ライフサイエンスコーパス: ILC2

1 Th2), eosinophils and innate lymphoid cells (ILC2).

2 ed Stat6 as a direct gene target of c-Myc in ILC2.

3 so provide additional signals for sustaining ILC2.

4 s and enhanced gene translation in activated ILC2.

5 -like phenotype atypical of adipose resident ILC2.

6 with wild type but not Il5(-/-) or Il13(-/-) ILC2.

7 n ST2(-) phenotype, but are not inflammatory ILC2.

8 ndicated a reparative function for Tregs and ILC2.

9 Strikingly, our results demonstrate that ILC2(10)s can utilize both autocrine and paracrine signa

10 Interestingly, ILC2(10)s demonstrated a metabolic dependency on the gly

11 mportant and previously unrecognized role of ILC2(10)s in diseases associated with ILC2s such as alle

12 as to characterize the effector functions of ILC2(10)s in the development and pathology of allergic a

13 ILC2(10)s were also adoptively transferred into Rag2(-/-

14 IL-4-stimulated ILC2(10)s were isolated to evaluate cytokine secretion,

15 2s in the lungs that actively produce IL-10 (ILC2(10)s).

16 Maf and Blimp-1 regulate IL-10 expression in ILC2(10)s.

17 Peripheral blood ILC2 abundance and phenotype were analyzed by flow cytom

18 ssue-resident group 2 innate lymphoid cells (ILC2) accumulate in the choroid plexus of aged brains.

19 In vitro, ASCs produced TSLP that supported ILC2 accumulation and activation.

20 on is RAGE-dependent and contributes to lung ILC2 accumulation and downstream eosinophilic inflammati

21 hways have both been implicated in promoting ILC2 accumulation during type 2 inflammation.

22 In this study, we show that ILC2 accumulation in the murine lung in response to syst

23 Although ILC2-activating factors have been identified, the mechan

24 sruption of LT signaling markedly diminishes ILC2 activation and downstream responses during type 2 i

25 ILC2 activation and eosinophil recruitment, TH2-related

26 ucers of type 2 cytokines, the regulation of ILC2 activation and function is not well understood.

27 dings uncover iTregs as potent regulators of ILC2 activation and implicate their utility as a therape

28 ysLT1R promotes LTC4- and Alternaria-induced ILC2 activation and lung inflammation.

29 ould further amplify the effects of IL-33 on ILC2 activation and lung inflammation.

30 Our findings reveal that PGE2 limits ILC2 activation and propose that selective EP2 and EP4 r

31 on, and suggest that NK cells serve to limit ILC2 activation and subsequent allergic airway inflammat

32 suggesting that more IL-33 was available for ILC2 activation and that a COX product(s) inhibited IL-3

33 kin microenvironment to induce chronic local ILC2 activation and their dissemination into the circula

34 c-Myc is essential for ILC2 activation and their in vivo pathogenic effects.

35 epithelial cytokines significantly amplified ILC2 activation and upregulated expression of the recept

36 The molecular pathways that drive ILC2 activation are not well understood.

37 However, molecular pathways that control ILC2 activation are not well understood.

38 uced PGD(2) is essential in cytokine-induced ILC2 activation because blocking of the COX-1/2 or HPGDS

39 meostasis, Runx deficiency induces excessive ILC2 activation due to overly active GATA-3 functions.

40 tenance of ILC2 at homeostasis but abolished ILC2 activation during allergic airway inflammation.

41 , a therapeutic target capable of modulating ILC2 activation has yet to be identified.

42 , we show that interleukin (IL)-33-dependent ILC2 activation in the lung is involved centrally in pro

43 dies identified a pathway where IL33 induces ILC2 activation in the lung within hours of HS/T.

44 However, the mechanism of this synergistic ILC2 activation is unknown.

45 Hence, fostering IL-9-mediated ILC2 activation may offer a novel therapeutic approach i

46 in IL-33- and LT-deficient mice, and optimal ILC2 activation reflects potent synergy between these pa

47 ILC2 activation requires tuft-cell-derived interleukin-2

48 cterized the gene programs that underlie the ILC2 activation state.

