ライフサイエンスコーパス: Th2 cell

1 D4(+) T cells that produce type 2 cytokines (Th2 cells).

2 (ILC2s) and recruited type 2 helper T cells (TH2 cells).

3 es the rapid activation of T helper 2 cells (Th2 cells).

4 n allergic patients control the viability of TH2 cells.

5 ice are unable to generate follicular Th and Th2 cells.

6 lminth-induced regulatory T cells (Tregs) or Th2 cells.

7 or of PGD2-induced cytokine release in human Th2 cells.

8 ress less DENND1B and phenocopy Dennd1b(-/-) TH2 cells.

9 -1 sites surrounding type-2 cytokine loci in Th2 cells.

10 and M2 macrophages in myeloma elimination by Th2 cells.

11 numbers but an increase in the proportion of Th2 cells.

12 numbers of T follicular helper and effector Th2 cells.

13 rotein 3-positive Treg cells while promoting TH2 cells.

14 d miR-27 upstream of genes known to regulate Th2 cells.

15 Gata3 mRNA is stabilized in Zc3h12a(-/-) TH2 cells.

16 +) T cell capability of differentiating into TH2 cells.

17 r functional profile with that of autologous TH2 cells.

18 by adoptively transferred Ag-specific CD4(+) Th2 cells.

19 tors derived from mast cells, which activate TH2 cells.

20 ramer(+) T cells and very low proportions of Th2 cells.

21 of fibrosis, is routinely ascribed to CD4(+) Th2 cells.

22 ession in Tfh cells rather than in canonical Th2 cells.

23 The tetramers defined bona fide Th2 cells.

24 ted with the loss of alpha2delta2 protein in TH2 cells.

25 ormal differentiation of human TH1 cells and TH2 cells.

26 transferred, traceable ovalbumin-experienced Th2 cells.

27 tributing to the cross-regulation of Th1 and Th2 cells.

28 ted mice from anaphylaxis, without affecting Th2 cells.

29 cultures identified CD200R as upregulated on Th2 cells.

30 -loop-mediated DSBs in TH1 cells relative to TH2 cells.

31 h preferential suppression of Th1 cells over Th2 cells.

32 e gene expression pattern related to Tfh and Th2 cells.

33 ecific highly differentiated IL-4(+) IL-5(+) Th2 cells.

34 erentiation and expansion of T reg, Th1, and Th2 cells.

35 ote effector differentiation of HDM-specific TH2 cells.

36 variant (Etv)5 regulates IL-10 production in Th2 cells.

37 is required for the development of ex-Foxp3 Th2 cells.

38 Salmonella independently of T regulatory or Th2 cells.

39 erived suppressor cells (MDSCs) and IL-13(+) Th2 cells.

40 L-4-producing CD4(+) T cells, namely TFH and Th2 cells.

41 regulatory networks that govern T helper-2 (Th2) cells.

42 ing and activated ILC2s and T helper type 2 (TH2) cells.

43 a, a serine/threonine kinase, is involved in TH2 cell activation and proliferation.

44 interaction of cysLTs with PGD2 in promoting TH2 cell activation is still poorly understood.

45 e had eosinophilic airway inflammation and a TH2 cell activation phenotype that was not different fro

46 Efficient TH2 cell activation required both an increased stability

47 IL-13 production in lung tissue, as well as TH2 cell activation.

48 crophages, type 2 innate lymphoid cells, and TH2 cells along with increased Il33 expression in the ai

49 Co-culture of LECs with TH2 cells also inhibits tube formation, but this effect

50 sion was selectively maintained in polarized TH2 cells and absent in TH1 or TH9 cells.

51 ted the terminal differentiation of effector TH2 cells and adaptive lung inflammation in a T cell-int

52 ependent requirement for IL-1R expression on TH2 cells and an important nonredundant role for T-cell-

53 at RNase 7 has immunomodulatory functions on TH2 cells and decreases the production of TH2 cytokines

54 mmune mechanisms important in asthma such as Th2 cells and eosinophils also manifest autophagy.

