ライフサイエンスコーパス: ILC

1 ILC cells exhibit anchorage-independent growth in ultra-

2 ILC depletion was associated with neutrophil infiltratio

3 ILC frequencies were lowest in HIV positive women who ex

4 ILC subsets expressed TNF receptor ligands, which limite

5 ILCs are also contributors of inflammatory diseases such

6 ILCs arise from lymphoid progenitors undergoing lineage

7 ILCs exhibit phenotypic and functional plasticity in res

8 ILCs from infected tissue that produced IFN-gamma also e

9 ILCs have been found at the maternal-fetal interface and

10 ILCs persisting in Mir142(-/-) mice demonstrated increas

11 ILCs were detected both in gingivitis and periodontitis.

12 e the current knowledge of mammalian group 1 ILC heterogeneity and propose new inclusive nomenclature

13 (miR-142) is a critical regulator of type 1 ILC biology.

14 egrates environmental cues for proper type 1 ILC homeostasis and defense against viral infection.

15 Specifically, group 1 ILCs (ILC1s) and group 3 ILCs (ILC3s) respond to infecti

16 ulatory ILC population distinct from group 1 ILCs (ILC1s), ILC2s, and ILC3s in (1) mice bred in our a

17 Mammalian group 1 ILCs are defined by the production of interferon (IFN)-g

18 hile recent studies demonstrate that group 1 ILCs consist of circulating mature natural killer (NK) c

19 human ILC1 and NK cells, comprising group 1 ILCs, is still elusive.

20 udy, it was found that liver-resident type 1 ILCs (ILC1s) expanded locally and persisted after the re

21 414 were upregulated in the infected type 1 ILCs and 128 in the infected type 2 ILCs.

22 virus genes were detected in infected type 1 ILCs and 27 in infected type 2 ILCs.

23 ostvaccination NKp44(+) and NKp44(+)IL-17(+) ILC frequencies were associated with delayed SIV acquisi

24 associated with a substantial loss of Type 2 ILC (ILC2) in the intestinal lamina propria.

25 pe 3 ILC-deficient mice compared with type 2 ILC-deficient mice.

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

27 After infection, type 2 ILCs expressed significantly higher levels of granulocyt

28 d type 1 ILCs and 128 in the infected type 2 ILCs.

29 fected type 1 ILCs and 27 in infected type 2 ILCs.

30 Th2) cells and innate lymphoid cells type 2 (ILCs), and increased airway smooth muscle mass via recru

31 bsence of type 1 and type 3, but not type 2, ILCs affects the survival of infected mice.

32 absence of type 1 or type 3, but not type 2, ILCs affects the survival of ocularly infected mice.IMPO

33 All 3 ILC populations expressed type 2 genes and induced airwa

34 and genes within intestinal type 1, 2, and 3 ILC subsets.

35 quency, trafficking, and function of group 3 ILC (ILC3) and NK cells using polychromatic flow cytomet

36 L6 as regulators affecting type 1 and type 3 ILC lineages.

37 ed survival of the infected type 1 or type 3 ILC-deficient mice compared with type 2 ILC-deficient mi

38 Type 1, type 2, and type 3 ILC-deficient mice were used to gain insights into the e

39 differed among the infected type 1, 2, and 3 ILCs in vitro While ILCs play no role or a redundant rol

40 Our results indicate that type 1, 2, and 3 ILCs respond differently to HSV-1 infection in vitro and

41 Using mouse models, we show that group 3 ILCs (ILC3s) accumulated rapidly in Mtb-infected lungs a

42 ecifically, group 1 ILCs (ILC1s) and group 3 ILCs (ILC3s) respond to infection with proliferation and

43 es negatively regulated RORgammat(+) group 3 ILCs (ILC3s), especially T-bet(+) ILC3s, and diminished

44 genes was seen in the HSV-1-infected type 3 ILCs, whereas 414 were upregulated in the infected type

45 s genes were detected in the infected type 3 ILCs, whereas only 11 herpesvirus genes were detected in

46 CL3, and CCL4 than infected type 1 or type 3 ILCs.

47 For 5 of 7 (71%) ILC patients, (18)F-FES PET/CT detected more metastatic

48 To determine how activated ILC cytokine production is regulated, ILC subsets were a

49 ction of both Helicobacter species activated ILCs and induced gut inflammation; however, these Helico

50 In addition, ILC frequencies in early pregnancy may serve as predicti

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

52 n of both IL-10Ralpha and TGF-betaR1 for all ILC subsets.

