ライフサイエンスコーパス: ILC2

1 M-MDSCs), and group 2 innate lymphoid cells (ILC2).

2 cells (DC) and/or innate lymphocytic cells (ILC2).

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

4 -like phenotype atypical of adipose resident ILC2.

5 natural cytotoxicity receptor NKp30 on human ILC2.

6 deficiencies that failed to generate plastic ILC2.

7 roduce IFN-gamma, thereby generating plastic ILC2.

8 onal heterogeneity of human peripheral blood ILC2.

9 they have not been shown to be expressed by ILC2.

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

11 onary RAGE is necessary for allergen-induced ILC2 accumulation in the lung.

12 se models, immunopathology and local Th2 and ILC2 accumulation is reduced in DR3-deficient mice despi

13 In contrast, ILC2 acquire gut homing receptors in a largely RA-indepe

14 itical role for IL-33, a hallmark peripheral ILC2-activating cytokine, in promoting the egress of ILC

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

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

17 ILC2 activation and eosinophil recruitment, TH2-related

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

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

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

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

22 e hypothesized that PKC-theta contributes to ILC2 activation and might be necessary for ILC2s to inst

23 Finally, IL-1beta potentiated ILC2 activation and plasticity in vivo, and IL-12 acted

24 mation, IL-33 release by FALC stromal cells, ILC2 activation and pleural B-cell activation in FALCs,

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

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

27 IFN-gamma inhibited ILC2 activation and Treg cell accumulation by IL-33 in i

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

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

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

31 Strategies to block ILC2 activation or the IL-33/IL-33 receptor pathway can

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

33 Mechanistically, ILC2 activation results in the proliferation of bipotent

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

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

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

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

38 ndings uncover Tregs as potent regulators of ILC2 activation; MaR1 targets Tregs and ILC2s to restrai

39 and compare it with that of the established ILC2 activators IL-25 and IL-33.

40 onses, particularly when combined with other ILC2 activators.

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

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

43 ate cytokine production plasticity for human ILC2 and further suggest that environmental cues can dic

44 ontact mechanism that mediates activation of ILC2 and identifies a potential target for the developme

45 ers of immunopathologic IL-5(+) and IL-13(+) ILC2 and IL-17A(+) ILC3 compared with RSV-infected wild-

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

47 can be phenotypically classified into ILC1, ILC2 and ILC3 subsets, the transcriptional control of co

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

49 tage, by transient expression of mixed ILC1, ILC2 and ILC3 transcriptional patterns, whereas, in cont

50 r programs specific to the ILC subsets ILC1, ILC2 and ILC3 was initiated later, at the common ILC pre

51 oth type 2 and type 3 innate lymphoid cells (ILC2 and ILC3), specifically in the portion of organs ex

52 al killer cells and helper-like cells (ILC1, ILC2 and ILC3).

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

54 Three ILC classes have emerged, ILC1, ILC2 and ILC3, with ILC1 and ILC3 including several subs

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

56 ble to AAI than WT littermates, whereby both ILC2 and Th2 cells were important cellular sources of IL

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

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

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

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

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

62 s involves type 2 immune cells, such as Th2, ILC2, and basophils exerting their effect by production

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

64 ILC1, ILC2, and ILC3 cells were cultured for 5 days with RA, 1

65 ursor (ILCP) strictly committed to the ILC1, ILC2, and ILC3 lineages.

66 f innate lymphoid cells (ILCs) such as ILC1, ILC2, and ILC3 populate the intestine, but how these ILC

67 ss- and gain-of-function studies reveal that ILC2- and eosinophil-derived type 2 cytokines stimulate

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

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

70 Group 2 innate lymphoid cells (ILC2) are important in effector functions for eliciting

71 ese data identify Arg1 as a key regulator of ILC2 bioenergetics that controls proliferative capacity

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

73 D4(+) Th2 and group 2 innate lymphoid cells (ILC2), but whether certain metabolic enzymes control dis

74 Surprisingly, human IL-13(+)ILC2 can acquire the capacity to produce IFN-gamma, ther

75 t an emerging concept that myeloid cells and ILC2 can coordinately regulate tissue damage at mucosal

76 as inhibited, while exogenous IL-33 restored ILC2 cell activation and type 2 cytokine expression.

77 ic CD4(+) Th2 cells, whereas CD4(+) Th17 and ILC2 cell numbers remained constant.

