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• W2016652854 abstract "The mechanisms that guide the development of mucosal-associated innate lymphoid cells (ILCs) producing IL-17, IL-22, and IFN-γ are the subject of intense interest. In this issue of Immunity, Hughes et al., 2010Hughes T. Becknell B. Freud A.G. McClory S. Briercheck E. Yu J. Mao C. Giovenzana C. Nuovo G. Wei L. et al.Immunity. 2010; 32 (this issue): 803-814Abstract Full Text Full Text PDF PubMed Scopus (158) Google Scholar identify a new role for IL-1β in regulating an IL-22-producing ILC. The mechanisms that guide the development of mucosal-associated innate lymphoid cells (ILCs) producing IL-17, IL-22, and IFN-γ are the subject of intense interest. In this issue of Immunity, Hughes et al., 2010Hughes T. Becknell B. Freud A.G. McClory S. Briercheck E. Yu J. Mao C. Giovenzana C. Nuovo G. Wei L. et al.Immunity. 2010; 32 (this issue): 803-814Abstract Full Text Full Text PDF PubMed Scopus (158) Google Scholar identify a new role for IL-1β in regulating an IL-22-producing ILC. Lymphoid tissues associated with mucosal surfaces harbor an elaborate immune defense system that plays a primary role in protection against invading pathogens. Developmentally related innate lymphoid cells (ILCs), including lymphoid tissue inducer (LTi) cells, IL-22-producing cells expressing natural cytotoxicity receptors (NK22, NCR22, and NKR-LTi), and classical NK cells have been identified in mucosal-associated lymphoid tissues (MALT) in both man and mouse (Colonna, 2009Colonna M. Immunity. 2009; 31: 15-23Abstract Full Text Full Text PDF PubMed Scopus (229) Google Scholar). These diverse ILCs produce a variety of cytokines (IL-17, IL-22, and IFN-γ) that are implicated in protection against infection. In addition, these cytokines influence tissue remodeling after stress or inflammation and, when deregulated, can lead to serious disease, including autoimmunity and cancer exacerbation. Accordingly, it is essential to understand the mechanisms that control the generation of these innate lymphocytes and that regulate their function. Hughes et al., 2010Hughes T. Becknell B. Freud A.G. McClory S. Briercheck E. Yu J. Mao C. Giovenzana C. Nuovo G. Wei L. et al.Immunity. 2010; 32 (this issue): 803-814Abstract Full Text Full Text PDF PubMed Scopus (158) Google Scholar provide an important advance by demonstrating that the IL-1R1 can be used to identify human ILCs within secondary lymphoid tissue (SLT) that have strong IL-22-producing capacity. Moreover, they provide evidence suggesting that IL-1β, derived from dendritic cells (DCs), can modulate the fate of developing ILCs at mucosal sites, favoring the production of IL-22+ ILC while inhibiting generation of classical IFN-γ+ NK cells. These findings suggest a mechanistic solution for ILC diversification and, along with a recent report (Cella et al., 2010Cella M. Otero K. Colonna M. Proc. Natl. Acad. Sci. USA. 2010; (in press. Published online June 1, 2010)https://doi.org/10.1073/pnas.1005641107Crossref PubMed Scopus (238) Google Scholar), demonstrate that regulation of IL-1β expression may fine-tune the functional activities of mucosal-associated ILCs under diverse conditions. IL-17, IL-22, and IFN-γ have essential roles in protecting mucosal surfaces from pathogen invasion. Among the ILC that produce these cytokines, LTi cells (that play a nonredundant role in lymphoid tissue organogenesis) as well as classical NK cells can be considered as innate “versions” of the adaptive Th17 and Th1 cells, respectively. Recently, a human ILC with properties of both LTi and NK cells was described. Dubbed “NK22” (Cella et al., 2009Cella M. Fuchs A. Vermi W. Facchetti F. Otero K. Lennerz J.K. Doherty J.M. Mills J.C. Colonna M. Nature. 