55 Activated TH2 cells and eosinophils are hallmarks of the allergic

56 4, and their combination in activating human TH2 cells and how such activation might allow the TH2 ce

57 acceleration both by live imaging of single Th2 cells and in an ex vivo Th1 malaria model by single-

58 PINB4 mRNA was measured in in vitro-cultured TH2 cells and in ex vivo CD27(-)CD4(+) cells and innate

59 orative interactions between acquired CD4(+) Th2 cells and innate ILC2s to drive the exacerbation of

60 helminths consists of adaptive responses by TH2 cells and innate responses by group 2 innate lymphoi

61 etting, we observed that Tigit expression in Th2 cells and its interaction with CD155 expressed in de

62 s into Th2 cells could concomitantly enhance Th2 cells and limit T reg cell-mediated suppression.

63 icularly those involving interaction between TH2 cells and neutrophils, such as in patients with seve

64 isms that regulate maintenance of persistent TH2 cells and potentiate allergic inflammation are not w

65 ype 2 innate lymphoid cells (ILC2s) resemble TH2 cells and produce the TH2 cytokines IL-5 and IL-13 b

66 hat Tfh cells are precursors of HDM-specific Th2 cells and reveal an unexpected role of B cells and T

67 nvestigating the correlations between ILC2s, Th2 cells and Th2 cytokines expression in CRS patients.

68 ited multiorgan inflammation by reducing Th1/Th2 cells and their associated cytokines.

69 -mediated proliferation of cocultured CD4(+) Th2 cells and their cytokine production, and promoted eo

70 he regulation of bronchial epithelial TJs by TH2 cells and their cytokines and their involvement in e

71 TH2 cells and their cytokines are associated with allerg

72 onstrate an anti-lymphangiogenic function of TH2 cells and their cytokines, suggesting a potential us

73 al inflammatory cells, such as activation of Th2 cells and tolerization of dendritic cells by suppres

74 e associated with improved survival, whereas Th2 cells and Tregs are associated with negative outcome

75 e have shown that simultaneous inhibition of Th2 cells and Tregs by using the pharmacological inhibit

76 ons in skin-infiltrating pathogenic effector Th2 cells and TSLP.

77 a(+) exosomal-mediated induction of IL-13(+) Th2 cells and tumor angiogenesis.

78 ophil counts, which might be orchestrated by TH2 cells and type 2 innate lymphoid cells though releas

79 iasis not only via modification/induction of Th2 cells and type II dendritic cells, but also via dire

80 iated by IL-5-expressing pathogenic effector Th2 cells and was independent of TCRgammadelta T cells a

81 nsgenic tools to characterize the lineage of th2(+) cells and demonstrate that they are dopaminergic.

82 le for interleukins derived from T-helper-2 (Th2) cells and innate lymphoid cells, such as interleuki

83 how the negative effects of T helper type 2 (TH2) cells and their cytokines on LV formation.

84 n contrast to constitutive ST2 expression on Th2 cells, and marked highly activated effector cells.

85 nt receptor-homologous molecule expressed on TH2 cells, and montelukast, an antagonist of cysteinyl l

86 ulated gene expression networks in ILC2s and TH2 cells, and reinforce the therapeutic potential of ta

87 se inhibitor 2A (Spi2A) was studied in mouse TH2 cells, and the serine protease inhibitor B3 (SERPINB

88 nse, including the expansion of eosinophils, Th2 cells, and type 2 innate lymphoid cells, associated

89 the Th1 phenotype, exacerbated generation of Th2 cells, and unaltered Th17 differentiation.

90 nt receptor-homologous molecule expressed on TH2 cells antagonists.

91 Th2 cells appear to be the critical IL-4/IL-13-expressin

92 Although we have learned much about how TH2 cells are differentiated, the TH2 checkpoint mechani

93 hypothesized that allergen- specific memory Th2 cells are present and the factors necessary for the

94 on factors that regulate IL-10 production in Th2 cells are still incompletely described.

