ライフサイエンスコーパス: ILC1

1 ILC1 subsets may contribute to the inflammatory bowel di

2 ILC1 were found to be the major TRAIL expressers during

3 ILC1, ILC2, and ILC3 cells were cultured for 5 days with

4 ILC1-derived interferon-gamma was necessary and sufficie

5 ILC1-like NK cells showed splenic residency and strong c

6 ILC1s acquired stable transcriptional, epigenetic and ph

7 ILC1s are enriched in tissues and hence generally consid

8 ILC1s produced interferon-y (IFN-y) in the absence of in

9 e inducer (LTi), and innate lymphoid cell 1 (ILC1) cells, but not ILC2 or ILC3 cells, were enriched i

10 involvement of innate lymphoid cells-type 1 (ILC1) in the pathogenesis of alopecia areata (AA), becau

11 s, liver innate lymphoid cells (ILC) type 1 (ILC1s) have been shown to represent a distinct lineage t

12 mpairs thymic generation of CCR10(+)NK1.1(+) ILC1s at adult, but not perinatal, stages.

13 nals promotes generation of CCR10(+)NK1.1(+) ILC1s from hematopoietic progenitors.

14 troma impairs generation of CCR10(+)NK1.1(+) ILC1s in adult thymi, but development of CCR10(+)NK1.1(+

15 t thymi, but development of CCR10(+)NK1.1(+) ILC1s in neonatal thymi is less dependent on Delta-like

16 ession of the IL-7R CD127 on thymic NK1.1(+) ILC1s, and deficiency of CD127 also impairs thymic gener

17 Interferon gamma produced by activated ILC1 is critical to licence CD11b(+)Ly6C(+) monocyte pro

18 ry cytokines IL-10 and TGF-beta on activated ILC1 and ILC2 populations ex vivo.

19 Ex vivo activated ILC1 and ILC2 subsets were also found to be a source of

20 Activated ILC1s produced interferon-gamma (IFN-gamma) and protecte

21 IFN-gamma released from activated ILC1s promoted the survival of hepatocytes through upreg

22 oride (CCl(4)) injection into mice activated ILC1s, but not natural killer (NK) cells, in the liver.

23 Reconstruction of the adipose ILC1 population in Prkdc(-/-)IL2rg(-/-) mice by adoptive

24 Adipose ILC1s were dependent on the transcription factors Nfil3

25 -culture experiments show that human adipose ILC1s promote adipose fibrogenesis and CD11c(+) macropha

26 Here we show that the number of adipose ILC1s increases in obese T2D patients and correlates wit

27 sis of parabiotic mice revealed that adipose ILC1s maintained long-term tissue residency.

28 While SMAD4 deficiency did not affect ILC1 differentiation, NK cells unexpectedly acquired an

29 Although all ILC1 subsets shared characteristics with Th1 cells, CD4(

30 An ILC1 gene signature also predicted survival of a subset

31 entiation, NK cells unexpectedly acquired an ILC1-like gene signature and were unable to control tumo

32 stered within inflamed areas and acquired an ILC1-like phenotype.

33 ty in the propensity of NK cells to adopt an ILC1-like phenotype in culture, characterized by the ste

34 nabled the conversion of these cells into an ILC1 phenotype in response to IL-12.

35 Interestingly, the adoption of an ILC1-like phenotype was independent of the effect of IL-

36 the conversion of circulating NK cells to an ILC1-like phenotype and have clarified the pathways resp

37 Full differentiation to an ILC1-like population required the additional loss of ROR

38 Genetic ablation of both NK cells and ILC1 (NK/ILC1(Delta) mice) led to reduced early IFNgamma

39 ersial whether natural killer (NK) cells and ILC1 cells are distinct cell types.

40 footpad infection, natural killer cells and ILC1 cells both limited joint colonization by Brucella.

41 that lack ICER specifically in NK cells and ILC1 phenocopied the worsened disease outcome of Icer(-/

42 ILCs had characteristic of both NK cells and ILC1.

43 cape accompanying CCR6- ILC3 development and ILC1 conversion solidified c-Maf as a gatekeeper of type

44 hemokines CXCL9/CXCL10, which recruit NK and ILC1 cells into the brain in a CXCR3-dependent manner.