2009; 457: 722-725Crossref PubMed Scopus (917) Google Scholar) or RORC+CD127+ NK-like cells (Cupedo et al., 2009Cupedo T. Crellin N.K. Papazian N. Rombouts E.J. Weijer K. Grogan J.L. Fibbe W.E. Cornelissen J.J. Spits H. Nat. Immunol. 2009; 10: 66-74Crossref PubMed Scopus (485) Google Scholar), these cells have LTi (RORC, LTA, LTB, and CCR6) and NK cell (CD56, NKp46, and NKp44) features. In the fetus, these cells produce mainly IL-17, whereas postnatal cells show strong IL-22 production, suggesting that these cells could represent innate Th17 cell-like and Th22 cell-like subsets, respectively. RORC+CD127+ NK-like cells could be derived after culture of human fetal or postnatal LTi cells in IL-2, suggesting a precursor-product relationship. These cultures also contained cells bearing NK markers (NKp30 and NKp44) and low amounts of granzyme B and IFN-γ, leading to the initial conclusion that human LTi cells were IL-15-responsive NK cell precursors (Cupedo et al., 2009Cupedo T. Crellin N.K. Papazian N. Rombouts E.J. Weijer K. Grogan J.L. Fibbe W.E. Cornelissen J.J. Spits H. Nat. Immunol. 2009; 10: 66-74Crossref PubMed Scopus (485) Google Scholar). This notion was not unheralded, given that Mebius and colleagues had shown that fetal mouse LTi cells could generate lytic NK1.1+ NK cells (and DC cells) after in vitro culture (Mebius et al., 1997Mebius R.E. Rennert P. Weissman I.L. Immunity. 1997; 7: 493-504Abstract Full Text Full Text PDF PubMed Scopus (541) Google Scholar). Still, both NK22 cells as well as RORC+CD127+ NK-like cells isolated ex vivo or generated in vitro were clearly phenotypically and functionally different from classical NK cells, lacking expression of killer cell Ig-like receptors (KIRs) and perforin (Cella et al., 2009Cella M. Fuchs A. Vermi W. Facchetti F. Otero K. Lennerz J.K. Doherty J.M. Mills J.C. Colonna M. Nature. 2009; 457: 722-725Crossref PubMed Scopus (917) Google Scholar, Cupedo et al., 2009Cupedo T. Crellin N.K. Papazian N. Rombouts E.J. Weijer K. Grogan J.L. Fibbe W.E. Cornelissen J.J. Spits H. Nat. Immunol. 2009; 10: 66-74Crossref PubMed Scopus (485) Google Scholar). Thus, the developmental relationships and frontiers between human LTi, NK22, RORC+CD127+, and classical NK cells remained fuzzy. The Caligiuri lab has proposed a five-stage model for human NK cell development in SLT on the basis of expression of CD34, CD117, and CD94 (Freud et al., 2006Freud A.G. Yokohama A. Becknell B. Lee M.T. Mao H.C. Ferketich A.K. Caligiuri M.A. J. Exp. Med. 2006; 203: 1033-1043Crossref PubMed Scopus (295) Google Scholar). In this scheme, immature NK cells (stage 3 iNK: CD34−CD117+CD94−) harbored NK cell but not T cell, B cell, or DC precursors. Interestingly, a subset of stage 3 cells expressed IL-22 and the transcription factor AHR that is required for inducible IL-22 expression, but lacked phenotypic and functional attributes of mature NK cells (Hughes et al., 2009Hughes T. Becknell B. McClory S. Briercheck E. Freud A.G. Zhang X. Mao H. Nuovo G. Yu J. Caligiuri M.A. Blood. 2009; 113: 4008-4010Crossref PubMed Scopus (105) Google Scholar). The collective observations were therefore consistent with a model in which immature NK cells could have a dual function, being precursors to mature NK cells but also providing a potential source of IL-22 in SLT that could impact on mucosal immune responses and help sustain tissue integrity during infection or inflammation (Figure 1). Although this “dual function” iNK cell model was attractive, an alternative model in which stage 3 iNK cells comprised several distinct lymphoid cell precursors needed to be considered, given that only a minor fraction of stage 3 iNK cells gave rise to bona fide NK cells after in vitro culture. In this case, true NK cell precursors would be distinct from IL-22+ cells, with the latter possibly representing NK22, RORC+CD127+ cells or related ILCs or their precursors (Figure 1). Hughes et al., 2010Hughes T. Becknell B. Freud A.G. McClory S. Briercheck E. Yu J. Mao C. Giovenzana C. Nuovo G. Wei L. et al.Immunity. 