ライフサイエンスコーパス: ILC

1 ILC numbers were preserved by antiretroviral therapy (AR

2 ILC-driven colitis depends on production of granulocyte

3 ILCs act as early orchestrators of immunity, responding

4 ILCs consist of conventional natural killer cells and he

5 ILCs contained detectable amounts of the transcription f

6 ILCs might also represent promising targets in the conte

7 ILCs present in the intestine also enter and exit crypto

8 ILCs were isolated and analyzed by flow cytometry.

9 ice, we identify a subset of adipose group 1 ILC (ILC1) and demonstrate a role for these cells in met

10 f the entire lymphoid and nonlymphoid type 1 ILC compartment appears to require the semiredundant act

11 s across the lymphoid and nonlymphoid type 1 ILC compartments.

12 l mediators of mucosal immunity, and group 1 ILCs (ILC1 cells) and group 3 ILCs (ILC3 cells) have bee

13 GR expression in group 1 ILCs is required to limit their IFN-gamma production, th

14 e-specific cis-regulatory element in group 1 ILCs that is demarcated by a long non-coding RNA.

15 ther with ILC1s, NK cells constitute group 1 ILCs, which are characterized by their capacity to produ

16 the function and lineage identity of group 1 ILCs, while being dispensable for early ILC development

17 ter of its neighboring gene, Id2, in group 1 ILCs.

18 In this Review, we focus on how group 2 ILC (ILC2) and group 3 ILC (ILC3) responses are regulate

19 s injury promotes an IL-33-dependent group 2 ILC (ILC2) response and that abrogation of this response

20 group 3 ILC, but not CD4(-) ILC1 or group 2 ILC, are increased in the peripheral blood of individual

21 Recently, group 2 ILCs (ILC2s) were found to promote the development and e

22 particular, IL-5- and IL-13-producing type 2 ILCs (ILC2s) have been implicated in repair mechanisms t

23 focus on how group 2 ILC (ILC2) and group 3 ILC (ILC3) responses are regulated and how these cells i

24 quencies of CD4(+) ILC1 and NKp44(+) group 3 ILC, but not CD4(-) ILC1 or group 2 ILC, are increased i

25 adult intestine, NK cells and group 2 and 3 ILCs were severely reduced.

26 y, and group 1 ILCs (ILC1 cells) and group 3 ILCs (ILC3 cells) have been shown to be functionally pla

27 s highly expressed in the nucleus of group 3 ILCs (ILC3s).

28 t3L increased the number of NKp46(-) group 3 ILCs in wild-type and even in Il7(-/-) mice, which gener

29 -17(+) cells were almost exclusively group 3 ILCs.

30 )) cells had markers consistent with group 3 ILCs.

31 mphocytes, PD-1 was upregulated on activated ILCs.

32 5 neutralizing Ab, or a depleting Ab against ILCs, can both effectively reduce intestinal eosinophili

33 All ILC subsets are functionally competent in vitro, and are

34 Human ILCPs robustly generate all ILC subsets in vitro and in vivo.

35 the fitness of the common progenitor of all ILCs.

36 Although ILCs have been extensively studied in model organisms, l

37 EILPs, all-lymphoid progenitors (ALPs), and ILC precursors (ILCps).

38 development and functions of CD4 T cell and ILC subsets and then summarize recent literature on quan

39 tified 20 and 4 supermodules for ER+/ER- and ILC/IDC comparisons, respectively.

40 c mice, we found that both ILC-intrinsic and ILC-extrinsic factors were responsible for this ILC dysr

41 five training and three testing studies, and ILC/IDC comparison with two training and two testing stu

42 Both CD4 T cells and ILCs can be classified into distinct lineages based on t

43 strictly required for the development of any ILC subset, as residual cells persist in the small intes

44 This effect occurred independently of DCs as ILC numbers were normal in mice in which DCs were consti

45 Diet-induced obesity impaired AT1-ILC killing ability.

46 Adipose type 1 innate lymphoid cells (AT1-ILCs) promote pro-inflammatory macrophages in obesity, b

47 Our findings reveal a role for AT1-ILCs in regulating ATM homeostasis through cytotoxicity

48 Depletion of AT1-ILCs and perforin deficiency resulted in alterations in

49 lammatory ATMs, and adoptive transfer of AT1-ILCs exacerbated metabolic disorder.