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

79 this conversion, and during viral infection, ILC2 cells clustered within inflamed areas and acquired

80 Thus, functional plasticity of ILC2 cells exacerbates anti-viral immunity, which may ha

81 he sentinel function of DCs is contingent on ILC2 cells for the generation of an efficient memory TH2

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

83 tly and negatively regulated mouse and human ILC2 cells in a manner dependent on the transcriptional

84 Notably, IL-12 converted human ILC2 cells into ILC1 cells, and the frequency of ILC1 ce

85 2 cell responses, with targeted depletion of ILC2 cells profoundly impairing TH2 cell localization to

86 I interferons, together with IL-27, regulate ILC2 cells to restrict type 2 immunopathology.

87 Here we found that group 2 ILCs (ILC2 cells) also exhibited phenotypic plasticity in resp

88 activation of group 2 innate lymphoid cells (ILC2 cells) and infection-associated type 2 immunopathol

89 Among these, type 2 ILCs (ILC2 cells) are able to produce type 2 cytokines.

90 Group 2 innate lymphoid cells (ILC2 cells) are important for type 2 immune responses an

91 While type 2 innate lymphoid cells (ILC2 cells) are the dominant innate producers of IL-13 i

92 , as well as production of IL-5 and IL-13 in ILC2 cells, and IFN-gamma in ILC1 and ILC3 cells.

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

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

95 ed that IL-1beta was a critical activator of ILC2 cells, inducing proliferation and cytokine producti

96 evelopment of ILC1 and ILC3 cells but not of ILC2 cells.

97 we demonstrate that group 2 innate lymphoid (ILC2) cells have a crucial role in memory TH2 cell respo

98 y, and activation of innate lymphoid type 2 (ILC2) cells was inhibited, while exogenous IL-33 restore

99 The cell population with phenotypic ILC2 characteristics, lineage(-)CD127(+)CRTH2(+) cells,

100 ILC2 cultures demonstrated that IFN-gamma(+)ILC2 clones could be derived and were stably associated

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

102 Here, we characterize the ILC2 compartment in CRS by investigating the correlation

103 ally sensitized with food allergens, and the ILC2 compartment was analyzed.

104 sulted in a deficiency or dysfunction of the ILC2 compartment, respectively, and resistance to experi

105 A usage and FA-dependent IL-13 production by ILC2 could represent a host adaptation to maintain barri

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

107 ILC2 cultures demonstrated that IFN-gamma(+)ILC2 clones

108 n supernatants from both stimulated PBMC and ILC2 cultures.

109 ines upregulated B7-H6, leading to increased ILC2 cytokine production.

110 allergen papain, they produced ILC3 but not ILC2 cytokines and caused increased airway infiltration

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

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

113 reduces ILC2 effector function and represses ILC2-dependent AHR, while decreasing expression of ILC2

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

115 tion at the site of inflammation and reduced ILC2-dependent immune responses in a number of models of

116 for RNase-mediated release of IL-33 inducing ILC2-dependent improvements in the metabolic status of o

117 In contrast, treatment with IL-9 promoted ILC2-dependent Treg activation and effectively induced r

118 Interestingly, ILC2 depletion correlated with less severe hepatitis and

119 , and alveolar lavage fluid was analyzed for ILC2-derived cytokines.

120 2 cells induced by ingested antigens enhance ILC2-derived IL-13 production, thereby promoting IgE-med

121 ated from IL-5-deficient mice, we found that ILC2-derived IL-5 is critically involved in the enhanced

122 ILC2-derived interleukin 13 (IL-13) is critical for elic

123 by T cells and innate lymphoid type 2 cells (ILC2), despite normal early induction of ILC2s.

124 e lysine methyltransferase G9a in regulating ILC2 development and function.

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

126 ion factor Gata3 is essential for T cell and ILC2 development from hematopoietic stem cells (HSCs) an

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

128 PD-1(hi)IL-25R(hi) as an early checkpoint in ILC2 development, which was abolished by deficiency in t

129 in the regulation of Id2 at the inception of ILC2 development.

130 r previously linked to T cell commitment, in ILC2 development.

131 , which is active both in T cells and during ILC2 development.

132 Although subsets of human CRTh2(+)ILC2 differentially express CD117 (c-kit receptor), some

133 cytokines and lipid mediators can influence ILC2, direct interaction of these cells with the microen

134 , effectively suppress the production of the ILC2-driven proinflammatory cytokines IL-5 and IL-13 bot

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

136 f a previously unappreciated IL-10 producing ILC2 effector cell population.