45 NK cells and ILC1s are developmentally distinct but share so many fea

46 , we show in this article that cNK cells and ILC1s are dispensable for initiation and progression of

47 NK cells and ILC1s both require the transcription factor T-bet for li

48 Despite their shared features, NK cells and ILC1s display profound differences among various tissue

49 However, neither depletion of cNK cells and ILC1s in NKT cell-deficient mice nor specific genetic de

50 distinct from both steady-state NK cells and ILC1s in uninfected mice.

51 Because NK cells and ILC1s share a common precursor (ILCP), we asked if AML a

52 files, placing natural killer (NK) cells and ILC1s together, but recent studies support their separat

53 NK cells and ILC1s were functionally impaired, with reduced cytotoxic

54 lymphoid cells (ILCs) encompass NK cells and ILC1s, which have non-redundant roles in host protection

55 In the present study we found that ILC3s and ILC1s in human tonsils represented the ends of a spectru

56 ILCs are traditionally classified as ILC1, ILC2 or ILC3 on the basis of their expression of s

57 oups of innate lymphoid cells (ILCs) such as ILC1, ILC2, and ILC3 populate the intestine, but how the

58 (P = 0.001), while in patients with asthma, ILC1s increased from baseline at Day 8 (P = 0.042).

59 on skewing with the infiltration of atypical ILC1 secreting inflammatory cytokines but reduced levels

60 tor GATA-3 and a concomitant switch to being ILC1 cells that produced interferon-gamma (IFN-gamma).

61 s were also differentially expressed between ILC1s and cNKs, indicating that PLZF together with other

62 Peripheral blood ILC1-3 subsets of 16 DOCK8-deficient patients recruited

63 -resident ILC1, IFN-gamma production by both ILC1 and cNK was minimal at this site of viral persisten

64 Both ILC1s and NK cells are essential for rapid responses aga

65 ICER expression by ILC1 promotes recruitment of IFNgamma(+) ILC1 in Leishma

66 iferative and IFN-gamma effector response by ILC1s and ILC3s, and loss of STAT4 signaling in the inna

67 1 in a unique cell population, which we call ILC1-like NK cells; during viral infection, Zfp683 was i

68 hared characteristics with Th1 cells, CD4(+) ILC1 also demonstrated significant phenotypic and functi

69 We also show that the frequencies of CD4(+) ILC1 and NKp44(+) group 3 ILC, but not CD4(-) ILC1 or gr

70 rmore, we demonstrate that CD4(+) and CD4(-) ILC1 are functionally divergent based on their IL-6Ralph

71 and functional features of CD4(+) and CD4(-) ILC1 suggest that they may have differing roles in the p

72 LC1 and NKp44(+) group 3 ILC, but not CD4(-) ILC1 or group 2 ILC, are increased in the peripheral blo

73 al killer (NK)/group 1 innate lymphoid cell (ILC1)-like NKp46(+) cells in the thymus and reduction in

74 to convert to a type 1 innate lymphoid cell (ILC1)-like phenotype in response to TGF-beta exposure.

75 m+) ILCs acquire an natural killer (NK) cell/ILC1-like phenotype.

76 AIL-expressing innate lymphoid type I cells (ILC1) but not conventional NK cells.

77 referred to as innate lymphoid type I cells (ILC1).

78 natural killer cells and helper-like cells (ILC1, ILC2 and ILC3).

79 ) derived from type 1 innate lymphoid cells (ILC1) enhances the migration of imNeu, but not mature ne

80 issue-resident type 1 innate lymphoid cells (ILC1) serve an essential early role in host immunity thr

81 3(-) NK1.1(+) group 1 innate lymphoid cells (ILC1) within the FRT, essential for recruitment of CD8(+

82 e recently identified innate lymphoid cells (ILC1, ILC2, and ILC3), and innate-like lymphocytes, incl

83 Group 1 innate lymphoid cells (ILC1s) are cytotoxic and interferon gamma-producing lymp

84 Group 1 innate lymphoid cells (ILC1s) are effectors of innate immunity and enriched in

85 losely related type 1 innate lymphoid cells (ILC1s) are enriched in the bone marrow of leukemic mice

86 at distinguish type 1 innate lymphoid cells (ILC1s) from natural killer (NK) cells is a gene signatur

87 ntification of type 1 innate lymphoid cells (ILC1s) has been problematic.