50 (HFD) showed differential trafficking of AT1-ILCs, particularly in response to short- and long-term H

51 ssue harbor heterogeneous populations of AT1-ILCs.

52 At steady state, AT1-ILCs displayed cytotoxic activity toward adipose tissue

53 However, because ILCs are finely tuned to perturbations within tissue mic

54 of a selective functional connection between ILC and the posteromedial portions of the VTA (pmVTA) an

55 o better understand the relationship between ILC subsets and their Th cell counterparts, we measured

56 ution and propose how the connection between ILCs and T cells contributes to the robustness of immuni

57 has demonstrated that the crosstalk between ILCs and their environment has a significant impact on h

58 es currently recognized to be shared between ILCs and T cells.

59 We found that human blood ILCs were severely depleted during acute viremic HIV-1 i

60 one marrow chimeric mice, we found that both ILC-intrinsic and ILC-extrinsic factors were responsible

61 bacterial uptake and killing is enhanced by ILC production of IL-17A, indicating that innate lymphoc

62 Invasive lobular carcinoma (ILC) is the second most common breast cancer subtype and

63 Invasive lobular carcinoma (ILC) is the second most frequently occurring histologica

64 CCR10(+) ILCs promoted the homeostasis of skin-resident T cells a

65 gramming and priming of skin-homing CCR10(+) ILCs in the sLNs.

66 quired for the proper generation of CCR10(+) ILCs.

67 human CD56(bright) cells and mouse CD127(+) ILC, or conserved networks of transcriptional regulation

68 D27(-)CD4(+) cells and innate lymphoid cell (ILC) 2 from patients with grass pollen allergy by using

69 l progenitor (ETP) and innate lymphoid cell (ILC) development remains unclear.

70 Commitment to the innate lymphoid cell (ILC) lineage is determined by Id2, a transcriptional reg

71 ation specified toward innate lymphoid cell (ILC) lineages, but their relationship with other describ

72 Little is known about innate lymphoid cell (ILC) populations in the human gut, and the turnover of t

73 ent of tissue-resident innate lymphoid cell (ILC) subsets.

74 Innate lymphoid cell (ILCs) subsets differentially populate various barrier an

75 Innate lymphoid cells (ILC) are a heterogeneous group of cellular subsets that

76 ntain tissue-resident innate lymphoid cells (ILC) in different microenvironments are incompletely und

77 Innate lymphoid cells (ILC) play an important role in many immune processes, in

78 ulates the balance of innate lymphoid cells (ILC), a diverse class of lymphocytes that are poised to

79 pecifically Th cells, innate lymphoid cells (ILC), and gammadelta T cells.

80 ly, several groups of innate lymphoid cells (ILC), distinct from NK cells in development and function

81 Group 2 innate lymphoid cells (ILC-2s) regulate immune responses to pathogens and maint

82 regulator of group 2 innate lymphoid cells (ILC-2s).

83 Innate lymphoid cells (ILCs) 'preferentially' localize into barrier tissues, wh

84 vely expressed in all innate lymphoid cells (ILCs) and is required for their development.

85 relationship between innate lymphoid cells (ILCs) and lymphoid tissue-inducer (LTi) cells is poorly

86 Innate lymphoid cells (ILCs) are a family of immune effector cells that have im

87 Innate lymphoid cells (ILCs) are a family of innate immune cells that have dive

88 Innate lymphoid cells (ILCs) are a new family of immune cells that play importa

89 Innate lymphoid cells (ILCs) are a recently identified population of immune cel

90 Innate lymphoid cells (ILCs) are critical mediators of mucosal immunity, and gr

91 Innate lymphoid cells (ILCs) are emerging as important regulators of homeostati

92 Innate lymphoid cells (ILCs) are important regulators in various immune respons

93 Innate lymphoid cells (ILCs) are increasingly acknowledged as important mediato

94 Innate lymphoid cells (ILCs) are innate immune cells that are ubiquitously dist

95 Innate lymphoid cells (ILCs) are known as first responders to infections and as

96 Innate lymphoid cells (ILCs) are rapidly-responding cells that are functionally

97 Innate lymphoid cells (ILCs) are the most recently discovered group of immune c

98 Innate lymphoid cells (ILCs) are tissue-resident "first responders" of the immu

99 Innate lymphoid cells (ILCs) are tuned to quickly respond to and amplify tissue

100 that IL-7R-dependent innate lymphoid cells (ILCs) block LIP of CD8(+) T cells in neonatal but not ad

101 Innate lymphoid cells (ILCs) communicate with other haematopoietic and non-haem

102 Innate lymphoid cells (ILCs) contribute to host defence and tissue repair but c

103 ts role in regulating innate lymphoid cells (ILCs) during fetal and adult life is not understood.