49 identify PKC-theta as a critical factor for ILC2 activation that contributes to TH2 cell differentia

50 t type 2 cytokine responses characterized by ILC2 activation, proliferation and eosinophil recruitmen

51 IL-33 in cadherin-11-deficient mice mediated ILC2 activation, resulting in higher IL-13 expression le

52 ry fate-mapping approaches and reporters for ILC2 activation, we show that ILC2s appeared in multiple

53 a establish an essential role for CBFbeta in ILC2 activation.

54 ocrine manner, essential in cytokine-induced ILC2 activation.

55 inding factor beta (CBFbeta) is required for ILC2 activation.

56 receptor expression on lung ILC2 to enhance ILC2 activation.

57 c-Myc expression is upregulated during ILC2 activation.

58 drives colonic group 2 innate lymphoid cell (ILC2) activation during infection and IL-33 activated IL

59 cally promoted group 2 innate lymphoid cell (ILC2) activation to induce innate allergic inflammation.

60 onses, particularly when combined with other ILC2 activators.

61 hibition of c-Myc by JQ1 treatment repressed ILC2 activity and suppressed Alternaria-induced airway i

62 Thus, Runx confers competence for sustained ILC2 activity at the mucosa, and contributes to allergic

63 blood and kidneys, and adoptive transfer of ILC2 also protected mice from IRI.

64 to investigate the relative contribution of ILC2 and adaptive TH2 cell responses in a murine model o

65 correlated with ACQ6 and AQLQ scores, while ILC2 and eosinophil numbers did not.

66 rofen significantly increased the numbers of ILC2 and IL-5 and IL-13 expression by ILC2 in the lung.

67 L-23 signaling attenuated cytokine-producing ILC2 and ILC3 responses in STAT1-deficient mice during R

68 allowed for clear phenotypic delineation of ILC2 and ILC3 subsets.

69 portions of the different ILC subsets (ILC1, ILC2 and ILC3) in gingivitis and periodontitis.

70 n of IL-33 and IL-23, cytokines that promote ILC2 and ILC3, respectively, compared with wild-type mic

71 ing PGD2, IL-13 and NKp30 partially restores ILC2 and M-MDSC levels and results in increased survival

72 nd peripheral eosinophilia is linked to both ILC2 and myeloid IL-33 signaling.

73 minth infection, ASC depletion impaired lung ILC2 and Th2 cell accumulation and function, which are i

74 High fat feeding alters both the number of ILC2 and their type II cytokine production.

75 rogated IL-33, group 2 innate lymphoid cell (ILC2) and eosinophilic responses to Alternaria allergen

76 ed lung IL-13+ innate lymphoid cells type 2 (ILC2) and IL-13+ gammadelta T cells.

77 deficient in group 2 innate lymphoid cells (ILC2), and C57BL/6 wild-type mice treated with anti-IL5

78 caused a reduction in innate lymphoid cell, ILC2, and IL-9(+) and IL-13(+) ILC2 numbers in the lung.

79 ve been shown to contain precursors of ILC1, ILC2, and ILC3.

80 tor ST2 on targets such as CD4(+) Th2 cells, ILC2, and mast cells.

81 Here, we show that ILC2 are present in para-aortic adipose tissue and lymph

82 Type-2 innate lymphoid cells (ILC2) are a prominent source of type II cytokines and ar

83 Group 2 innate lymphoid cells (ILC2) are stimulated by IL-33 to increase IL-5 and IL-13

84 Group 2 innate lymphoid cells (ILC2) are tissue-resident innate effector cells that can

85 Group 2 innate lymphoid cells (ILC2) are tissue-resident, long-lived innate effector ce

86 of CBFbeta did not impair the maintenance of ILC2 at homeostasis but abolished ILC2 activation during

87 The role of IL-33/ILC2 axis in RSV-induced AHR inflammation and eosinophil

88 establish miRNAs as important regulators of ILC2 biology, reveal overlapping but nonidentical miRNA-

89 Our results show that ILC2 can still arise from what are normally considered t

90 1 days of altitude therapy, CRTH2-expressing ILC2, CD4(+) and CD8(+) T cells and Treg cells showed at

91 lete c-Myc in primary murine lung ILC2 or an ILC2 cell line.

