman R.M. Munz C. Human dendritic cells activate resting natural killer (NK) cells and are recognized via the NKp30 receptor by activated NK cells.J Exp Med. 2002; 195: 343-351Crossref PubMed Scopus (847) Google Scholar and in a process of DC “editing” able to select DCs with the most efficient antigen-presenting capability.2Ferlazzo G. Morandi B. Cross-Talks between natural killer cells and distinct subsets of dendritic cells.Front Immunol. 2014; 5: 159Crossref PubMed Scopus (121) Google Scholar, 3Moretta L. Ferlazzo G. Bottino C. Vitale M. Pende D. Mingari M.C. et al.Effector and regulatory events during natural killer-dendritic cell interactions.Immunol Rev. 2006; 214: 219-228Crossref PubMed Scopus (245) Google Scholar Our current results unveil a similar but even more effective bridge between innate and adaptive immunity in which group 3 innate lymphoid cells (ILC3s), potent effectors of the very early immune response, can receive an activating signal by DCs through cellular ligands able to engage the activating receptor DNAX accessory molecule 1 (DNAM-1) and in turn act as early and strong activators of DCs. ILC3s are characterized by expression of the transcription factor retinoic acid–related orphan receptor (ROR) γt. In addition to RORγt, they homogenously express the IL-7 receptor (CD127) and the stem cell factor receptor c-Kit (or CD117) and can be further dissected according to NKp44 expression (see Fig E1, A, in this article's Online Repository at www.jacionline.org). DNAM-1 is known to be expressed on NK cells, monocytes, and subsets of T cells and has recently been described also on the surface of mouse ILC3s.4Verrier T. Satoh-Takayama N. Serafini N. Marie S. Di Santo J.P. Vosshenrich C.A. Phenotypic and functional plasticity of murine intestinal NKp46+ group 3 innate lymphoid cells.J Immunol. 2016; 196: 4731-4738Crossref PubMed Scopus (28) Google Scholar We have here shown that human ILC3s express DNAM-1 at levels comparable with those on NK cells (Fig 1, A) and provided first evidence that engagement of DNAM-1 receptor on ILC3s is required for inducing GM-CSF production by ILC3s during DC/ILC3 interaction, whereas neither NKp44 nor NKp30 are involved (Fig 1, B). In turn, GM-CSF released by ILC3s stimulates IL-1β release by the interacting DCs (Fig 1, C and D), and remarkably, this latter cytokine can be responsible for DC maturation in an autocrine and, most likely, paracrine fashion on surrounding DCs, as assessed by upregulation of costimulatory/activation molecules on DC surfaces (Fig 1, E). Of note, DC activation induced by ILC3s was, at least in this experimental setting, significantly more efficient than that induced by autologous NK cells (Fig 1, E). On the other hand, IL-1β produced by DCs during their cross-talk with ILC3s plays a relevant role also for ILC3 proliferation and production of IL-22 (Fig 1, F), thus resulting crucial for inducing reciprocal cell activation during the cross-talk between DCs and ILC3s. It is noteworthy that during coculture with autologous DCs, ILC3s proliferate more vigorously than NK cells, which are known to proliferate upon interaction with DCs (Fig 1, G).1Ferlazzo G. Tsang M.L. Moretta L. Melioli G. Steinman R.M. Munz C. Human dendritic cells activate resting natural killer (NK) cells and are recognized via the NKp30 receptor by activated NK cells.J Exp Med. 2002; 195: 343-351Crossref PubMed Scopus (847) Google Scholar The robust proliferation of ILC3s occurring upon interaction with DCs provides a possible explanation for accumulation of these innate lymphocytes in secondary lymphoid organs, in mucosal sites, and at epithelial barriers, where DCs are present as sentinel cells and abundantly recruited during inflammation. Accordingly, the frequency of NKp44+ ILC3s in human inflamed tonsils apparently correlated with the degree of inflammation and in vitro appeared to be the prominent ILC subset activated by DCs (see Fig E1, B-E). Remarkably, we showed that IL-1β–producing DCs and ILC3s harbor in the