104 Innate lymphoid cells (ILCs) function to protect epithelial barriers against pa

105 Innate lymphoid cells (ILCs) functionally resemble T lymphocytes in cytotoxicit

106 lar, the discovery of innate lymphoid cells (ILCs) has opened entirely new avenues for research.

107 Innate lymphoid cells (ILCs) have an important role in the immune system's resp

108 Innate lymphoid cells (ILCs) have been classified into "functional subsets" acc

109 In recent years, innate lymphoid cells (ILCs) have emerged as innate correlates to T cells.

110 ential involvement of innate lymphoid cells (ILCs) in allergic airway disease exacerbation caused by

111 ted the importance of innate lymphoid cells (ILCs) in multiple immune responses.

112 et-dependent NKp46(+) innate lymphoid cells (ILCs) in the initiation of CD4(+) TH17-mediated neuroinf

113 Innate lymphoid cells (ILCs) patrol environmental interfaces to defend against

114 Innate lymphoid cells (ILCs) play critical roles in immune homeostasis and immu

115 d recently identified innate lymphoid cells (ILCs) play important roles in host defense and inflammat

116 Innate lymphoid cells (ILCs) play key roles in host defense, barrier integrity,

117 Recent findings that innate lymphoid cells (ILCs) regulate adaptive T cell responses led us to exami

118 Innate lymphoid cells (ILCs) represent innate versions of T helper and cytotoxi

119 he development of all innate lymphoid cells (ILCs) that express the interleukin 7 receptor alpha-chai

120 nv)-dependent mucosal innate lymphoid cells (ILCs) that produce interleukin (IL)-17, as well as with

121 acteristics of sorted innate lymphoid cells (ILCs) were defined by using quantitative PCR.

122 Additionally, innate lymphoid cells (ILCs), important producers of cytokines necessary for in

123 mal identification of innate lymphoid cells (ILCs), increased the understanding of their tissue distr

124 ts directly on type 3 innate lymphoid cells (ILCs), promoting their homeostasis and driving them to p

125 y deleted in NKp46(+) innate lymphoid cells (ILCs), we demonstrated a major role for the HPA pathway

126 , comprised mainly of innate lymphoid cells (ILCs); approximately 90% of IL-17-producing (IL-17(+)) c

127 in chronic disease and remaining circulating ILCs were activated but not apoptotic.

128 overpris et al. (2016) find that circulating ILCs are lost early and irreversibly during HIV infectio

129 ic T cells that differentiate from committed ILC precursors (ILCPs).

130 m of dopamine control, through a concomitant ILC-mediated activation of the pmVTA.

131 we found that under steady-state conditions, ILCs in skin-draining lymph nodes (sLNs) were continuous

132 nic mice, we demonstrate that Flt3L controls ILC numbers by regulating the pool of alpha4beta7(-) and

133 s generally assumed that infralimbic cortex (ILC) and prelimbic cortex, two adjacent areas of the med

134 l connection between the infralimbic cortex (ILC) and the posteromedial portions of the ventral tegme

135 Cells were further stained to define ILC subsets and a donor-specific or recipient-specific H

136 ated tissue specifications of Rorc-dependent ILCs across lymphoid and nonlymphoid organs.

137 Our findings demonstrate that donor-derived ILCs persist long-term after transplantation and support

138 Donor-derived ILCs were found to persist greater than 8 years after tr

139 but their relationship with other described ILC progenitors is still unclear.

140 suggest that environmental cues can dictate ILC phenotype and function for these tissue-resident inn

141 s, revealing common features among different ILC subsets as well as important distinctions.

142 port a model of tissue ILC differentiation ("ILC-poiesis"), whereby diverse ILC subsets are generated

143 erentiation ("ILC-poiesis"), whereby diverse ILC subsets are generated in situ from systemically dist

144 be lymphoid tissue inducer cells among donor ILCs was far higher than that among recipient ILCs.

145 verview of the molecular alterations driving ILC and have explored links with therapy response.