88 Although type 1 innate lymphoid cells (ILC1s) have been originally found as liver-resident ILCs

89 ccumulation of type 1 innate lymphoid cells (ILC1s) in sarcoidosis.

90 ntraepithelial type 1 innate lymphoid cells (ILC1s) that positively associated with patient survival.

91 " NK cells and type 1 innate lymphoid cells (ILC1s) to characterize the dynamics of their homeostatic

92 monstrate that type 1 innate lymphoid cells (ILC1s) were the major immune force providing early prote

93 Liver type 1 innate lymphoid cells (ILC1s), also known as liver-resident natural killer (LrN

94 (NK) cells and type 1 innate lymphoid cells (ILC1s).

95 cNK) cells and type 1 innate lymphoid cells (ILC1s).

96 liver-resident type-1 innate lymphoid cells (ILC1s).

97 In line, ICER deficiency in NK cells/ILC1 resulted in higher lesional parasite burden with fe

98 nuclear receptor alpha (Rora) in LrNK cells/ILC1s and conventional natural killer (cNK) cells had de

99 lear receptor alpha (Roralpha) in LrNK cells/ILC1s and conventional natural killer (cNK) cells had de

100 killer (cNK) cells had decreased LrNK cells/ILC1s but normal numbers of cNK cells.

101 killer (cNK) cells had decreased LrNK cells/ILC1s but normal numbers of cNK cells.

102 d effector molecule expression of LrNK cells/ILC1s.

103 d effector molecule expression of LrNK cells/ILC1s.

104 nuclear receptor alpha (RORa) in LrNK cells/ILC1s.

105 lear receptor alpha (RORalpha) in LrNK cells/ILC1s.

106 he number of ILC1s in the blood; circulating ILC1 numbers decrease as a result of metabolic improveme

107 exhibited an 8-fold increase in circulating ILC1s, which correlated with treatment status.

108 p 1 innate lymphoid cells (ILCs), comprising ILC1s and natural killer cells (NK cells), belong to a l

109 By contrast, ILC1s were found scattered, enriched in the ectocervix a

110 In contrast, ILC1s are poised in uninfected barrier tissues and respo

111 reviously unreported population of converted ILC1-like cells in the mouse small intestine post-transp

112 DOCK8-deficient ILC1-3 subsets had defective proliferation, expressed lo

113 At a lower density, ILC1s prevent LSCs from differentiating into leukemia pr

114 lls can give rise to Eomes(-) Tbet-dependent ILC1-like cells that circulate widely and persist indepe

115 In addition, aceNKP-derived ILC1/NK cells effectively ameliorate tumor burden in a m

116 oreover, in contrast to previously described ILC1 subsets they could be efficiently differentiated in

117 We were not able to detect ILC1 cells in any of the tissues assessed, however, we i

118 d cytokine-producing helper-like ILCs (i.e., ILC1s, ILC2s, ILC3s).

119 Three ILC classes have emerged, ILC1, ILC2 and ILC3, with ILC1 and ILC3 including severa

120 secrete little T(H) 2 cytokines, but exhibit ILC1-like properties, including a capacity to produce IF

121 tance, loss of IFN-gamma or T-bet-expressing ILC1s in Rag1(-/-) mice increased susceptibility to C. d

122 supports a model in which circulating fetal ILC1-like NKPs travel to secondary lymphoid tissues to i

123 s tumor growth, whereas intestinal Rorc(fm-) ILC1s or NK cells fail to inhibit tumor progression.

124 c distinctions are particularly apparent for ILC1 populations, whose distribution was markedly altere

125 s for some ILCs and overlapping patterns for ILC1 cells and NK cells, whereas other ILC subsets remai

126 Our findings reveal a novel role for ILC1 to recruit effector CD8(+) T-cells to prevent virus

127 These data demonstrate a critical role for ILC1s in defense against C. difficile.

128 cells and are developmentally distinct from ILC1 cells.