53 ed precursors with potential to generate all ILC subsets and natural killer (NK) cells, and also perm

54 Precursors to all ILC subsets (ILC precursors [ILCP]) have been identified

55 2, and Th17 cells are well characterized, an ILC subset strictly equivalent to IL-10-secreting regula

56 duced miR-142 expression, whereas global and ILC-specific miR-142-deficient mice exhibited a cell-int

57 Mucosal memory-like NK and ILC subsets in rectal and vaginal tissues of chronically

58 ulate IL-22 production by CD4(+) T cells and ILCs are not clear.

59 omote IL-22 production by CD4(+) T cells and ILCs through G-protein receptor 41 (GPR41) and inhibitin

60 ucing IL-22 production in CD4(+) T cells and ILCs to maintain intestinal homeostasis.

61 As ILC is nearly always (95%) estrogen receptor (ER)-positi

62 ay contribute to reported plasticity between ILC subsets.

63 rstanding of functional interactions between ILCs and the adaptive immune system, discuss limitations

64 The expression of IFN-gamma/TNF-alpha by ILCs and NK cells combined likely triggers a pathway tha

65 Invasive lobular carcinoma (ILC) accounts for 8%-14% of all breast cancer cases.

66 Invasive lobular carcinoma (ILC) demonstrates lower conspicuity on (18)F-FDG PET tha

67 Invasive lobular carcinoma (ILC) is a histological subtype of breast cancer with dis

68 e 2 ER/PR+ HER2- invasive lobular carcinoma (ILC).

69 f the phenotype of peripheral blood CD117(+) ILCs, which revealed the presence of three major subsets

70 was correlated with mucosal NKp44(+)CD16(+) ILCs.

71 xcessive activation of innate lymphoid cell (ILC) 2 during allergic lung inflammation.

72 are also required for innate lymphoid cell (ILC) development and maintenance, and consequently for g

73 vestigated NK cell and innate lymphoid cell (ILC) dynamics and function in rhesus macaque rectal tiss

74 oth the T cell and the innate lymphoid cell (ILC) lineages in mammals.

75 ective loss of group 3 innate lymphoid cell (ILC) number and function in a Dock8-deficient mouse mode

76 r flow cytometry human innate lymphoid cell (ILC) subsets can be detected in the circulation, in rela

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

78 Although innate lymphoid cells (ILC) and natural killer (NK) cells are found throughout

79 Innate lymphoid cells (ILC) are a heterogeneous family of immune cells regulati

80 Innate lymphoid cells (ILC) are lymphocytes that lack an antigen-specific recep

81 cells are a subset of innate lymphoid cells (ILC) capable of recognizing stressed and infected cells

82 , T cells, Tregs, and innate lymphoid cells (ILC) from peripheral blood using flow cytometry.

83 Innate lymphoid cells (ILC) play critical roles in regulating immunity, inflamm

84 Innate lymphoid cells (ILCs) and CD4(+) T cells produce IL-22, which is critica

85 tion of skin-resident innate lymphoid cells (ILCs) and modulation of sebaceous glands by a subset of

86 Innate lymphoid cells (ILCs) are critical for host defense and tissue repair bu

87 Innate lymphoid cells (ILCs) are enriched at barrier surfaces of the mammalian

88 Innate lymphoid cells (ILCs) are generated early during ontogeny and persist pr

89 ng the development of innate lymphoid cells (ILCs) are mostly unknown.