same area of human inflamed tonsils (Fig 1, H), thus suggesting that early release of IL-1β by DCs encountering ILC3s at these sites would play a central role in the initiation and also maintenance of inflammatory processes. Hence, in the context of the early phase of the immune response, the role played by ILC3s in activating the subsequent adaptive response might be more relevant than previously appreciated, particularly in settings in which activation of DCs by pathogen/danger signals might be inefficient, including cancer. Of note, when compared with BDCA3+ DCs, BDCA1+ DCs induced stronger ILC3 proliferation and release of IL-22, GM-CSF, and IL-8 (Fig 2, A; see Fig E2 in this article's Online Repository at ww.jacionline.org), whereas IL-2, TNF-α, and IL-17 were not produced by ILC3s upon stimulation by both DC subsets (see Fig E2, A). The evidence that BDCA1+ DCs derived from tonsils (as well as from peripheral blood; see Fig E4 in this article's Online Repository at www.jacionline.org) appear particularly prone to activate human ILC3s is in agreement with their specific greater capability in production of IL-1β when compared with other human DC subsets.5Jongbloed S.L. Kassianos A.J. McDonald K.J. Clark G.J. Ju X. Angel C.E. et al.Human CD141+ (BDCA-3)+ dendritic cells (DCs) represent a unique myeloid DC subset that cross-presents necrotic cell antigens.J Exp Med. 2010; 207: 1247-1260Crossref PubMed Scopus (805) Google Scholar DC/ILC3 interaction also results in expression of NKp44 accompanied at the same time by upregulation of NKp46, and again, BDCA1+ DCs are more potent than BDCA3+ DCs in inducing this effect (see Fig E3, A-C, in this article's Online Repository at www.jacionline.org). We also observed that activation of ILC3s in response to DCs is more prominent in ILC3s expressing NKp44 both in terms of proliferation and cytokine secretion (Fig 2, B), with the exception of GM-CSF, which is released in similar amounts by NKp44− and NKp44+ ILC3s exposed to DCs (Fig 2, B). The evidence that steady-state NKp44− ILC3s can produce relevant amounts of GM-CSF upon interaction with DCs is in agreement with a model in which the release of GM-CSF by ILC3s acts as a triggering factor for completing the reciprocal activation between DCs and ILC3s. Release of other ILC3-associated cytokines, such as IL-22, is known to be sustained by both IL-1β and IL-23. We observed that, along with IL-1β release, encounter with ILC3s induced upregulation of IL-23 expression in BDCA1+ DCs (Fig 2, C), thus further supporting the strong capacity of the latter to boost IL-22 production by interacting ILC3s. In tissues, IL-22 levels are regulated by epithelium-derived cytokines, such as IL-25 and thymic stromal lymphopoietin (TSLP), which are able to suppress IL-22 production by ILC3s.6Giacomin P.R. Moy R.H. Noti M. Osborne L.C. Siracusa M.C. Alenghat T. et al.Epithelial-intrinsic IKKalpha expression regulates group 3 innate lymphoid cell responses and antibacterial immunity.J Exp Med. 2015; 212: 1513-1528Crossref PubMed Scopus (65) Google Scholar Nevertheless, in cases of chronic epithelial damage dampening the production of IL-25 and TLSP, reciprocal activation between DCs and ILC3s should lead to an exacerbating loop of the initial inflammatory process, potentially playing a critical role in the maintenance and progression of the starting lesions. At the same time, DC activation would reduce their production of IL-22–binding protein, another factor able to control IL-22 activity.7Martin J.C. Bériou G. Heslan M. Chauvin C. Utriainen L. Aumeunier A. et al.Interleukin-22 binding protein (IL-22BP) is constitutively expressed by a subset of conventional dendritic cells and is strongly induced by retinoic acid.Mucosal Immunol. 