129 ad reduced numbers of antiviral IFN-gamma(+) ILC1 and increased numbers of immunopathologic IL-5(+) a

130 e of Immunity, identify T-bet(+)IFN-gamma(+) ILC1 that accumulate in the inflamed intestine of IBD pa

131 ls, interferon gamma-positive (IFN-gamma(+)) ILC1s, interleukin (IL)-13(+) ILC2s, and for IL-22(+), b

132 imulates generation of NK, NK-T, gammadelta, ILC1, and memory CD8 T cells.

133 early progenitors and a highly heterogeneous ILC1, ILC3, and NK precursor cell cluster.

134 s without PGD exhibited significantly higher ILC1 frequencies before reperfusion, accompanied by elev

135 How ILC1s and ILTCKs may be targeted to broaden the scope of

136 Here we characterized a human ILC1 subset that produced interferon-gamma (IFN-gamma) i

137 ity and developmental relation between human ILC1 and NK cells, comprising group 1 ILCs, is still elu

138 cross tissues through investigation of human ILC1 diversity by single-cell RNA sequencing and flow cy

139 Collectively, these findings identify ILC1s as anticancer immune cells that might be suitable

140 however, we identified intra-epithelial (ie)ILC1-like cells that represent a broader category of NK

141 a1 signaling; however, transfer of Ifng(-/-) ILC1s has no effect on adipose fibrogenesis.

142 by ILC1 promotes recruitment of IFNgamma(+) ILC1 in Leishmania infections important for development

143 we identify a subset of adipose group 1 ILC (ILC1) and demonstrate a role for these cells in metaboli

144 he subset previously defined as group 1 ILC (ILC1) contains CD4(+) CD8(-), CD4(-) CD8(+), and CD4(-)

145 Increased ILC2:ILC1 ratio in patients with asthma correlated with clini

146 ity analysis identified an intermediate ILC3-ILC1 cluster, which had strong directionality toward ILC

147 A transitional ILC3-ILC1 population was also detected in the human intestine

148 f T-bet(+) IFN-gamma-producing group 1 ILCs (ILC1 and natural killer cells), CD8(+) cytotoxic T cells

149 ators of mucosal immunity, and group 1 ILCs (ILC1 cells) and group 3 ILCs (ILC3 cells) have been show

150 Specifically, group 1 ILCs (ILC1s) and group 3 ILCs (ILC3s) respond to infection wit

151 conventional NK (cNK) cells and type 1 ILCs (ILC1s) as the two major subsets.

152 t was found that liver-resident type 1 ILCs (ILC1s) expanded locally and persisted after the resoluti

153 alling in a distinct subset of group 1 ILCs (ILC1s) instructed an unconventional immune-regulatory tr

154 Group 1 ILCs (ILC1s) produce interferon gamma and depend on Tbet, grou

155 y ILC population distinct from group 1 ILCs (ILC1s), ILC2s, and ILC3s in (1) mice bred in our animal

156 hereas proinflammatory type 1 NKp44(-) ILCs (ILC1s) were higher.

157 killer cells (cNK) and tissue-resident ILCs (ILC1s) that can be distinguished based on their location

158 ree subsets of innate lymphoid cells (ILCs), ILC1s, ILC2s and ILC3s, which is not reversed by ART.

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

160 gulating NF-kappaB signaling, thus impairing ILC1 proliferation and cytotoxicity in vitro and in vivo

161 -5 and IL-13 in ILC2 cells, and IFN-gamma in ILC1 and ILC3 cells.

162 al natural killer cells and inhibiting it in ILC1.

163 NKp46 activation in ILC1s therefore constitutes a previously unrecognized, c

164 Conditional deletion of Inpp4b in ILC1s and NK cells reveals that it is necessary for the

165 ng antigen-specific receptors, which include ILC1s and natural killer (NK) cells.

166 reciated cytokine-secreting cells, including ILC1 (IFN-gamma-expressing NK cells), ILC2 (IL-5 and IL-

167 cells through cell-cell contact, increasing ILC1 production of IFN-gamma and TNF, and enhancing cyto

168 mpact on ILC homeostasis or cytokine-induced ILC1 or ILC3 responses but significantly diminishes ILC2

169 by a Th1 response activated by infiltrating ILC1, NK, and LTi cells.