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

91 Innate lymphoid cells (ILCs) are strategically positioned at mucosal barrier su

92 Innate lymphoid cells (ILCs) are the most recently identified leukocytes of the

93 Innate lymphoid cells (ILCs) are tissue-resident lymphocytes categorized on the

94 Innate lymphoid cells (ILCs) are tissue-resident lymphocytes that promote immun

95 Innate lymphoid cells (ILCs) are tissue-resident sentinels that are essential f

96 Innate lymphoid cells (ILCs) consist of a heterogeneous family of lymphocytes t

97 Intestinal innate lymphoid cells (ILCs) contribute to the protective immunity and homeosta

98 Although innate lymphoid cells (ILCs) functionally analogous to T helper type 1 (Th1), T

99 Innate lymphoid cells (ILCs) guard epithelial tissue integrity during homeostas

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

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

102 an emerging group of innate lymphoid cells (ILCs) in health and disease.

103 r, the involvement of innate lymphoid cells (ILCs) in immune responses to infection with Mycobacteriu

104 ol the development of innate lymphoid cells (ILCs) in the bone marrow.

105 CRTH2(-)IL7Ralpha(-) innate lymphoid cells (ILCs) is unknown.

106 F-alpha]) produced by innate lymphoid cells (ILCs) located in the colon secondary to simian immunodef

107 Depleting group I innate lymphoid cells (ILCs) or infecting Trail(-/-) mice completely restored p

108 Although innate lymphoid cells (ILCs) play fundamental roles in mucosal barrier function

109 Innate lymphoid cells (ILCs) play important functions in immunity and tissue ho

110 Innate lymphoid cells (ILCs) play important roles in host defense and inflammat

111 e what roles, if any, innate lymphoid cells (ILCs) play in HSV-1 infection.

112 Innate lymphoid cells (ILCs) play strategic roles in tissue homeostasis and imm

113 Innate lymphoid cells (ILCs) promote tissue homeostasis and immune defense but

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

115 are cytotoxic type 1 innate lymphoid cells (ILCs) that defend against viruses and mediate anti-tumor

116 ohorts, we found that innate lymphoid cells (ILCs) were depleted in the blood and gut of people with

117 Innate lymphoid cells (ILCs) were originally classified based on their cytokine

118 endritic cells (DCs), innate lymphoid cells (ILCs), and natural killer (NK) cells.

119 all three subsets of innate lymphoid cells (ILCs), ILC1s, ILC2s and ILC3s, which is not reversed by

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

121 oduction from group 3 innate lymphoid cells (ILCs), whereas IL-6 administration during the late phase

122 tics of skin-resident innate lymphoid cells (ILCs).

123 garded as a subset of innate lymphoid cells (ILCs).

124 an important role for innate lymphoid cells (ILCs).

125 utant, is produced by innate lymphoid cells (ILCs).

126 covery of a family of innate lymphoid cells (ILCs): ILC1s, ILC2s, and ILC3s.

127 menclature parallel those of T helper cells, ILCs do not require adaptive immune programming.

128 arkedly expand current concepts of NK cells, ILCs, and their potential conversion.

129 periodontitis soft tissue and characterized ILC subsets including RANKL expression in single-cell su

130 An examination of circulating ILC subsets revealed surface expression of IL-10Ralpha a

131 ratory loads (inspiratory load compensation, ILC).

132 onal regulatory networks (TRNs) that control ILC function are largely unknown.

133 ha and DN ILCs were similar to that of CRTH2 ILCs in the blood and lung.

134 nscription factor reporter mice to delineate ILC precursor states by revealing the multifaceted expre

135 ce and relative proportions of the different ILC subsets (ILC1, ILC2 and ILC3) in gingivitis and peri

136 ed with HIV-1 infection irreversibly disrupt ILCs.

137 termines the fates and functions of distinct ILC progenitors.

138 metry for single-cell resolution of distinct ILC subsets.

139 red efforts to profile anatomically-distinct ILCs in humans.

140 iptomic analysis of CRTH2, IL7Ralpha, and DN ILCs confirmed the expression of mRNA for type 2 transcr

141 of type 2 cytokine-positive IL7Ralpha and DN ILCs were similar to that of CRTH2 ILCs in the blood and

142 fusion.Conclusions: The composition of donor ILC subsets is altered after allograft reperfusion and i

143 We predicted the "core" TFs driving ILC identities, organized TFs into cooperative modules c

144 l11b, Gata3, RORgammat, and RORalpha) during ILC development in the bone marrow.