95 However, Th2 cells are the major source of IL-4 during HDM sensit

96 ls (ILC2s) and CD4(+) type 2 helper T cells (TH2 cells) are defined by their similar effector cytokin

97 oid cells (ILC2s) and type 2 helper T cells (Th2 cells) are the primary source of interleukin 5 (IL-5

98 r proportion of skin-homing cells expressing TH2 cell-associated chemokine receptors.

99 dermatitis produced by overexpression of the TH2 cell-associated cytokine, IL-31 (IL-31Tg mice).

100 ion controls the innate effector function of Th2 cells at the site of inflammation.

101 IL-33), which induces type-2 helper T cells (Th2 cells) at the site of infection to produce IL-13, th

102 ata indicate that dysregulation of ILC2s and TH2 cells attenuates DEP-enhanced allergic airway inflam

103 is critical for eliciting production of the TH2 cell-attracting chemokine CCL17 by IRF4(+)CD11b(+)CD

104 Their CD4(+) T cells exhibit a "Th2" cell bias ex vivo and when cultured in vitro, contr

105 ified targets not previously associated with Th2 cell biology which regulated IL-4 production in unbi

106 e of miR-24 and miR-27 reveals regulators of Th2 cell biology.

107 pression of GATA3 and production of IL-13 by Th2 cells both in vitro and in vivo.

108 nificant decrease of Th9- and IL-4-producing Th2 cells but an increase of Th17 cells in lung tissue i

109 elminth-elicited Il4(gfp+)alphabeta(+)CD4(+) TH2 cells but not in TH1, TH17, or Treg cells.

110 transcription factor expression with CD4(+) Th2 cells, but functional diversity of the ILC2 lineage

111 ich is crucial for the induction of IL-13(+) Th2 cells, but it also participates in the induction of

112 t differences to conventional Th1, Th17, and Th2 cells, but no major changes between healthy and LTBI

113 As a consequence, in vitro polarized Th2 cells, but not Th9 cells, are able to release IL-31.

114 ucial role in regulating IL-10 production in Th2 cells by facilitating the binding of IL-10-inducing

115 Moreover, human TH2 cells carrying asthma-associated DENND1B variants ex

116 IL-17RB(+)CD4(+) polyp-derived TH2 cells coexpressed ST2 (IL-33 receptor) and responded

117 nd here that helminth-infected mice had more TH2 cells compared to uninfected mice, and thes e cells

118 Th2 cells contribute to the development of disease throu

119 fied subset of immune cells that, along with Th2 cells, contribute to the pathogenesis of asthma by p

120 ecognized regulator of TCR downmodulation in TH2 cells, contributes to asthma pathogenesis and how DE

121 gs indicate that converting T reg cells into Th2 cells could concomitantly enhance Th2 cells and limi

122 Functional inhibition of Dkk-1 impaired Th2 cell cytokine production and leukocyte infiltration,

123 the kinases p38 MAPK and SGK-1, resulting in Th2 cell cytokine production.

124 ese findings indicate that IL-4, a canonical Th2 cell cytokine, can sometimes promote rather than imp

125 allergic (DCs driving the differentiation of TH2 cells [DC2s]) phenotype and investigate whether chan

126 As DENND1B interacts with AP-2 and Rab35, TH2 cells deficient in AP-2 or Rab35 also exhibit enhanc

127 TFH and TH2 cells demonstrated unique phenotypes, tissue localiz

128 ergen exposure induces an IgG4 response in a TH2 cell-dependent manner.

129 demonstrate that a significant proportion of Th2 cells derive from Foxp3(+) cells after Heligmosomoid

130 In this study, we asked whether ex-T reg Th2 cells develop and contribute to type-2 immunity.

131 the initial exposure to HDM did not lead to Th2 cell development but instead promoted the formation

132 ancer eradication mediated by tumor-specific Th2 cells did not require B cells, natural killer T cell

133 promoted peanut-specific IgE production than Th2 cells did.

134 We found that tissue ILC2s and TH2 cells differentiated independently but shared overla

135 y the Zc3h12a gene) regulates IL-5-producing TH2 cell differentiation and TH2-mediated inflammation.