2014; 7: 101-113Crossref PubMed Scopus (111) Google Scholar This hypothesis might particularly hold true in patients with inflammatory skin diseases characterized by a hyperproliferative epidermis, in which ILC3s expressing CCR6 and the skin-homing receptor cutaneous lymphocyte antigen (CLA)8Teunissen M.B.M. Munneke J.M. Bernink J.H. Spuls P.I. Res P.C.M. Te Velde A. et al.Composition of innate lymphoid cell subsets in the human skin: enrichment of NCR(+) ILC3 in lesional skin and blood of psoriasis patients.J Invest Dermatol. 2014; 134: 2351-2360Abstract Full Text Full Text PDF PubMed Scopus (236) Google Scholar would migrate to damaged epidermis and engage with BDCA1+ DCs, which are abundantly represented in inflamed skin.9Zaba L.C. Fuentes-Duculan J. Eungdamrong N.J. Abello M.V. Novitskaya I. Pierson K.C. et al.Psoriasis is characterized by accumulation of immunostimulatory and Th1/Th17 cell-polarizing myeloid dendritic cells.J Invest Dermatol. 2009; 129: 79-88Abstract Full Text Full Text PDF PubMed Scopus (351) Google Scholar At these sites, ILC3/DC cross-talk might initiate a self-maintaining loop of reciprocal activation that results in expansion of ILC3s, as well as in long-term release of IL-22, which is responsible for continuous proliferation of epidermal cells, an event frequently occurring in several chronic inflammatory skin diseases. Our current observation that upon interaction with ILC3s, along with IL-1β, DCs can also increase IL-23 expression, which is recognized as a crucial player in psoriasis pathogenesis, is in agreement with this hypothesis. On the same line, ILC3s expressing CLA, a homing receptor that facilitates targeting of lymphocytes to inflamed skin, were abundantly represented in both peripheral blood of patients with psoriasis and in inflamed tonsils (Fig 2, D). Remarkably, CLA+ ILC3s can produce high levels of GM-CSF and accounted for most of the IL-22–producing ILC3s upon interaction with DCs (Fig 2, E). In this context, it is worth mentioning that IL-22 production is mainly restricted to ILC3s expressing NKp44, a subset not detectable in the peripheral blood of healthy subjects8Teunissen M.B.M. Munneke J.M. Bernink J.H. Spuls P.I. Res P.C.M. Te Velde A. et al.Composition of innate lymphoid cell subsets in the human skin: enrichment of NCR(+) ILC3 in lesional skin and blood of psoriasis patients.J Invest Dermatol. 2014; 134: 2351-2360Abstract Full Text Full Text PDF PubMed Scopus (236) Google Scholar but considerably accumulated and activated following interaction with DCs. Moreover, in support of the model proposed here, the inflamed papillary dermis of psoriatic skin reveals a massive presence of both IL-1β–producing DCs and ILC3s (Fig 2, F). Our current results represent an advance in understanding ILC3-activating signals as well as their interactions with other players in innate immunity and might be informative for designing modern immunotherapeutic strategies targeting either DC or ILC activation. All samples were collected after obtaining informed consent and with approval of tissue-specific protocols by the Ethical Committee of the University Hospital Policlinico G.Martino, Messina, Italy. Peripheral blood was also obtained from healthy donors and patients affected by active psoriasis. Tonsillar tissues were processed, as previously described.E1Carrega P. Loiacono F. Di Carlo E. Scaramuccia A. Mora M. Conte R. et al.NCR(+)ILC3 concentrate in human lung cancer and associate with intratumoral lymphoid structures.Nat Commun. 2015; 6: 8280Crossref PubMed Scopus (172) Google Scholar Total CD127hi ILCs were sorted to high purity (>98%) by using the FACSAria II cell sorter (BD Biosciences, Franklin Lakes, NJ) as lineage (LIN)− (CD3, CD19, CD94, CD14, CD34, and BDCA2) CD127hi cells. Among ILCs, ILC3s were sorted as LIN−CRTH2−c-Kit+CD127hiNKp44+/−, and group 1 innate lymphoid cells (ILC1s) were sorted as LIN−CRTH2−c-Kit−CD127hiNKp44− cells. NK cells were sorted as LIN+NKp46+ cells. DCs were sorted as LIN−HLA-DR+CD11c+ or LIN−HLA-DR+ BDCA1+ or BDCA3+ cells. Intracellular staining for cytokine detection was performed on freshly isolated tonsillar ILC3s or NK cells stimulated for 18 hours with autologous total myeloid DCs or, in selected experiments, with either autologous tonsillar