145 ations killing 50% of the zebrafish embryos (ILC(50)) were calculated from the measured BCF and LC(50

146 astrointestinal listeriosis in mice, we find ILCs to be essential for control of early replication of

147 ry cytokine IL-10, raising the potential for ILC-mediated regulation of immune cells.

148 gamma chain-containing receptor required for ILC development, significantly reduced endometrial innat

149 at additional perturbations are required for ILC formation.

150 duced actomyosin relaxation was required for ILC initiation, but not progression.

151 r, these data illustrate a critical role for ILCs in the early responses to gastrointestinal infectio

152 nstrated that pulmonary ILC3s descended from ILC precursors that populated a niche defined by fibrobl

153 lasts or deletion of the IGF-1 receptor from ILC precursors interrupted ILC3 biogenesis and rendered

154 Furthermore, ILCs are dysregulated in multiple human diseases.

155 However, the percentage of IFN-gamma(+) ILCs in infected colons was 5- to 10-fold higher than th

156 C3 expansion and survival, and more globally ILC cytokine signaling and proliferation.

157 arrier functionality and tissue homeostasis, ILC-related mechanisms underlying intestinal barrier fun

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

159 Here, we examined how ILCs are maintained and renewed within tissues.

160 ive study of anchorage independence in human ILC cell lines provides mechanistic insights and clinica

161 at ID1 and ID3 expression is higher in human ILC tumors as compared to IDC, correlated with worse pro

162 donors, here we have provided a map of human ILC heterogeneity across multiple anatomical sites.

163 noikis resistance, herein we show that human ILC cell lines exhibit enhanced cell proliferation in UL

164 elated cell surface-expressed genes in human ILCs by RNA sequencing.

165 In contrast to mice, human ILCs are less strictly compartmentalized and tissue loca

166 tantly, CD62L expression was absent on human ILCs expressing NKp44 in tonsils and PB of Crohn disease

167 Recently, human ILCs that express CD117 and CD127 but lack CRTH2 and NKp

168 Group I ILCs are comprised of two subsets, conventional natural

169 specific, tissue-resident subset of group I ILCs.

170 Further, we investigated if ILCs express receptor activator of nuclear factor kappa-

171 atlas of lung ILC2s and found that Il18r1(+) ILCs comprise circulating and tissue-resident ILC progen

172 15 equally sustains wild-type and Il7ra(-/-) ILC survival in vitro and compensates for IL-7R deficien

173 and tissue localization selectively impacts ILC distribution in a subset-dependent manner.

174 ndow during ontogeny, may dominantly imprint ILC phenotypes in adult tissues.

175 recipients is associated with alterations in ILC subset composition within the allograft.Methods: We

176 er prospective trials of (18)F-FES PET/CT in ILC should be considered to evaluate ER-targeted imaging

177 -RSK pathways specifically in ULA culture in ILC cells.

178 family transcription factors ID1 and ID3 in ILC ULA culture, the knockdown of which diminished the a

179 and PI3K pathway activation via PTEN loss in ILC development.

180 ifferences in the survival rates of infected ILC-deficient mice and wild-type mice, there was signifi

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

182 Analysis of isolated ILCs in vitro revealed that all three subtypes could be

183 revealing the multifaceted expression of key ILC-associated transcription factors (Id2, Bcl11b, Gata3

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

185 In contrast, KLRG1(+) ILCs predominantly differentiate into ILC2s.

186 Epigenetic profiling of KLRG1(+) ILCs is consistent with the broad differentiation potent

187 ngle-cell cultures demonstrate that KLRG1(+) ILCs can also differentiate into other ILC subsets depen

188 chomatis, suggesting a role for group 3-like ILCs in endometrial innate immunity.

189 ory function of the responsible group 3-like ILCs was not dependent on the natural killer cell recept

190 e mutant, indicating a role for group 3-like ILCs.

191 colon by evading IFN-gamma from group 3-like ILCs.

192 In these locations ILC respond to tissue perturbations by producing factors

193 g the fate of LTi progenitors versus non-LTi ILC progenitors.