136 IL-4Ralpha) chain on CD4(+) T cells leads to TH2 cell differentiation in vitro, implying that IL-4Ral

137 1beta, IL-6, and IL-23, whereas HDM-specific TH2 cell differentiation was hampered by increased IL-12

138 ctor for ILC2 activation that contributes to TH2 cell differentiation, which is associated with IRF4

139 lls uncovered multiple miRNAs that inhibited Th2 cell differentiation.

140 demonstrates that IL-37 is able to ablate a TH2 cell-directed allergic inflammatory response and the

141 -4 and IL-13, released from T-helper type 2 (Th2) cells, drive macrophage polarization toward an alte

142 dust mite (HDM), often leads to T helper 2 (Th2) cell-driven allergic responses.

143 cells to suppress the deleterious effects of Th2 cells during cryptococcal infection.

144 a previously unappreciated role for effector TH2 cells during TCR-independent innate-like immune resp

145 apid activation of memory CD4(+) T helper 2 (TH2) cells during allergic inflammation requires their r

146 A levels of IgG4 and IgE, genes specific for Th2 cells, eosinophils, and neutrophils were over-expres

147 Ex-Foxp3 Th2 cells exhibit characteristic Th2 effector functions

148 e for autophagy in directly limiting mucosal TH2 cell expansion.

149 Mouse and human TH2 cells express mainly Cavbeta1, beta3, and alpha2delt

150 subsets, including naive CD4(+) T cells and TH2 cells, express a distinct transcript of Runx3 that i

151 , and GATA-3 assemble at the Il4 promoter in Th2 cells expressing IL-4 but not in Th2 cells not expre

152 unity, IL-33 interacts with dendritic cells, Th2 cells, follicular T cells, and regulatory T cells, w

153 we tested the efficacy of idiotype-specific Th2 cells for the treatment of mice with MHC class II-ne

154 ocused on the lung parenchyma by transfer of Th2 cells from a novel TCR transgenic mouse, specific fo

155 cells in vitro and in vivo as well as human Th2 cells from allergic patients.

156 Th2 cells from asthmatic subjects expressed higher level

157 suggesting enhanced activation potential of Th2 cells from asthmatic subjects.

158 rgic disease and has been shown to work with TH2 cells from atopic asthmatic patients.

159 IGIT expression was upregulated in activated Th2 cells from mice with experimental allergic disease a

160 In vitro-polarized TH2 cells from patients with grass pollen allergy expres

161 SERPINB3) and SERPINB4 genes were studied in TH2 cells from patients with grass pollen allergy.

162 here were lower levels of in vitro-polarized TH2 cells from Spi2A knockout mice (P < .005) and in viv

163 whether there are qualitative differences in Th2 cells from subjects with allergic asthma, rhinitis,

164 absence of other T-cell subsets or even when TH2 cell functions were severely compromised.

165 f PGD2, LTE4, and their combination on human TH2 cell gene expression were defined by using a microar

166 th the receptor TNFRSF14 (HVEM), can support TH2 cell generation and longevity and promote airway rem

167 d microenvironment instructed pDC-driven Th9/Th2 cell generation.

168 , our transcriptomic analysis of circulating Th2 cells has identified several molecules that are like

169 IFNgamma-producing Th1 cells, tumor-specific Th2 cells have been largely neglected for ACT due to the

170 TH2 cells have long been believed to play a pivotal role

171 Th2 cells have long been considered responsible for the

172 to induction of activated MDSCs and IL-13(+) Th2 cells have not yet been identified.

173 eakiness in asthmatic patients is induced by TH2 cells, IL-4, and IL-13 and HDAC activity.

174 d exposure to pathogens, urban dwellers have TH2 cell immune activity and atopic disease in a more st

175 Supernatant of activated TH1 and TH2 cells impaired epithelial integrity, while treatment

176 miR-126a(+) exosomes further induce IL13(+) Th2 cells in a positive feed-back loop manner.