146 Increasing evidence implicates dysregulated ILC responses as drivers of disease pathogenesis in mult

147 Yet how Id2 expression is regulated in each ILC subset remains poorly understood.

148 ponsive to extracellular cues unique to each ILC subset represent a key regulatory layer for controll

149 up 1 ILCs, while being dispensable for early ILC development and homeostasis of ILC2s and ILC3s.

150 ement of transcription factors key for early ILC development.

151 phenotype, lymphoid tissue-derived Rorc(fm+) ILCs acquire an natural killer (NK) cell/ILC1-like pheno

152 that only lymphoid-tissue resident Rorc(fm+) ILCs can suppress tumor growth, whereas intestinal Rorc(

153 By adoptively transferring Rorc(fm+) ILCs into recipient mice, we show that ILCs distribute a

154 ntestinal Rorc fate map-positive (Rorc(fm+)) ILCs show a clear ILC3 phenotype, lymphoid tissue-derive

155 transcription factors, is indispensable for ILC differentiation.

156 ison, and 'extracellular matrix pathway' for ILC/IDC comparison.

157 tations in additional genes are required for ILC formation in mice.

158 that have not been previously described for ILCs.

159 factor inhibitor ID2, a critical factor for ILCs, and these cells were unable to expand in cytokine-

160 stimulation of glutamatergic terminals from ILC.

161 of ILCs and transcription factors that guide ILC lineage specification and commitment.

162 ght into the molecular mechanisms that guide ILC migration into peripheral tissues, revealing common

163 tration of a PD-1 antibody depleted PD-1(hi) ILCs and reduced cytokine levels in an influenza infecti

164 ssue and systemic metabolism, as well as how ILC biology can be regulated by environmental changes in

165 We also highlight studies showing how ILC-intrinsic metabolism influences their activation, pr

166 cytokine production of both mouse and human ILC-2s.

167 ental signals and pathways involved in human ILC development.

168 3BP2 were also frequently aberrated in human ILC, highlighting these genes as drivers of a novel onco

169 tumors of which the majority resembled human ILC in terms of morphology and gene expression.

170 ddition, the growing complexity of the human ILC family in terms of previously unrecognized functiona

171 Although the majority of human ILCs are characterized by the functional loss of E-cadhe

172 view on the function and plasticity of human ILCs in tissue homeostasis and disease.

173 slowly unraveling, the development of human ILCs is far from understood.

174 Our analysis shows that human ILCs are highly heterogeneous cell types between individ

175 15 equally sustains wild-type and Il7ra(-/-) ILC survival in vitro and compensates for IL-7R deficien

176 among transcription factors known to impact ILC or NK cell development, GATA3, TCF7 (TCF-1), AHR, SO

177 e the most frequent molecular alterations in ILC.

178 ently higher uptake of (18)F-fluciclovine in ILC requires confirmation in a larger cohort.

179 ion of an epigenetic regulatory mechanism in ILC development and function.

180 e coordination with T-bet, another key TF in ILC biology.

181 effector genes is selectively accessible in ILCs prior to high-level transcription upon activation.

182 A recent study reveals how inflammatory ILC responses can be suppressed by a newly defined subse

183 entral node in the TF network that instructs ILC development, homeostasis, and function and provide m

184 Increase in KLRG1(+) ILC-2 cell numbers was attributed to an intrinsic defect

185 ing PD-1 with an antibody increased KLRG1(+) ILC-2 cell number and reduced disease burden.

186 an important negative regulator of KLRG1(+) ILC-2 function in both mice and humans.

187 fection, a significant expansion of KLRG1(+) ILC-2 subsets occurred in Pdcd1(-/-) mice and, upon adop

188 the number, and hence function, of KLRG1(+) ILC-2s.

189 upon adoptive transfer, Pdcd1(-/-) KLRG1(+) ILC-2s significantly reduced worm burden.

190 T5 is critical for accumulation of all known ILC subsets in mice and reveal a hierarchy of STAT5 depe

191 unique in its ability to generate all known ILC subsets, including natural killer (NK) cells, but no

192 All type 1 innate lymphocytes (ILCs) express the transcription factor T-bet, but cNKs a

193 current paradigm states that all newly made ILCs originate from common lymphoid progenitors in the b

194 at IL-33 receptor-positive ILC2s are a major ILC subtype in the kidney of humans and mice.

195 Three major ILC subsets are recognized in mice and humans.

196 Notably, many ILC functions appear to be regulated by mechanisms disti

197 man peripheral blood NK cells and all mature ILC populations expressed RORgammat.