2010; 32 (this issue): 803-814Abstract Full Text Full Text PDF PubMed Scopus (158) Google Scholar now provide further evidence for heterogeneity within stage 3 cells by identifying a subset of cells expressing the interleukin-1 receptor one (IL-1R1). By separating and analyzing IL-1R1hi and IL-1R1lo subsets, they provide evidence that IL-22 and AHR expression was restricted to the IL-1R1hi subset; this subset concomitantly expressed CD127, CD161, LTA, and CCR7 (LTi cell-like features) but also CD56 and NKp44, suggesting that they were closely related to the previously described NK22 and RORC+CD127+ cells. In contrast, the IL-1R1lo subset (representing ∼20% of stage 3 cells) lacked expression of these markers. Hughes et al., 2010Hughes T. Becknell B. Freud A.G. McClory S. Briercheck E. Yu J. Mao C. Giovenzana C. Nuovo G. Wei L. et al.Immunity. 2010; 32 (this issue): 803-814Abstract Full Text Full Text PDF PubMed Scopus (158) Google Scholar then assess the impact of exogenous IL-1β on the development of NK cells from stage 3 iNK cells. As expected, only the IL-1R1hi subset responded to IL-1β, which enhanced cell proliferation in the presence of IL-15 resulting in higher overall cell yields. IL-1β in the absence of IL-15, however, was not sufficient for growth. Interestingly, IL-1β+IL-15 clearly sustained IL-22 expression in IL-1R1hi cells; this was associated with continued AHR expression, reinforcing the parallels between IL-22-producing ILC and Th22 cells (Colonna, 2009Colonna M. Immunity. 2009; 31: 15-23Abstract Full Text Full Text PDF PubMed Scopus (229) Google Scholar). In the absence of IL-1β, IL-22 and AHR expression from IL-15-stimulated IL-1R1hi stage 3 cells was lost. These results suggest a critical role for IL-1β in regulating the function of IL-22-producing ILCs, although the results are also compatible with overgrowth of a minor IL-1R1hi subset lacking AHR and IL-22 expression. IL-1β was also able to influence the development of classical NK cells from stage 3 cells. This effect was also restricted to the IL-1R1hi subset and resulted in an overall suppression of CD56 and CD94 expression and a reduction in IFN-γ production and CD107a mobilization (a surrogate marker for NK lytic granule exocytosis). IL-1R1lo cells, in contrast, appeared as precursors for classical NK cells. A clonal analysis of IL-1R1hi and IL-1R1lo stage 3 cells were consistent with the observations made in bulk cultures; IL-1β sustained IL-22 in IL-1R1hi cells while reducing IL-15-dependent CD94 expression. These results suggest that IL-1β could provide a molecular switch that dictates development of IL-22-producing ILCs versus classical NK cells from common Id2-dependent precursors (Figure 1). Do the results of Hughes et al. distinguish the “dual function” from the “dual precursor” model (Figure 1)? For the moment, the jury is still deliberating. Although IL-22 expression appears restricted to the IL-1R1hi stage 3 subset, this population is clearly heterogeneous (for CD127, CD161, CD56, and NKp44) providing ample opportunity for distinct lineage-specific precursors of the dual precursor model. Indeed, a recent report showed that stage 3 iNK cells contain a CD127+ cell subset with features of IL-22 ILC, whereas the CD127− cell subset contained precursors that could differentiate into classical NK cells (Crellin et al., 2010Crellin N.K. Trifari S. Kaplan C.D. Cupedo T. Spits H. J. Exp. Med. 2010; 207: 281-290Crossref PubMed Scopus (216) Google Scholar). In the mouse, fate-mapping experiments have clearly shown that Rorc+ precursors of IL-22+ ILCs are distinct from NK cell precursors for classical NK cells (Satoh-Takayama et al., 2010Satoh-Takayama N. Lesjean-Pottier S. Vieira P. Sawa S. Eberl G. Vosshenrich C.A. Di Santo J.P. J. Exp. Med. 2010; 207: 273-280Crossref PubMed Scopus (241) Google Scholar), supporting a dual precursor model in this species. The observation by Hughes et al., 2010Hughes T. Becknell B. Freud A.G. McClory S. Briercheck E. Yu J. Mao C. Giovenzana C. Nuovo G. Wei L. et al.Immunity. 