137 ic agonist with alpha7nAChR on ILC2s reduces ILC2 effector function and represses ILC2-dependent AHR,

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

139 We also detected IL-13(+)IFN-gamma(+)ILC2 ex vivo in intestinal samples from Crohn's disease

140 data reveal ETS1 as a critical regulator of ILC2 expansion and cytokine production and implicate ETS

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

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

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

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

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

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

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

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

149 A subset of ex vivo and cultured ILC2 express NKp30 that upon interaction with its cognat

150 ILC2 expressed higher levels of both SERPINB3 and SERPIN

151 pletion of Tregs interrupted MaR1 control of ILC2 expression of IL-13 in vivo.

152 Exogenous MaR1 reduced lung inflammation and ILC2 expression of IL-5 and IL-13 and increased amphireg

153 Mechanistically, dexamethasone upregulated ILC2 expression of IL-7 receptor alpha, which augmented

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

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

156 signaling pathway is critically involved in ILC2 function and homeostasis.

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

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

159 ll-intrinsic metabolic pathways that control ILC2 function are undefined.

160 FN-gamma) and interleukin 27 (IL-27) altered ILC2 function dependent on the transcription factor STAT

161 However, the upstream signals that regulate ILC2 function during pulmonary inflammation remain poorl

162 ate cell-derived IL-2 as a major cofactor of ILC2 function during pulmonary inflammation.

163 This suggested that an altered ILC2 function in BALB/c mice might mediate the increased

164 ed IL-2 is a critical cofactor in regulating ILC2 function in pulmonary type 2 pathology.

165 mined the consequences of PLZF deficiency on ILC2 function in response to innate and adaptive immune

166 rstand the role of IL-2 in the regulation of ILC2 function in the lung.

167 -2, but the importance of endogenous IL-2 in ILC2 function in vivo remains unclear.

168 ckout and reporter mice to dissect pulmonary ILC2 function in vivo.

169 ever, the effect of prostaglandin (PG) I2 on ILC2 function is unknown.

170 in treating allergic diseases by suppressing ILC2 function.

171 fined male-specific factors are required for ILC2 function.

172 out to investigate how PGE2 regulates human ILC2 function.

173 teraction are important in the regulation of ILC2 function.

174 After ILC2 gene expression analysis we investigated the role o

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

176 or and establish that Bcl11b sustains mature ILC2 genetic and functional programs and lineage fidelit

177 producing ILC1, plasticity of human or mouse ILC2 has not been shown.

178 discovery of group 2 innate lymphoid cells (ILC2) has increased our understanding of the initiation

179 Group 2 innate lymphoid cells (ILC2) have been implicated in the pathogenesis of allerg

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

181 ells constitutively express IL-25 to sustain ILC2 homeostasis in the resting lamina propria in mice.

182 airway inflammation by negatively regulating ILC2 homeostasis, thereby limiting their capacity to exp

183 in specifying type II innate lymphoid cell (ILC2) identity and blocks their conversion to ILC3s.

184 We report the existence of an inflammatory ILC2 (iILC2) population responsive to interleukin 25 (IL

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

186 Induction of the IL-33/ILC2/IL-13 circuit in a murine biliary injury model prom

187 ILC2 IL5 up-regulation induces further IL5 expression by

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

189 e we show that type 2 innate lymphoid cells (ILC2), important mediators of barrier immunity, predomin

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

191 L-13 and CCL17 and had impaired expansion of ILC2 in damaged lung tissue compared with wild-type cont

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

193 Given the role of IL-5 produced by ILC2 in regulating eosinophil development and survival,

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

195 w focuses on the important messenger role of ILC2 in translating epithelial-derived alarmins into dow

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

197 2 cytokine-producing innate lymphoid cells (ILC2) in the FALC.

198 sed numbers of innate lymphoid type 2 cells (ILC2) in the lung, which also exhibited elevated mRNA ex

199 Group 2 innate lymphoid cells (ILC2) include IL-5- and IL-13-producing CRTh2(+)CD127(+)

200 sensitization and anaphylaxis while reducing ILC2 induction.

201 bsence of RAGE does not affect IL-33-induced ILC2 influx in the spleen, type 2 cytokine production in

202 ILC2 infusion was associated with reduced donor proinfla

203 Unexpectedly, ILC2-intrinsic IL-33 activation was required for Treg ce

204 ependent AHR, while decreasing expression of ILC2 key transcription factor GATA-3 and critical inflam

205 ILC2 lack rearranged Ag-specific receptors, and although

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

207 In agreement with the foregoing, IL-33 and ILC2 levels were increased in the airways of asthmatic p

208 ivating cytokine, in promoting the egress of ILC2 lineage cells from the bone marrow.