177 ces in understanding the origins of atypical TH2 cells in asthmatic patients, the role of TH1 cells a

178 decreased the number of functional ILC2s and TH2 cells in DEP+HDM-exposed mice, resulting in an impai

179 development of IL-4-producing TFH cells and TH2 cells in draining lymph nodes after airway exposure

180 ght to investigate the role of histamine and TH2 cells in driving epithelial barrier dysfunction in A

181 f Th1 and Th17 cells and decreased the Fo of Th2 cells in INF individuals.

182 Although frequencies of antigen-specific TH2 cells in peripheral blood determined by using HLA cl

183 tracellular cytokine expression in ILC2s and TH2 cells in the bronchoalveolar lavage fluid and lung t

184 responses, the DC subpopulations that induce Th2 cells in the intestine are unidentified.

185 - and IL-13-producing but not IL-4-producing TH2 cells in the lung.

186 nd establish a fundamental role for TSLP and Th2 cells in tumor immunity against early-stage cancers.

187 Although the prominent role of TH2 cells in type 2 immune responses is well established

188 ssed by effector cells, including pathogenic TH2 cells in ulcerative colitis, but is expressed poorly

189 It is predominantly expressed in mouse Th2 cells in vitro and in vivo as well as human Th2 cell

190 of inosine on the differentiation of Th1 and Th2 cells in vitro depended on adenosine A2A receptors,

191 and proliferation rate holds both in Th1 and Th2 cells in vivo and in vitro, indicating that this is

192 owever, their role in priming IL-4-producing Th2 cells in vivo is not fully understood.

193 mphoid cells (ILC2s) resemble type 2 helper (Th2) cells in cytokine production and contribute to anti

194 and induced diverse functional responses in TH2 cells, including cell adhesion, migration, and survi

195 Treg cells with distinct characteristics of TH2 cells increased in the lungs of mice undergoing IL-3

196 Upon transfer, Th2 cells induced a type II inflammation at the tumor si

197 IL-25 and CD4(+) TH2 cells induced by ingested antigens enhance ILC2-deri

198 fferentiation of IL-5-producing Zc3h12a(-/-) TH2 cells is mediated through Notch signaling and Gata3

199 nt receptor-homologous molecule expressed on TH2 cells) is implicated in the pathogenesis of asthma,

200 ing in the substantial generation of Th1 and Th2 cells, leads us to propose that the critical CD28/B7

201 ormance (T-helper Type 17 [Th17]/Th2 and Th1/Th2 cell levels) were performed according to Th cell res

202 e acquisition by Treg cells of a T helper 2 (Th2)-cell-like phenotype, also found in peripheral-blood

203 depletion of ILC2 cells profoundly impairing TH2 cell localization to the lungs and skin of sensitize

204 TH2 cells made important contributions to HDM-induced an

205 rized by increased numbers of lamina propria TH2 cells, mast cells, and eosinophils, shock (hypotherm

206 In addition, the effect of activated TH1 and TH2 cells, mast cells, and neurons was tested in vitro.

207 ndicates that inhibition or reprogramming of Th2 cells may be very effective for the treatment of all

208 Thus, ACT with tumor-specific Th2 cells may represent a highly efficient immunotherapy

209 l CD28/B7 interactions, required to generate Th2 cells, may directly occur between CD4 T cells engage

210 Additionally, CD4+ Th2 cells mediated the antitumor effects of TSLP, challe

211 e that innate TLR2 signals convert transient TH2 cell-mediated dermatitis into persistent inflammatio

212 Most commonly associated with Th2 cell-mediated diseases, we describe a role for eosin

213 the IL-17 family of cytokines that promotes Th2 cell-mediated inflammatory responses.

214 zation phase or Tfh cell depletion prevented Th2 cell-mediated responses following challenge.

215 The efficacy of PIT on different T helper 2 (Th2) cell memory populations is unknown.

216 Mast cells and TH2 cells might decrease epithelial barrier integrity in

217 Blocking PKC or Cav1.2 channel activation in TH2 cells might represent new strategies to treat allerg

218 L-4 contributes to IL-10 production and that Th2 cells modulate Th1 cultures towards a self-regulator

219 Allergen-specific TH2 cells most closely paralleled the transient clinical

220 oter in Th2 cells expressing IL-4 but not in Th2 cells not expressing it.