or allogeneic blood-derived BDCA1+ or BDCA3+ DCs at a ratio of 2:1. Monensin (2 μmol/L; Sigma-Aldrich, St Louis, Mo) and brefeldin (10 μg · mL−1; Sigma-Aldrich) were added during the last 6 hours of culture to inhibit cell secretion. Detection of intracellular cytokines in blood BDCA1+ DCs was performed coculturing them for 36 hours with tonsillar NKp44+ ILC3s and monensin and brefeldin were added during the last 12 hours of culture. Cells were then fixed in 1% paraformaldehyde, permeabilized with saponin 0.1% in PBS and stained with the following antibodies: phycoerythrin (PE)–conjugated anti–IL-22, PE-conjugated anti-GM–CSF, PE-conjugated anti–IFN-γ, PE-conjugated anti–TNF-α, PE-conjugated anti–IL-8 and PE-conjugated anti–IL-2, and fluorescein isothiocyanate–conjugated anti–IL-1β. Samples were then acquired, about 3 × 103 events were collected for each subset analyzed by using the FACSCanto II (BD Biosciences) cytometer, and data were analyzed with FlowJoVX (Tree Star, Ashland, Ore) software. Freshly isolated fluorescence-activated cell–sorted human ILCs were plated at 5 × 104 cells · mL−1 in RPMI 1640 plus FBS 10% supplemented with penicillin/streptomycin in 96-well round-bottom plates. For DC-mediated ILC proliferation, purified LIN−CD127hi cells were cultured with autologous LIN−HLA-DR+CD11c+ DCs for 6 days. For DC-mediated ILC activation, cells were cocultured for 48 hours. For ILC3 and NK cell proliferation experiments, cells were stimulated with autologous tonsillar BDCA1+ or BDCA3+ DCs, or blood BDCA1+ DCs at a ratio of 2:1 for 6 days in the presence of IL-7 (50 ng · mL−1; Miltenyi Biotec, Bergisch Gladbach, Germany). Where indicated, cells were stimulated with recombinant IL-1β (50 ng · mL−1; Miltenyi Biotec). Proliferation was assessed by using flow cytometry with carboxyfluorescein succinimidyl ester fluorescence or Ki67 staining. For BDCA1+ DC maturation, purified BDCA1+ DCs from peripheral blood were cultured with freshly isolated ILC3s or NK cells for 24 hours and then analyzed for expression of CD80, CD83, and CD40. The level of expression was measured as the geometric mean fluorescence intensity. IL-1β production was assessed on purified blood BDCA1+ DCs cultured for 24 hours with or without ILC3s by using both intracellular staining and real-time PCR analysis. Alternatively, IL-1β was measured by using flow cytometry on BDCA1+ DCs stimulated with 25 ng · mL−1 recombinant GM-CSF (Sargamostim; Genzyme, Cambridge, Mass). In selected experiments, neutralizing anti-IL-1β (clone 2805; R&D Systems, Minneapolis, Minn), anti–GM-CSF (clone 3209; R&D Systems), anti-NKp44 (IgM, KS38), anti-NKp30 (IgM, F252), and anti-DNAM-1 (IgM, F5; the last 3 were produced in our laboratories and/or kindly provided by Alessandro Moretta, University of Genoa, Italy) antibodies or matched isotype controls were added at the beginning of culture. mRNA was isolated from cells by using the RNeasy MicroKit (Qiagen, Hilden, Germany). cDNA was synthesized by using QuantiTect Reverse Transcription Reagents (Qiagen) and assayed by using quantitative PCR in duplicates with the Quant Studio DX real-time PCR system (Thermo Fisher Scientific, Waltham, Mass). The IL-1β and IL-23 TaqMan Gene Expression Assay (Thermo Fisher Scientific) was used, and mRNA content was normalized to glyceraldehyde-3-phosphate dehydrogenase expression. Mean relative gene expression was determined by using the ΔΔ cycle threshold method. Formalin-fixed, paraffin-embedded palatine tonsils from pediatric tonsillectomies and skin biopsy specimens from patients with psoriasis were collected from the archives of the Department of Anatomic Pathology, “SS. Annunziata” Hospital of Chieti, Chieti, Italy. For histology, tonsillar tissue samples were fixed in 4% neutral buffered formalin, embedded in paraffin, sectioned at 4 μm and stained with hematoxylin and eosin. For immunohistochemistry, formalin-fixed, paraffin-embedded sections were treated with 3% H2O2 for 5 minutes and then washed in H2O to inhibit endogenous