194 wever, whether changes in donor-derived lung ILC populations are associated with PGD development has

195 We studied human blood and lung ILCs from asthmatic and control subjects by flow cytomet

196 sing (18)F-FES PET/CT to evaluate metastatic ILC patients with synchronous (18)F-FDG and (18)F-FES PE

197 on of metastases in patients with metastatic ILC.

198 Moreover, ILC levels were reduced in pregnancies resulting in spon

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

200 he endometrial tissue, confirming that mouse ILCs contribute significantly to endometrial innate immu

201 ucosal NKp44(+) and suppress double-negative ILCs are likely desirable.

202 , whereas, NKG2A(-) NKp44(-) double-negative ILCs positively correlated with viral load, indicating a

203 We found protective type 3 NKp44(+) ILCs (ILC3s) to be significantly diminished in newly tra

204 n chronically SIV-infected animals, NKp44(+) ILCs negatively correlated with viral load, further sugg

205 Mucosal NKp44(+) ILCs increased postvaccination and returned to prelevels

206 Thus, the data suggest NKp44(+) ILCs and Deltagamma cells contribute to SIV infection ou

207 ths, whereas proinflammatory type 1 NKp44(-) ILCs (ILC1s) were higher.

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

209 les and transcriptome revealed that NKp46(+) ILCs predominantly develop into ILC3s; some of them can

210 Tuberculosis increased accumulation of ILC subsets in the human lung, coinciding with a robust

211 Proteomic comparison of ILC and IDC cell lines identified induction of PI3K/Akt

212 implications for metastatic dissemination of ILC and implicates ID1 and ID3 as novel drivers and ther

213 on variant of ASPP2 (t-ASPP2) as a driver of ILC in mice with mammary-specific loss of E-cadherin.

214 minished the anchorage-independent growth of ILC cell lines through cell cycle arrest.

215 nscriptional and functional heterogeneity of ILC progenitors, and studied the precursor-product relat

216 required for the function and maintenance of ILC subsets in humans.

217 tion and tissue adaptation as a mechanism of ILC maintenance and phenotypic diversification.

218 and identify STAT4 as a central modulator of ILC-mediated protection.

219 Changes in the percentage of ILC subsets with reperfusion or PGD (grade 3 within 72 h

220 TCF-1 promotes developmental progression of ILC precursors, while constraining their dendritic cell

221 actor 1 (IGF1) supports the proliferation of ILC precursors and protects from infection.

222 analysis identified two successive stages of ILC development within T cell factor 1-positive (TCF-1(+

223 cluded 92 patients, of whom 14 (15%) were of ILC histology.

224 kines with IL-22 is linked to the ability of ILCs to coexpress T-bet and RORgammaT/Ahr.

225 In this study, single-cell RNA analysis of ILCs isolated from inflamed tissues indicates that RORal

226 cells has provided a molecular definition of ILCs and their tissue-specific functions.

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

228 d functional similarities and differences of ILCs between the skin and other organs and highlight fut

229 he heterogeneity and functional diversity of ILCs, which have revealed striking similarities to T cel

230 Despite the low frequency of ILCs in circulation, ex vivo experiments have demonstrat

231 The main hallmark of ILCs is the functional loss of the cell-cell adhesion pr

232 Consequently, loss of ILCs resulted in sebaceous hyperplasia with increased pr

233 The majority of ILCs, in both conditions, were ILC1s.

234 t heterogeneity, and functional potential of ILCs in non-diseased human tissues.

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

236 Our discovery of the presence of ILCs both in gingivitis and periodontitis and concomitan

237 ient to predict the functional properties of ILCs.

238 A distinct subset of ILCs scored highly for a CGRP-specific gene signature af

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

240 Here we show that circulating subsets of ILCs are depleted from the blood of participants with pu

241 Here, we identified opposing effects on ILCs by two Helicobacter species, Helicobacter apodemus

242 No differences in NK cell or ILC frequencies or cytokine production were seen between

243 opment but is also highly expressed by other ILC subsets where its function remains poorly defined.

244 ILC common progenitor, which generates other ILC subsets and is defined by the expression of the tran

245 G1(+) ILCs can also differentiate into other ILC subsets depending on the signals they receive.

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

247 n between maternal HIV infection, peripheral ILC frequencies and preterm birth.