170 hat differ from those of liver or intestinal ILC1s or NK cells.

171 tably, IL-12 converted human ILC2 cells into ILC1 cells, and the frequency of ILC1 cells in patients

172 asma gondii infection converts NK cells into ILC1-like cells that are distinct from both steady-state

173 e ILCs can be phenotypically classified into ILC1, ILC2 and ILC3 subsets, the transcriptional control

174 conclude that ILC3s undergo conversion into ILC1-like cells in human tissues in vivo, and that tissu

175 r, tumors may induce NK cell conversion into ILC1-like cells that are limited to the tumor microenvir

176 uce the cytokine interleukin-22 convert into ILC1-like cells that produce interferon-gamma in vitro,

177 o ILC3s; some of them can differentiate into ILC1/NK-like cells, but they are unable to develop into

178 e 1 effector features and fully convert into ILC1s.

179 l phenotype (ftILCPs) and differentiate into ILC1s, ILC2s and ILC3s in vitro.

180 Intraepithelial ILC1 were amplified in Crohn's disease patients and cont

181 well as liver and intestinal intraepithelial ILC1 have markers that denote tissue residency and trans

182 In mice, intraepithelial ILC1 were distinguished by CD160 expression and required

183 T cells share this profile, intraepithelial ILC1 may be their innate counterparts.

184 eptor-alpha, indicating that intraepithelial ILC1 are distinct from conventional NK cells.

185 Thus, intraepithelial ILC1 may initiate IFN-gamma responses against pathogens

186 xpressing very little, indicating that it is ILC1 that curtail replication via TRAIL in the absence o

187 ether these results highlight TRAIL as a key ILC1-utilized effector molecule that can operate in defe

188 Ablation of Zfp683-dependent liver ILC1 lead to increased viral load in the presence of int

189 antly in Prdm1-deficient cNK cells and liver ILC1s.

190 ukin-12-driven IFN-gamma production by liver ILC1s.

191 activation and IFN-gamma production of liver ILC1s.

192 Thus, liver ILC1s acquire adaptive features in an MCMV-specific mann

193 From their frontline tissue locations, ILC1s can even induce an antiviral state in uninfected t

194 ent insights into the balance between mature ILC1 and ILC3 based on these TFs and how they interact w

195 s, aceNKPs give rise to a spectrum of mature ILC1/NK cells (regardless of their tissue location) that

196 Memory ILC1 responses were dependent on the MCMV-encoded glycop

197 In mice, ILC1s differ from NK cells, as they develop independentl

198 roinflammatory cytokines resulted in a mixed ILC1-ILC2 phenotype but was able to convert only a small

199 rsor stage, by transient expression of mixed ILC1, ILC2 and ILC3 transcriptional patterns, whereas, i

200 Functionally, NKp46 expressed on mouse ILC1s interacts with tumor cells through cell-cell conta

201 were committed ILC progenitors with multiple ILC1, ILC2 and ILC3 potential at the clonal level.

202 advancing our understanding of the human NK-ILC1 spectrum.

203 severe colitis with an increase in T(H)1/NK/ILC1 effector genes in LPLs, while Prdm1(fl/fl)Cd4(Cre)

204 netic ablation of both NK cells and ILC1 (NK/ILC1(Delta) mice) led to reduced early IFNgamma expressi

205 vity that supports the differentiation of NK/ILC1-like cells.

206 Furthermore, expression of Inpp4b by NK/ILC1s is necessary for their presence in the intratumora

207 tlas of tissue-associated and circulating NK/ILC1s.

208 Human NKp46(+) ILC1s exhibit stronger cytokine production and cytotoxic

209 ease in IFN-gamma-expressing, T-bet+, NKp46+ ILC1s and a concomitant increase in IL-22-expressing, RO

210 oup 3 innate lymphoid cells (ILC3s), but not ILC1s or ILC2s, were similarly responsive to IGF signali

211 in inefficient development of ILC2s, but not ILC1s or ILC3s.