198 tion of Rorc (encoding ROR-gammat) in mature ILCs also did not impair cytokine response in the steady

199 ption factors and cytokine outputs of mature ILCs but have these signature loci in an epigenetically

200 For 1-alkyl-3-methylimidazolium ILCs, linear correlations of ionic volumes with the occu

201 A signature of genes present in mouse ILC except NK cells, defined by Immunological Genome Pro

202 Deletion of mouse ILC-intrinsic Arg1 abrogated type 2 lung inflammation by

203 Although the ontogeny of mouse ILCs is slowly unraveling, the development of human ILCs

204 Whether RAS activation, mucosal ILCs and antibodies to V2 are also important hallmarks o

205 t a foreign Ag are not inhibited by neonatal ILCs.

206 detrimental role of T-bet-dependent NKp46(+) ILCs in the development of CNS autoimmune disease.

207 T-bet-dependent NKp46(+) ILCs localized in the meninges and acted as chief coordi

208 Loss of T-bet specifically in NKp46(+) ILCs profoundly impaired the ability of myelin-reactive

209 e the current knowledge on the appearance of ILC subsets during evolution and propose how the connect

210 intense study has elucidated many aspects of ILC development, phenotype, and function, numerous chall

211 These effects were a direct consequence of ILC-intrinsic RA signaling, because retinoic acid-relate

212 ntal trajectory and signalling dependence of ILC progenitors are not fully understood.

213 , comprehensive, and detailed description of ILC heterogeneity in humans across patients and tissues.

214 ular processes that drive the development of ILC are still largely unknown.

215 right) cells show preferential expression of ILC-associated IL7R (CD127), TNFSF10 (TRAIL), KIT (CD117

216 , numerous challenges remain in the field of ILC biology.

217 Positive regulation of ILC-2s through ICOS has been recently elucidated.

218 ionally provides new candidate regulators of ILC development and clearly defines the stage of require

219 acterization may help to tailor treatment of ILC through the application of specific targeted, chemo-

220 cent studies that demonstrate the ability of ILCs to influence tissue and systemic metabolism, as wel

221 s have hampered adequate characterization of ILCs in humans.

222 been used to delineate the contributions of ILCs versus those of T cells and review the current unde

223 Furthermore, depletion of ILCs with an anti-CD90 antibody, followed by T-cell reco

224 d, thus paving the way to rational design of ILCs by combining suitably sized ions.

225 and to suppress the aberrant development of ILCs, including ILC2s and lymphoid-tissue-inducer-like c

226 stine and in the spatio-temporal dynamics of ILCs in the intestinal inflammatory response.

227 studies that have elucidated the effects of ILCs on the maintenance of tissue homeostasis and the co

228 echanisms that regulate the establishment of ILCs in barrier tissues are poorly understood.

229 ays that control development and function of ILCs, the epigenetic mechanisms that regulate ILC biolog

230 for controlling the identity and function of ILCs.

231 s important to understand which functions of ILCs are specialized and which are redundant with those

232 rature regarding the regulatory functions of ILCs in adaptive immunity, and suggest that lung ILC2s p

233 n and has established essential functions of ILCs in diverse physiological processes.

234 ding of the specialized in vivo functions of ILCs.

235 c impairment in GVHD associated with loss of ILCs could be improved by restoration of IL-22 signaling

236 ice, which generally have reduced numbers of ILCs.

237 L-23, have been shown to shape plasticity of ILCs, little is known about how the tissue microenvironm

238 ed us to examine the regulatory potential of ILCs in the context of cancer.

239 view we discuss the developmental program of ILCs and transcription factors that guide ILC lineage sp

240 ient to predict the functional properties of ILCs.

241 owever, our current knowledge on the role of ILCs in humoral immunity is limited.

242 nnate lymphoid cells (ILC2s) are a subset of ILCs that play a protective role in the response to helm

243 n be suppressed by a newly defined subset of ILCs with regulatory function.

244 Subsets of ILCs have phenotypes that mirror those of polarized help

245 ighted the impact of tissue-specific cues on ILC migration, and the importance of the local immunolog

246 at the frequency of IL-6Ralpha expression on ILC is altered in SSc.

247 ing the impact of tissue microenvironment on ILC development.

248 central to pathology, the impact of HIV-1 on ILCs remains unknown.

249 iagnosis of locally advanced IDC (n = 19) or ILC (n = 8) underwent PET/CT of the chest after intraven

250 ros expression than ILC precursors and other ILC subsets.