92 Antibody-mediated PD-1 blockade relieves ILC2 cell-intrinsic PD-1 inhibition to expand TILC2s, au

93 e found high expression of CD200R on Th2 and ILC2 cells and basophils.

94 sed in purified CD3+ CD4+, CD14+, CD19+, and ILC2 cells from affected family members, as were IL-5 pr

95 nsis infection is as follows: CD4(+) T cells/ILC2 cells, IgG, and FcRgamma>mast cells>IgE and Fcepsil

96 une responses showed that CD4(+) T cells and ILC2 cells, IgG, FcRgamma, and, to a lesser extent, IgE

97 suggest context-specific regulation of tuft-ILC2 circuits within the small intestine.

98 analysed B cells from NP or tonsil, or after ILC2 coculture, by flow cytometry.

99 ne expression analysis identified a discrete ILC2-committed population and delineated transition stat

100 in genes in the thymus drastically increased ILC2 counts in the thymus and other organs where ILC2 no

101 In mouse models, mast cell-ILC2 crosstalk can drive local inflammation.

102 n supernatants from both stimulated PBMC and ILC2 cultures.

103 ng increases allergen-induced IL-33 release, ILC2 cytokine production, and airway inflammation.

104 -5 and IL-13 while TGF-beta had no effect on ILC2 cytokine production.

105 ergic inflammation was marginally reduced in ILC2-deficient mice that received combined DEP+HDM, it w

106 n receptor alpha (RORalpha)(fl/fl)IL7R(Cre) (ILC2-deficient), and recombination-activating gene (Rag)

107 ve as a promising therapeutic target against ILC2-dependent asthma.

108 tentially new therapeutic approach to target ILC2-dependent inflammation.

109 ILC2-dependent suppression of NK cells is elaborated via

110 Interestingly, ILC2 depletion correlated with less severe hepatitis and

111 CCR10(+) ILC2 depletion, as well as blocking of IFN-gamma activit

112 ILC2-derived IL-13 was sufficient for RSV-driven AHR, si

113 Consequently, ILC2-derived IL-4 and IL-13 feed back to induce eotaxin

114 variectomy, abolishes the sex differences in ILC2 development and restores IL-33-mediated lung inflam

115 ranscription factor RORalpha is required for ILC2 development but is also highly expressed by other I

116 Here, we show that ILC2 development is greatly influenced by male sex hormo

117 and decreased cytokines and ILC2 markers in ILC2 differentiated from the bone marrow of NIP45(-/-) m

118 n of a transcriptional network important for ILC2 differentiation.

119 TLR9 activation alleviates ILC2-driven AHR and airway inflammation through direct s

120 ILC2-driven innate type 2 inflammation is accompanied by

121 h helminths in the intestine also induces an ILC2-driven, IL-13-dependent goblet cell hyperplasia and

122 egs), effectively suppress the production of ILC2-driven, pro-inflammatory cytokines IL-5 and IL-13.

123 rized the effects of autophagy deficiency on ILC2 effector functions and metabolic balance.

124 acrine signaling to suppress proinflammatory ILC2 effector functions in vitro.

125 hat IL-33 plays a critical role in promoting ILC2 egress from the bone marrow.

126 Deletion of Cysltr1 blunted LTC4-induced ILC2 expansion and eosinophilia but did not alter IL-33

127 led that miR-155 is needed for IL-33-induced ILC2 expansion and eosinophilic airway inflammation.