peroxidases. Antigen was unmasked by means of heat-induced epitope retrieval in EDTA buffer at pH 8. Slices were then left at room temperature for 20 minutes. Sections were washed in PBS/Tween-20 and then incubated with the primary antibody anti-CD83 (clone 1H4b; Gentaur Srl, Bergamo, Italy) or anti–IL-1β antibody (Santa Cruz Biotechnology, Dallas, Tex) for 30 minutes. The resulting immune complexes were detected with the Bond Polymer Refine Detection Kit (Leica Biosystems, Wetzlar, Germany), according to the manufacturer's protocol. Negative controls were performed by replacing the primary antibody with 10% non-immune serum. Double immunohistochemistry was performed, as previously reported,E4Di Meo S. Airoldi I. Sorrentino C. Zorzoli A. Esposito S. Di Carlo E. Interleukin-30 expression in prostate cancer and its draining lymph nodes correlates with advanced grade and stage.Clin Cancer Res. 2014; 3: 585-594Google Scholar with anti-CD83 antibody in combination with anti–IL-1β antibody by using the Bond Polymer Refine Red Detection Kit (Leica Biosystems) and anti-NKp46 antibody (clone 195314; R&D Systems) in combination with anti-RORγt (clone MAB F81; Merck Millipore, Billerica, Mass) by using the Ferangi Blue Chromogen Kit (Biocare Medical, Concord, Calif). Statistical significance was determined with the Student t test or linear regression test. GraphPad Prism software (GraphPad Software, La Jolla, Calif) was used. P values of less than .05 were considered statistically significant. In human tonsils ILC3s represent the most prominent subset among CD127hi ILCs, accounting for about 6 × 105 ± 5 × 104 cells per tonsil, whereas ILC2s are barely detectable (Fig E1, A).E2Bernink J.H. Peters C.P. Munneke M. te Velde A. Meijer S.L. Weijer K. et al.Human type 1 innate lymphoid cells accumulate in inflamed mucosal tissues.Nat Immunol. 2013; 14: 221-229Crossref PubMed Scopus (726) Google Scholar Within the ILC3 population, ILC3s that express NKp44 represent the most abundant subset (Fig E1, A), and interestingly, we observed that their amount correlated with total peripheral blood leukocyte counts, with neutrophilia, as well as in the tonsils, with both the frequency of B cells and the percentage of proliferating B cells within the tonsils (Fig E1, B). Because of this apparent association between inflamed tonsillar reactivity and the frequency of NKp44+ ILC3s, we hypothesized that accessory cells, such as DCs, might play a role in ILC3 activation, proliferation, or both. To evaluate the ability of tonsil-derived myeloid DCs to instruct ILCs, LIN−HLA-DR+CD11c+ cells were sorted from tonsillar tissue and cocultured with autologous CD127hi ILCs. On 6 days of coculture of total CD127hi ILC population with autologous tonsil-derived DCs, the frequency of NKp44+ ILC3s was significantly increased to the detriment of NKp44− ILC3s, whereas no difference was observed for ILC1s (Fig E1, C). In agreement with these data, only NKp44+ ILC3s acquired expression of the Ki67 proliferation marker (Fig E1, D). Confirming their activating ability, tonsil-derived DCs induced elevated production of IL-22 in autologous ILC3s (Fig E1, E). In contrast to high levels of IL-22, tonsillar DCs were, at least in this setting, poor stimulators of IFN-γ production by ILC1s and when we compared tonsillar NK cells and ILC1s, the latter produced much lower amounts of IFN-γ (Fig E1, E). Functional analyses of ILC populations have shown their major role in early cytokine production. ILC3s are able to switch between IL-22 or TNF production depending on the activating signals involved. Engagement of NKp44 triggers production of TNF-α and IL-2 by ILC3s, whereas cytokine stimulation (IL-23, IL-1β, and IL-7) preferentially induces IL-22 and GM-CSF expression.E1Carrega P. Loiacono F. Di Carlo E. Scaramuccia A. Mora M. Conte R. et al.NCR(+)ILC3 concentrate in human lung cancer and associate with intratumoral lymphoid structures.Nat Commun. 