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

210 ly unknown role for IL-1beta in facilitating ILC2 maturation and plasticity.

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

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

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

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

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

216 tial therapeutic target for the treatment of ILC2-mediated asthma.

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

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

219 ic activity disrupted multiple components of ILC2 metabolic programming by altering arginine cataboli

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

221 s cytokine production and AHR in a humanized ILC2 mouse model.

222 ) that complemented IL-33-responsive natural ILC2 (nILC2) cells.

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

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

225 e effect of IL-2 administration on pulmonary ILC2 numbers and function in mice in the steady state an

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

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

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

229 The increase in ILC2 numbers in the lung has been largely attributed to

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

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

232 ILC2 numbers increase in the mouse lung not only through

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

234 ILC2 numbers significantly increased in nasal mucosal sa

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

236 xposure resulted in increased IL-33-mediated ILC2 numbers, TH2 cell numbers, and steroid-resistant AH

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

238 ow and concurrently increased blood and lung ILC2 numbers.

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

240 tration, airway mucus, airway reactivity, or ILC2 numbers.

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

242 of enforced Gata3 expression in T cells and ILC2 on the susceptibility of mice to allergic airway in

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

244 IL-1beta also governed ILC2 plasticity by inducing low expression of the transc

245 The inductive mechanism for ILC2 plasticity was mapped to the IL-12-IL-12R signaling

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

247 ssion of ILC3-associated genes in developing ILC2 populations.

248 er mice, we show that Bcl11b is expressed in ILC2 precursors in the BM and maintained in mature ILC2s

249 Together, these results reveal that ILC2 preferentially use FAs to maintain their function i

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

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

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

253 ETS1-deficient ILC2 progenitors failed to up-regulate messenger RNA for

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

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

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

257 ogenic strains of RSV induce IL-13-producing ILC2 proliferation and activation through a TSLP-depende

258 ated type 2 lung inflammation by restraining ILC2 proliferation and dampening cytokine production.

259 which IL-2 production from T cells promotes ILC2 proliferation and IL-13 production.

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

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

262 n line with this observation, PGE2 decreased ILC2 proliferation.

263 Interestingly, ILC2 recruitment to the lung occurred independently of T

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

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

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

267 asthma pathogenesis; however, mechanisms for ILC2 regulation remain to be determined.

268 substantial convergence of Th2 cells toward ILC2 regulomes.

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

270 rovide evidence suggesting that an analogous ILC2 response is operational in acute wounds of human sk

271 GI2 may be a potential therapy to reduce the ILC2 response to protease-containing aeroallergens, such

272 LPR KO mice did not mount an IL-13-producing ILC2 response to RSV infection.

273 y attenuated the RSV-induced IL-13-producing ILC2 response.

274 ury promotes an IL-33-dependent group 2 ILC (ILC2) response and that abrogation of this response impa

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

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

277 in human WAT and demonstrate that decreased ILC2 responses in WAT are a conserved characteristic of

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

279 ata extract for 4 consecutive days to induce ILC2 responses, and these were quantified.

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

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

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

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

284 of cysLTs and their relationship with other ILC2 stimulators in the activation of human ILC2s.

285 S ligand cell contact for Treg cell-mediated ILC2 suppression alongside the suppressive cytokines TGF

286 ntially express CD117 (c-kit receptor), some ILC2 surface phenotypes are unstable and can be modulate

287 ial nutrient, such as vitamin A, is limited, ILC2 sustain their function and selectively maintain int

288 olecularly distinct subset of activated lung ILC2, termed ILC210.

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

290 for IL-5 and IL-13 production by T cells and ILC2, the role for Gata3 in the generation or function o

291 lates T cells and type 2 innate lymphocytes (ILC2) through its receptor DR3 (Tnfrsf25).

292 mplexes drove group 2 innate lymphoid cells (ILC2) to produce IL-5 and proliferate.

293 , a member of group 2 innate lymphoid cells (ILC2), to secrete Th2 type-cytokines.

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 n factor, acted directly upstream of the key ILC2 transcription factor Gfi1 to maintain its expressio

297 accumulation in vivo and was independent of ILC2 type 2 cytokines but partially dependent on direct

298 Only ILC1 and ILC3, but not ILC2, undergo the RA-dependent homing receptor switch in

299 IL-12 acted as the switch that determined an ILC2-versus-ILC1 response.

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