128 n sensitized wild-type mice markedly boosted ILC2 expansion and IL-5/IL-13 generation in a CysLT2R-de

129 uronal signaling is critical for suppressing ILC2 expansion and maintaining homeostasis of the type 2

130 n immature mice and are required for maximum ILC2 expansion and mucous metaplasia.

131 to elucidate the contribution of miR-155 in ILC2 expansion using experimental murine models of aller

132 RV-induced mucous metaplasia, ILC2 expansion, airway hyperresponsiveness, and epitheli

133 Thus, CysLT2R signaling, IL-33-dependent ILC2 expansion, and IL-33-driven mast cell activation ar

134 ency increased airway epithelial activation, ILC2 expansion, and T(H) 2 differentiation.

135 Il5, Il13, muc5ac, and gob5 mRNA expression, ILC2 expansion, mucus metaplasia, and airway hyperrespon

136 ation through a cell-intrinsic inhibition of ILC2 expansion.

137 ILC2 expressed higher levels of both SERPINB3 and SERPIN

138 d significantly decreased the number of lung ILC2 expressing IL-5 and IL-13 following Alt-Ext-challen

139 tron microscopy demonstrates that mouse lung ILC2 expressing PSGL-1 have platelets attached to their

140 CGRP induced marked changes in ILC2 expression programs in vivo and in vitro, attenuati

141 before reperfusion, accompanied by elevated ILC2 frequencies after allograft reperfusion.Conclusions

142 Loss of NMU-NMUR1 signalling reduced ILC2 frequency and effector function, and altered transc

143 ILC2 frequency was associated with detectable IL-13 in t

144 ILC2 from asthma patients expressed increased amounts of

145 ht to address the role of pDCs in regulating ILC2 function and ILC2-mediated airway hyperreactivity (

146 s AHR and airway inflammation by suppressing ILC2 function and survival.

147 ne the role of TLR9 activation in regulating ILC2 function and to evaluate the therapeutic utility of

148 2 proliferation and Th2 cytokines suggesting ILC2 function is influenced by attachment to platelets.

149 ed, the overall effect of the COX pathway on ILC2 function is inhibitory in Alternaria-induced innate

150 urther show that IFN-gamma directly inhibits ILC2 function through a STAT1-dependent mechanism.

151 c tools for allergic diseases by controlling ILC2 function.

152 mplications of such endogenous production on ILC2 function.

153 out to investigate how PGE2 regulates human ILC2 function.

154 teraction are important in the regulation of ILC2 function.

155 in treating allergic diseases by suppressing ILC2 function.

156 Finally, TSLP was required for maximal ILC2 gene expression in response to IL-25 and IL-33.

157 CBFbeta promoted expression of key ILC2 genes at both transcriptional and translational lev

158 the physiological requirements for miRNAs in ILC2 homeostasis and immune function and compared the gl

159 uced by Alternaria, suggesting commonly used ILC2 identification practices do not accurately enumerat

160 ting a role for this cytokine in maintaining ILC2 identity.

161 Lung ILC2, IL-5 and IL-13 production, and BAL inflammatory ce

162 Moreover, these results underline the ILC2/IL-13 axis as a targetable pathway to curtail the M

163 ILC2 IL5 up-regulation induces further IL5 expression by

164 This IL33-ILC2-IL5-neutrophil axis defines a novel regulatory role

165 hil axis defines a novel regulatory role for ILC2 in acute lung injury that could be targeted in trau

166 ILC2 in asthma patients exhibit an activated phenotype.

167 Selective genetic ablation of ILC2 in Ldlr(-/-) mice accelerates the development of at

168 nction accompanied with an increase Treg and ILC2 in lymphoid and renal compartments, augmented anti-

169 ion of IL-5, IL-6, IL-9, IL-13 and GM-CSF by ILC2 in response to IL-33, with inhibition of p38 having

170 in infants and suggest an important role of ILC2 in shaping the immune response early during RSV inf

171 ILC2 in the aged brain are long-lived, are relatively re

172 Targeting ILC2 in the aged brain may provide new avenues to combat

173 ers of ILC2 and IL-5 and IL-13 expression by ILC2 in the lung.