251 those of natural killer (NK) cells and other ILCs.

252 both modalities available (n = 14), primary ILCs (n = 4) demonstrated (18)F-fluciclovine avidity (me

253 is a key orchestrator of cytokine-producing ILC responses during viral infection via ILC-extrinsic r

254 tionally, the percentages of IL-22-producing ILCs were reduced in the absence of dietary vitamin A.

255 n factors to accurately identify and profile ILCs across healthy and inflamed tissue types.

256 e-like B cells (NKB) induce these protective ILC responses.

257 natural killer (NK) cells, the prototypical ILC subset, and provide a systems-based molecular ration

258 LCs was far higher than that among recipient ILCs.

259 Regarding ILC-extrinsic mechanisms, we found that STAT1-deficient

260 LCs, the epigenetic mechanisms that regulate ILC biology are unknown.

261 Notably, the presence of these regulatory ILCs in TIL cultures corresponded with a striking reduct

262 es abrogated the ability of these regulatory ILCs to suppress T cell expansion.

263 However, the presence of renal ILCs in humans has not been reported.

264 ecular cues, we profiled mouse lung-resident ILCs using single-cell RNA sequencing at steady state an

265 ow ILCPs give rise to mature tissue-resident ILCs remains unclear.

266 detailed characterization of kidney-residing ILC populations revealed that IL-33 receptor-positive IL

267 ompensates for IL-7R deficiency, as residual ILCs are depleted in mice lacking both molecules.

268 loping field that showcase the critical role ILCs play in directing immune responses through their ab

269 Thus, TGF-beta induces SG ILC differentiation by suppressing Eomes.

270 Finally, TGF-beta imprinting of SG ILCs was synchronized with SG development, highlighting

271 Transcriptome analysis demonstrated that SG ILCs had characteristic of both NK cells and ILC1.

272 Salivary gland (SG) ILCs as well as liver and intestinal intraepithelial ILC

273 ation of infralimbic cortex-accumbens shell (ILC-NAc shell) inputs or treatment with the antibiotic,

274 llectively, these data demonstrate that siLP ILCs are not completely IL-7R dependent, but can persist

275 tinal ILC3s had lower Ikaros expression than ILC precursors and other ILC subsets.

276 uring acute viremic HIV-1 infection and that ILC numbers did not recover after resolution of peak vir

277 The results demonstrate that ILC excitatory afferents directly modulate the extracell

278 In this study, we show that ILC populations are present in the healthy human kidney.

279 (fm+) ILCs into recipient mice, we show that ILCs distribute among various organs and phenotypically

280 arly ART administration protects against the ILC loss, and this might be clinically beneficial to HIV

281 ace marker and cytokine expression among the ILC subsets that may further delineate their migration a

282 elease from glutamatergic terminals from the ILC exert a significant modulation of extracellular conc

283 lls represent the prototypical member of the ILC family.

284 ent mechanisms of the differentiation of the ILC lineage and LTi cell lineage and establish a high-re

285 progenitors become committed to each of the ILC lineages further underscores the relationship betwee

286 Disruption of the ILC-IL-22 axis impairs PGE2-mediated inhibition of syste

287 Manipulation of the ILC-IL-22-TEC axis may be useful for augmenting immune r

288 orchestrated T cell fate and suppressed the ILC transcription signature by activating the expression

289 How these ILC lineages develop and are maintained is not clear.

290 This ILC-based inhibition of LIP ensures the generation of a

291 -extrinsic factors were responsible for this ILC dysregulation during viral infection in STAT1-defici

292 is review we discuss the impact of the three ILC subsets and the signature cytokines they release on

293 lls and inhibiting the elimination of thymic ILCs improved thymopoiesis in an IL-22-dependent fashion

294 Our results support a model of tissue ILC differentiation ("ILC-poiesis"), whereby diverse ILC

295 together, Flt3L significantly contributes to ILC and Peyer's patches development by targeting lymphoi

296 emonstrate that a previously uncharacterized ILC population regulates the activity and expansion of t

297 vers of a novel oncogenic pathway underlying ILC development.

298 We identified a unique ILC population that inhibits tumor-infiltrating lymphocy

299 utamate release (in vivo microdialysis) upon ILC electrical stimulation.

300 ing ILC responses during viral infection via ILC-extrinsic regulation of IL-33 and IL-23.