2010; 32 (this issue): 803-814Abstract Full Text Full Text PDF PubMed Scopus (158) Google Scholar that IL-1β impacts on classical NK cell development in vitro would appear to support the dual function model of a common IL-1R1hi precursor (Figure 1), however, the existence of dedicated IL-1R1hi subsets (CD127+ for IL-22+ ILC; CD127- for NK cells) needs to be assessed in clonal assays. Because NK22 and RORC+CD127+ cells retain some phenotypic markers of classical NK cells, analysis should include discriminating markers (perforin, granzyme B) that are only highly expressed by classical NK cells. Hughes et al., 2010Hughes T. Becknell B. Freud A.G. McClory S. Briercheck E. Yu J. Mao C. Giovenzana C. Nuovo G. Wei L. et al.Immunity. 2010; 32 (this issue): 803-814Abstract Full Text Full Text PDF PubMed Scopus (158) Google Scholar also identify conventional DCs as a potential source of IL-1β in SLT. This makes sense considering that cDCs are known to transpresent IL-15-IL-15Rα complexes required for homeostasis of NK cells (and perhaps other distinct ILCs). Because DCs also produce key cytokines involved in the process of T cell polarization (IL-12, IL-18, and IL-23, for example), the proximity of cDCs with IL-1R1hi stage cells suggests a DC-controlled regulation of ILC function within SLT and by analogy, MALT. Along these lines, recent studies have demonstrated extensive flexibility of cytokine production by NK22 and RORC+CD127+ cells after in vitro culture with combinations of IL-1β, IL-2, IL-7, IL-12, and/or IL-23 (Cella et al., 2010Cella M. Otero K. Colonna M. Proc. Natl. Acad. Sci. USA. 2010; (in press. Published online June 1, 2010)https://doi.org/10.1073/pnas.1005641107Crossref PubMed Scopus (238) Google Scholar, Crellin et al., 2010Crellin N.K. Trifari S. Kaplan C.D. Cupedo T. Spits H. J. Exp. Med. 2010; 207: 281-290Crossref PubMed Scopus (216) Google Scholar). The identification by Hughes et al., 2010Hughes T. Becknell B. Freud A.G. McClory S. Briercheck E. Yu J. Mao C. Giovenzana C. Nuovo G. Wei L. et al.Immunity. 2010; 32 (this issue): 803-814Abstract Full Text Full Text PDF PubMed Scopus (158) Google Scholar of an IL-1R1hi subset of IL-22-producing innate lymphoid cells provides another example of a DC “crosstalk” within innate immune system. This DC-ILC dialog may operate at multiple levels to direct specific ILC subset development as well as adapt ILC effector functions during infection, inflammation, and tissue regeneration. Interleukin-1β Selectively Expands and Sustains Interleukin-22+ Immature Human Natural Killer Cells in Secondary Lymphoid TissueHughes et al.ImmunityJune 25, 2010In BriefAmong human natural killer (NK) cell intermediates in secondary lymphoid tissue (SLT), stage 3 CD34−CD117+CD161+CD94− immature NK (iNK) cells uniquely express aryl hydrocarbon receptor (AHR) and interleukin-22 (IL-22), supporting a role in mucosal immunity. The mechanisms controlling proliferation and differentiation of these cells are unknown. Here we demonstrate that the IL-1 receptor IL-1R1 was selectively expressed by a subpopulation of iNK cells that localized proximal to IL-1β-producing conventional dendritic cells (cDCs) within SLT. Full-Text PDF Open Archive" @default.
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• W2016652854 date "2010-06-01" @default.
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• W2016652854 title "An IL-1β-Dependent Switch in Innate Mucosal Immunity?" @default.
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