174 ytokine production in gammadelta T cells and ILC2 in the lungs, which may contribute to the observed

175 sed each other's receptor expression on lung ILC2 in vivo and in vitro.

176 ortion of ST2-bearing innate lymphoid cells (ILC2) in blood and kidneys, and adoptive transfer of ILC

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

178 phocytes resulted in selective impairment of ILC2(INFLAM) responses and increased susceptibility to h

179 omotes the generation of inflammatory ILC2s (ILC2(INFLAM)) via induction of the enzyme tryptophan hyd

180 ILC2 infusion was associated with reduced donor proinfla

181 uced Bcl-2 expression in intestinal Itk(-/-) ILC2 is also restored to WT levels after IL-2 complex tr

182 he clinical findings that both the IL-33 and ILC2 levels are elevated in patients with allergic airwa

183 ILC2 levels were significantly higher in D816V(+) patien

184 viral load, and type 2 innate lymphoid cell (ILC2) levels in nasal aspirates, collected within 24 hou

185 ) Th2 cells, but functional diversity of the ILC2 lineage has yet to be fully explored.

186 expressing IL-25 and decreased cytokines and ILC2 markers in ILC2 differentiated from the bone marrow

187 ings suggest a role for ILC2s and pathogenic ILC2-mast cell crosstalk in mastocytosis.

188 IL-33 and ILC2 may also serve as biomarkers for disease classifica

189 Type 2 innate lymphoid cells (ILC2) mediate inflammatory immune responses in the conte

190 Ms, as well as group-2 innate lymphoid cell (ILC2)-mediated AAM activation.

191 Cs through Toll-like receptor 7/8 suppresses ILC2-mediated AHR and airway inflammation and that deple

192 oduction, thus inhibiting the development of ILC2-mediated AHR.

193 role of pDCs in regulating ILC2 function and ILC2-mediated airway hyperreactivity (AHR) and lung infl

194 Treatment with CBFbeta inhibitors prevented ILC2-mediated airway hyperresponsiveness in a mouse mode

195 -alpha signaling increased IL-33 release and ILC2-mediated airway inflammation.

196 (ER-alpha, Esr1) or ER-beta (Esr2) increased ILC2-mediated airway inflammation.

197 a therapeutic approach for the treatment of ILC2-mediated allergic asthma and respiratory disease.

198 otentially a therapeutic target for treating ILC2-mediated allergic lung inflammation.

199 ation of IL-2 and IL-33 to enhance Treg- and ILC2-mediated protection from AKI, bears strong therapeu

200 indings reveal a novel regulatory pathway in ILC2-mediated pulmonary inflammation with important clin

201 However, the mechanisms regulating prolonged ILC2-mediated T(H)2 cytokine production under chronic in

202 Additionally, PD-1 deficiency shifts ILC2 metabolism toward glycolysis, glutaminolysis and me

203 LC2s in response to IL-33 was due to altered ILC2 migration patterns.

204 xis potently induces cytokine production and ILC2 migration.

205 o control airway inflammation in a humanized ILC2 mouse model.

206 counts in the thymus and other organs where ILC2 normally reside.

207 RV-induced type 2 cytokine immune responses, ILC2 number, and mucus metaplasia, while decreasing IL-1

208 ministered during allergen challenge reduced ILC2 numbers and activation, as well as airway inflammat

209 ILC2 numbers are increased in asthmatic patients compare

210 We sought to determine whether ILC2 numbers change in peripheral blood and the nasal mu

211 Furthermore, blood ILC2 numbers during the reaction correlated with time fo

212 evels in BAL fluid correlated with decreased ILC2 numbers in blood (P = .004, respective P = .024).

213 allenge (P < .05), whereas at the same time, ILC2 numbers in blood were reduced (P < .05).

214 Intestinal ILC2 numbers in Itk(-/-) mice are restored by the admini

215 ministration of Alternaria challenge reduced ILC2 numbers in the bone marrow and concurrently increas

216 ymphoid cell, ILC2, and IL-9(+) and IL-13(+) ILC2 numbers in the lung.