248 TH2(-)IL7Ralpha(-) type 2 cytokine-producing ILCs and their disease relevance.

249 th investigating whether IFN-gamma-producing ILCs also improve endometrial resistance to sexually tra

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

251 ct mechanisms through which t-ASPP2 promotes ILC initiation and progression.

252 ructed expansion and maturation of pulmonary ILC precursors.

253 Our findings suggest that reduced ILC frequencies may be a link between maternal HIV infec

254 ural killer cells and a trend toward reduced ILC populations, regardless of diagnosis (interstitial l

255 e TRNs suggest means to selectively regulate ILC effector functions, while our network approach is br

256 ivated ILC cytokine production is regulated, ILC subsets were activated in the presence or absence of

257 rn, adaptive immunity reciprocally regulates ILCs, which indicates that these interactions are a cruc

258 the role of the gut microbiota in regulating ILC development and maintenance still remains elusive.

259 port the absence of an intestinal regulatory ILC population distinct from group 1 ILCs (ILC1s), ILC2s

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

261 LCs comprise circulating and tissue-resident ILC progenitors (ILCP) and effector-cells with heterogen

262 have been originally found as liver-resident ILCs, their pathophysiological role in the liver remains

263 helia-derived signals maintain skin-resident ILCs that regulate microbial commensalism through sebace

264 our recent understanding of tissue-resident ILCs and the signals that regulate their contribution to

265 ly modulate the responses of tissue-resident ILCs has remained unclear.

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

267 The resulting ILC(50) were independent of external pH.

268 sebaceous glands by a subset of RORgammat(+) ILCs residing within hair follicles in close proximity t

269 tion of intestinal Th17- and IL-17-secreting ILCs.

270 icrobiota are critically involved in shaping ILC function.

271 emely large per cell quantities of signature ILC cytokines following activation.

272 , we discuss advances demonstrating how skin ILCs contribute to tissue homeostasis by regulating micr

273 striction and the development of specialized ILC subsets.

274 Precursors to all ILC subsets (ILC precursors [ILCP]) have been identified in human per

275 As such, ILCs function as a double-edged sword, balancing the inf

276 Therefore, we hypothesized that ILCs are key contributors to the early immune response i

277 However, emerging evidence indicates that ILCs also have a complex role in directly influencing th

278 Here, we show that ILCs isolated from mice can be infected with herpes simp

279 Overall, our findings show that ILCs may play a key role in regulating ITx graft homeost

280 ciated with PGD development, suggesting that ILCs may be involved in regulating lung injury in lung t

281 The ILC network revealed alternative-lineage-gene repression

282 owever, these cells are not derived from the ILC common progenitor, which generates other ILC subsets

283 ue monkeys and determined the make-up of the ILC subpopulations and the cytokines they expressed cons

284 n transcription factors greatly promotes the ILC fate while impairing B and T cell development.

285 during acute HIV-1 infection reproduced the ILC and NK cell abnormalities ex vivo.

286 riptome-sequencing (RNA-seq) analysis of the ILCs 24 h after HSV-1 infection revealed that 77 herpesv

287 sed to gain insights into the effects of the ILCs on the outcome of ocular HSV-1 infection.

288 However, these ILCs have not been extensively characterized.

289 ivo experiments have demonstrated that these ILCs release extremely large per cell quantities of sign

290 so associated with lower levels of all three ILC subsets in early pregnancy.

291 associated with reduced levels of all three ILC subsets.

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

293 ineage potential and enforcing commitment to ILC fate.

294 Sorted total ILCs from DOCK8- or STAT3-mutant patients and healthy co

295 Recent data suggest that a TSLP/ILC axis may mediate steroid resistance in asthma.

296 subsets and revealed hitherto unappreciated ILC precursor heterogeneity.

297 s highlights the importance of understanding ILC-regulated immunity for the design of future therapeu

298 nfected type 1, 2, and 3 ILCs in vitro While ILCs play no role or a redundant role in the outcomes of

299 th worse prognosis uniquely in patients with ILC and associated with upregulation of angiogenesis and

300 Seven of 14 patients with ILC had (18)F-FDG PET/CT performed within 5 wk of the re