212 The frequency of the novel ILC1-like NK cell progenitor (NKP) significantly decline

213 In humanized mice, the acquisition of ILC1 features by ILC3s showed tissue dependency.

214 e mechanisms include increased activation of ILC1, ILC2, and ILC3 populations, enhanced expression of

215 Furthermore, the degree of ILC1 population heterogeneity differed substantially in

216 was essential for the normal development of ILC1 and ILC3 cells but not of ILC2 cells.

217 r in the lineage-specific differentiation of ILC1 and ILC3 cells.

218 142-deficient mice exhibited an expansion of ILC1-like cells concurrent with increased transforming g

219 Raggammac(-/-) mice upregulate expression of ILC1- or ILC3-associated proteins following C. difficile

220 cells into ILC1 cells, and the frequency of ILC1 cells in patients with chronic obstructive pulmonar

221 studies have discovered the heterogeneity of ILC1 and ILC3 in the gastrointestinal tract.

222 om NK cells represented a major mechanism of ILC1 generation.

223 n status, characterized by overexpression of ILC1/NK cell-related genes and downregulation of type 3

224 p44 have been shown to contain precursors of ILC1, ILC2, and ILC3.

225 We found that reconstitution of ILC1, ILC2, and NCR(-)ILC3 was slow compared with that o

226 Although a limited set of ILC1 genes depended on PLZF for expression, characterist

227 Runx3 controlled the survival of ILC1 cells but not of ILC3 cells.

228 ia, deletion of NKp46 impairs the ability of ILC1s to control tumor growth and reduces survival.

229 uninfected animals upon genetic ablation of ILC1s or antibody-based neutralization of IFN-y.

230 thermore, inhibiting adipose accumulation of ILC1s using IL-12 neutralizing antibodies attenuates adi

231 Here, we show that a high density of ILC1s induces leukemia stem cell (LSC) apoptosis in mice

232 ion, ultimately resulting in an expansion of ILC1s.

233 elf, controlled the identity and function of ILC1s by promoting chromatin accessibility and depositio

234 mice, TET1 suppresses the hyperactivation of ILC1s to maintain intestinal homeostasis.

235 ontogenies and cancer-sensing mechanisms of ILC1s and ILTCKs in murine genetic cancer models as well

236 LZF(+) ILC precursors generated a mixture of ILC1s, ILC2s and ILC3s that lacked cytotoxic potential.

237 h glycemic parameters and with the number of ILC1s in the blood; circulating ILC1 numbers decrease as

238 Conversely, the antileukemia potential of ILC1s wanes when JAK-STAT or PI3K-AKT signaling is inhib

239 e iNK stage, with a striking predominance of ILC1s over cNKs early in ontogeny.

240 we studied the developmental progression of ILC1s and demonstrated substantial overlap with stages p

241 clusive nomenclature to clarify the roles of ILC1s and NK cells during homeostasis and disease.

242 Deletion of NKp46 reduces IL-2Ralpha on ILC1s by downregulating NF-kappaB signaling, thus impair

243 Only ILC1 and ILC3, but not ILC2, undergo the RA-dependent ho

244 uence abundance or phenotype of cNK cells or ILC1s in the kidney.

245 sis and plasticity that limits physiological ILC1 conversion.

246 parasite burden with fewer IFNgamma-positive ILC1 than in control mice.

247 reversibly give rise to IFN-gamma-producing ILC1, plasticity of human or mouse ILC2 has not been sho

248 can convert into interferon-gamma-producing ILC1s.

249 ed abundance of circulating ILC progenitors, ILC1s, and ILC3s, whereas males presented with diminishe

250 Interleukin-15 (IL-15) promoted ILC1 granzyme A expression and cytotoxicity, and IL-15 e

251 conventional dendritic cells (cDC1) promoted ILC1 production of IFN-gamma in a STAT4-dependent manner

252 All of these effects, which require ILC1s to produce interferon-gamma after cell-cell contac

253 despite high TRAIL expression by SG-resident ILC1, IFN-gamma production by both ILC1 and cNK was mini

254 ) as an important enzyme for tissue-resident ILC1 and NK cell survival, signal transduction, and anti

255 Thus, adipose-resident ILC1s contribute to obesity-related pathology in respons

256 eration and accumulation of adipose-resident ILC1s in a manner dependent on the IL-12 receptor and ST

257 P4B as a hallmark feature of tissue-resident ILC1s and intratumoral NK cells using an scRNA-seq atlas

258 ssary for the homeostasis of tissue-resident ILC1s but not circulating NK cells at steady-state.