217 beta2 integrins (CD18) significantly reduced ILC2 numbers in the lungs but did not alter ILC2 prolife

218 ILC2 numbers increase in the mouse lung not only through

219 The magnitude of increases in nasal mucosal ILC2 numbers positively correlated with maximum symptom

220 ILC2 numbers significantly increased in nasal mucosal sa

221 Mice lacking PKC-theta had reduced ILC2 numbers, TH2 cell numbers and activation, airway hy

222 d both the HDM-induced lung inflammation and ILC2 numbers, whereas transfer of CD3(-)NK1.1(+) NK cell

223 rins or alpha4 integrins did not affect lung ILC2 numbers.

224 n the lungs and was associated with elevated ILC2 numbers.

225 ow and concurrently increased blood and lung ILC2 numbers.

226 used to delete c-Myc in primary murine lung ILC2 or an ILC2 cell line.

227 innate lymphoid cell 1 (ILC1) cells, but not ILC2 or ILC3 cells, were enriched in the expression prof

228 ncy of proinflammatory and anti-inflammatory ILC2 phenotypes.

229 unlike the latter, a majority of peripheral ILC2 pools were generated de novo during the postnatal w

230 This ILC2 population is likely to contribute to asthma.

231 er these two pathways coordinate to regulate ILC2 population size in the tissue in vivo remains undef

232 L-33 and PGD(2)-CRTH2 pathways that regulate ILC2 population size will be useful in understanding how

233 mergence of a TSLP receptor-positive IL-9(+) ILC2 population, and an increase in intraepithelial mast

234 FR2, we identified a previously unrecognized ILC2 population.

235 , identified a previously unrecognized human ILC2 population.

236 that unconventional ST2- and CD127-negative ILC2 populations are present in mouse lung and are induc

237 nes IL-10 and TGF-beta on activated ILC1 and ILC2 populations ex vivo.

238 Adoptive transfer of bone marrow ILC2 precursors confirms a cell-intrinsic role for ITK.

239 Il7ra(-/-) ILC2 primarily express an ST2(-) phenotype, but are not

240 This period was accompanied by systemic ILC2 priming and acquisition of tissue-specific transcri

241 Administration of IL-5, a major ILC2 product, was sufficient to repress aging-associated

242 derived suppressor cells (MDSCs) mediated by ILC2 production of IL-13, improved GI tract barrier func

243 quired for the generation and maintenance of ILC2 progenitors (ILC2p).

244 Male mice have reduced numbers of ILC2 progenitors (ILC2Ps) and mature ILC2s in peripheral

245 ent of ILC2s but retained significantly more ILC2 progenitors in the bone marrow via augmented expres

246 ulmonary fungal allergen challenge mobilized ILC2 progenitors to exit the bone marrow.

247 In mice, the absence of IL-9 impaired ILC2 proliferation and activation of regulatory T (Treg)

248 The effects of PGE2 on human ILC2 proliferation and intracellular cytokine and transc

249 ace and that platelet depletion reduces lung ILC2 proliferation and Th2 cytokines suggesting ILC2 fun

250 Finally, we observed increased ILC2 proliferation and type 2 cytokine production as wel

251 ILC2 numbers in the lungs but did not alter ILC2 proliferation, apoptosis, and function.

252 This effect was not a result of reduced ILC2 proliferation, increased apoptosis or cell death, o

253 Indomethacin also increased ILC2 proliferation, the percentages of eosinophils, and

254 ed IL-5 but constrained IL-13 expression and ILC2 proliferation.

255 Upon activation, mature ILC2 rapidly secrete large amounts of type-2 cytokines a

256 The most pronounced ILC2 recruitment was observed in subjects with elevated

257 These findings expand our understanding of ILC2 regulation and may have important implications for

258 type 2 immune responses after trauma through ILC2 regulation of neutrophil IL5 production.