2015; 6: 8280Crossref PubMed Scopus (172) Google Scholar, E3Glatzer T. Killig M. Meisig J. Ommert I. Luetke-Eversloh M. Babic M. et al.RORgammat(+) innate lymphoid cells acquire a proinflammatory program upon engagement of the activating receptor NKp44.Immunity. 2013; 38: 1223-1235Abstract Full Text Full Text PDF PubMed Scopus (137) Google Scholar We evaluated the cytokine production profile of ILC3s upon stimulation with DCs. Remarkably, BDCA1+ DCs were strong inducer of the release of IL-22, IL-8, and GM-CSF by ILC3s, whereas BDCA3+ DCs could only induce the release of a limited amount of IL-22 (Fig 2, A). Conversely, IL-2, TNF-α, and IL-17 were not produced by ILC3s upon interaction with both DC subtypes (Fig E2, A). Then we investigated the pattern of cytokines induced by DCs on both NKp44− and NKp44+ ILC3 subsets. As expected, IL-22 production was mainly restricted to the NKp44+ ILC3s, IL-8 levels were significantly greater on NKp44+ compartments, and no differences in GM-CSF production could be observed among the 2 different subsets on both BDCA1+ DC (Fig 2, B) and BDCA3+ DC stimulation (Fig E2, B). The high frequency of NKp44+ ILC3s observed in human inflamed tonsils (Fig E1, A) might result from locoregional proliferation of this ILC subset but also by conversion of NKp44− ILC3s into NKp44+ cells. Thus we investigated whether the 2 distinct subsets of DCs might also display the potential to drive differentiation from NKp44− ILC3s to their NKp44-expressing counterpart. NKp44− ILC3s were sorted and cultured for 5 days with DCs or, alternatively, with each of the 2 DC subsets. Tonsillar myeloid DCs efficiently induced expression of NKp44 on ILC3s, and again, BDCA1+ DCs were mainly responsible for this induction (Fig E3, A and B). It is noteworthy that the prominent acquisition of NKp44 induced by BDCA1+ DCs was accompanied by significant upregulation of NKp46 expression on ILC3s (Fig E3, C). In our experimental conditions, tonsillar DCs were able to activate ILC3s in the absence of exogenous stimuli able to trigger DC activation. Thus, we wondered whether a possible explanation could rely on the activated status of DCs, which were isolated from inflamed tonsils. To address this question, BDCA1+ DCs were sorted also from peripheral blood and cocultured with tonsillar ILC3s. Also in this case BDCA1+ DCs could strongly activate ILC3s inducing high amounts of cytokines (Fig E4), thus indicating that tonsil- and blood-derived DCs display similar ILC3-activating properties.Fig E2Both BDCA1+ and BDCA3+ DC subsets are poor inducers of TNF-α, IL-2, and IL-17 by ILC3s, and BDCA3+ DCs have a modest effect on IL-22, IL-8, and GM-CSF. A, Intracellular cytokine expression of fluorescence-activated cell-sorted ILC3s stimulated as indicated was measured by using flow cytometry. B, Intracellular cytokine expression of fluorescence-activated cell-sorted NKp44+ and NKp44− ILC3s on BDCA3+ DC stimulation. *P <.05 and **P < .01. n.s., Not significant. FSC, Forward scatter.View Large Image Figure ViewerDownload Hi-res image Download (PPT)Fig E3BDCA1+ DCs efficiently induce expression of NKp44 on ILC3s. Acquisition of NKp44 and upregulation of NKp46 on fluorescence-activated cell-sorted NKp44− ILC3s cultured with total DCs (A) or BDCA1+/BDCA3+ subsets (B and C). *P <.05.View Large Image Figure ViewerDownload Hi-res image Download (PPT)Fig E4Blood-derived BDCA1+ DCs can efficiently activate NKp44+ ILC3s. Intracellular cytokine expression of fluorescence-activated cell-sorted NKp44+ ILC3s stimulated by BDCA1+ DCs isolated from peripheral blood. FSC, Forward scatter.View Large Image Figure ViewerDownload Hi-res image Download (PPT)" @default.
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• W2951733935 title "Dendritic cell recognition by group 3 innate lymphoid cells through DNAX accessory molecule 1 triggers proinflammatory reciprocal cell activation" @default.
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• W2951733935 isRetracted "false" @default.
• W2951733935 magId "2951733935" @default.
• W2951733935 workType "article" @default.