259 the homeostatic turnover of tissue-resident ILC1s is much slower than that of circulating NK cells.

260 atural killer (NK) cells and tissue-resident ILC1s, the functional, phenotypic, and developmental pro

261 ct groups based on their cytokine secretion: ILC1 produce IFN-gamma, ILC2 secrete IL-5 and IL-13, and

262 Stimulated ILC1 production of IFN-gamma was decreased by TGF-beta a

263 In healthy subjects, ILC1s increased from baseline at Day 3 (P = 0.001), whil

264 ffector programs specific to the ILC subsets ILC1, ILC2 and ILC3 was initiated later, at the common I

265 ve proportions of the different ILC subsets (ILC1, ILC2 and ILC3) in gingivitis and periodontitis.

266 DNA hydroxymethyltransferase TET1 suppresses ILC1 but not ILC2 or ILC3 differentiation.

267 er IFN-gamma-producing lineages such as Th1, ILC1, and intraepithelial gammadelta T cells.

268 e discuss recent findings demonstrating that ILC1s provide several critical layers of innate antivira

269 Findings from these studies imply that ILC1s in different tissues and organs share a common sig

270 These findings suggest that ILC1s are critical for tissue protection during acute li

271 Mounting evidence also suggests that ILC1s may have enhanced secondary responses to viral inf

272 ant expression of RANKL on a fraction of the ILC1 population suggest that these cells may be of impor

273 ey originated from different precursors, the ILC1 and cNK lineages followed a parallel progression at

274 C precursor (ILCP) strictly committed to the ILC1, ILC2, and ILC3 lineages.

275 RCC tumor tissue positively tracked with the ILC1 response.

276 expression was detected on a fraction of the ILC1s.

277 Mechanistically, these ILC1 cells augmented virus-induced inflammation in a man

278 Thus, ILC1 contribute an essential role in viral immunosurveil

279 2 innate lymphoid cell (ILC2) conversion to ILC1s is closely involved in silicosis progression, whic

280 convert only a small population of ILC2s to ILC1s, which were found post-transplant.

281 re also increased and expanded, similarly to ILC1s, in greater proportion compared with ILC3s.

282 HIF-1alpha in NKp46+ cells prevents ILC3-to-ILC1 conversion, increases the expression of IL-22-induc

283 ster, which had strong directionality toward ILC1s.

284 revealed that AML skewing of the ILCP toward ILC1s and away from NK cells represented a major mechani

285 t be clearly segregated into the traditional ILC1 and NK subsets, suggesting that group 1 ILCs consti

286 ate immune cells, including a PD1(+)TRAIL(+) ILC1 population.

287 Despite being deemed different cell types, ILC1s and NK cells share many common features both pheno

288 Unexpectedly, ILC1-like cells lacked Tbet expression and failed to pro

289 Here we identify highly variable ILC1 subtypes across tissues through investigation of hu

290 urrent knowledge of NK cells and the various ILC1 subsets.

291 as the switch that determined an ILC2-versus-ILC1 response.

292 e majority of ILCs, in both conditions, were ILC1s.

293 d protective interleukin-22 (IL-22), whereas ILC1s produced proinflammatory interferon-gamma (IFN-gam

294 d protective interleukin-22 (IL-22), whereas ILC1s produced proinflammatory interferon-gamma (IFN-y)

295 lunted in the absence of tuft cells, whereas ILC1s were unaffected.

296 We studied mice in which ILC1s and NK cells lacked SMAD4, a signal transducer tha

297 SERPINB4 mRNA (both P < .0005) compared with ILC1.

298 sses have emerged, ILC1, ILC2 and ILC3, with ILC1 and ILC3 including several subsets.

299 Together with ILC1s, NK cells constitute group 1 ILCs, which are chara

300 cosa, Zfp683 expression correlated well with ILC1s; in salivary glands, Zfp683 was coexpressed with t