259 results convey the potent role of DR3 as an ILC2 regulator and introduce DR3 agonistic treatment as

260 We conclude that ILC2 represent a major innate cell source of IL-5 and IL

261 riven AHR, since reconstitution of wild-type ILC2 rescued RSV-driven AHR in IL-13-deficient mice.

262 R(-/-) mice had reduced lung eosinophils and ILC2 responses after exposure to the fungal allergen Alt

263 33, Tph1, and ICOS in promoting inflammatory ILC2 responses and type 2 immunity at mucosal barriers.

264 Without CGRP signaling, ILC2 responses and worm expulsion were enhanced.

265 ine milieu that promotes ILC2 responses, how ILC2 responses are regulated by other stimuli remains po

266 Critically, NMB stimulation inhibited ILC2 responses from control but not basophil-depleted mi

267 While the molecular understanding of ILC2 responses has advanced, the complexity of microenvi

268 ing effects of PGD(2), PGE(2), and PGI(2) on ILC2 responses have been previously reported, the overal

269 ous CGRP is a critical negative regulator of ILC2 responses in vivo.

270 Elevated IL-33 levels and ILC2 responses were observed in the lungs most likely du

271 ILC2 responses, airway inflammation and airway hyperresp

272 Thus, NMUR1 signalling promotes inflammatory ILC2 responses, highlighting the importance of neuro-imm

273 erstanding the cytokine milieu that promotes ILC2 responses, how ILC2 responses are regulated by othe

274 PGDS enzymes or the CRTH2 receptor abolishes ILC2 responses.

275 uced pulmonary group 2 innate lymphoid cell (ILC2) responses and IL-33 release.

276 lminth-induced group 2 innate lymphoid cell (ILC2) responses are exaggerated in the absence of basoph

277 on, and TH and group 2 innate lymphoid cell (ILC2) responses.

278 Deletion of c-Myc in ILC2 results in reduced proliferation, decreased cytokin

279 ntracerebroventricular transfer of activated ILC2 revitalized the aged brain and enhanced the cogniti

280 Type 2 innate lymphoid cells (ILC2) share cytokine and transcription factor expression

281 MYC expression was examined in ILC2 sorted from peripheral blood of healthy controls an

282 c-Kit and CCR6 define this ILC2 subpopulation that exhibits ILC3 features, includin

283 we identify a group 2 innate lymphoid cell (ILC2) subpopulation that can convert into interleukin-17

284 s associated with selective reduction of the ILC2 subset after reperfusion.

285 ngle-cell analysis reveals that the CCR10(+) ILC2 subset is enriched in cells expressing amphiregulin

286 Ex vivo activated ILC1 and ILC2 subsets were also found to be a source of the immun

287 GD(2) and its metabolites can be detected in ILC2 supernatants.

288 indicating a tissue-specific role for ITK in ILC2 survival in the intestine.

289 Unlike most activated ILC2, the ILC210 population contracts after cessation of

290 and each other's receptor expression on lung ILC2 to enhance ILC2 activation.

291 therapeutic strategy that augments Treg and ILC2 to not only inhibit renal injury, but also promote

292 ovide a niche for multifaceted dialogue with ILC2 to sustain a type-2 immune environment in WAT.

293 ted Tregs and group 2 innate lymphoid cells (ILC2) to prevent renal injury.

294 Finally, IL-33 enhanced ILC2 trafficking to the lungs in a parabiosis mouse mode

295 The role of beta1 and beta2 integrins in ILC2 trafficking to the lungs was assessed by in vivo bl

296 es have accelerated these efforts, revealing ILC2 transcriptional programs that are coordinated with

297 Group-2 innate lymphoid cells (ILC2), type-2 cytokines, and eosinophils have all been i

298 sthma phenotypes as well as the frequency of ILC2 was significantly reduced in EA after altitude trea

299 In vitro, ILC2 were increased and potently expressed IL-13 in the

300 TSLPR and ST2 expression on lung ILC2 were measured by flow cytometry after treatment of