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

222 TH2 cell numbers and levels of their cytokines, IL-4 and

223 and IL-13(+) innate lymphoid cell (ILC) and TH2 cell numbers but similar airway hyperresponsiveness

224 ed in increased IL-33-mediated ILC2 numbers, TH2 cell numbers, and steroid-resistant AHR.

225 Lung IL-33 levels, IL-13(+) ILC numbers, TH2 cell numbers, IL-13 levels, and AHR remained increas

226 effects of TSLP, challenging the notion that Th2 cells only promote cancer.

227 ine-secreting alphabeta(+)CD4(+) T-helper 2 (TH2) cells orchestrate the type-2-driven immune response

228 Transferred Th2 cells persisted in vivo and conferred long-lasting i

229 Because Th2 cells play a pathogenic role in both these diseases

230 ), lymphoid infiltrates, comprised mainly of Th2 cells, predict a poor survival outcome in patients.

231 ells on DC phenotype, maturation status, and TH2 cell priming potential.

232 In Th cell subsets, Th2 cells produce considerable amounts of IL-10.

233 Type 2 helper T cells (TH2 cells) produce interleukin 13 (IL-13) when stimulate

234 consists of GATA-3(+) ILC2s, TC2 cells, and TH2 cells producing IL-4, IL-5, and IL-13, which induce

235 TGF-beta together drove their suppression of TH2 cell proliferation.

236 In patients with allergic asthma, TH2 cells promote IgE-mediated sensitization, airway hyp

237 fferentiation and to be induced by activated Th2 cells raises the possibility that TSLP may be involv

238 nding of the TF GATA-3 to the locus encoding TH2-cell-related cytokines and diminished intrachromosom

239 Interruption of Th2 cell reprogramming of Treg cells might thus provide

240 ctivation and expansion, which in turn drove Th2 cell reprogramming of Treg cells.

241 requisite for IL-33-induced IL-13 secretion, Th2 cells required the expression of the epidermal growt

242 ls for the generation of an efficient memory TH2 cell response.

243 cells, which together induce a HDM-specific Th2 cell response.

244 both clusters in T cells displayed increased Th2 cell responses and tissue pathology in a mouse model

245 nditional Klf4 deletion within cDCs impaired Th2 cell responses during Schistosoma mansoni infection,

246 e relative contribution of ILC2 and adaptive TH2 cell responses in a murine model of DEP-enhanced all

247 and immunopathology caused by induced type 2 Th2 cell responses in animal models.

248 mice lacking lung rEos showed an increase in Th2 cell responses to inhaled allergens.

249 We found that Th2 cell responses, and related events such as eosinophi

250 , IFN regulatory factor 4, to dampen harmful Th2 cell responses, as well as mediate chemokine retenti

251 AIG in DEREG mice is associated with strong Th2 cell responses, including dominant IgG1 autoantibodi

252 d (ILC2) cells have a crucial role in memory TH2 cell responses, with targeted depletion of ILC2 cell

253 of Abeta42-specific effector (Th1, Th17, and Th2) cell responses at later immunization times.

254 T-helper 2 (Th2) cell responses defend against parasites.

255 llergen extracts are used to study T helper (Th2) cell responses to HDM, which are implicated in the

256 ell ablation, the increase or loss of CD4(+) Th2 cells resulted in an enhanced or reduced IL-13 produ

257 Instead, only CD4(+) Foxp3(-) IL-4(+) Th2 cells showed increased IL-10 production upon infecti

258 ts of Dkk-1 polarized T cells to T helper 2 (Th2) cells, stimulating a marked simultaneous induction

259 through its ability to both directly induce Th2 cell survival and to impair regulatory T-cell suppre

260 In Th2 cells, T cell receptor (TCR) signaling activates the

261 of highly polarized transgenic CD4 effector Th2 cells, termed BT-II, followed by repeated inhalation

262 s into tumor-promoting T helper type 2 cell (Th2 cell), Th17 cell, and regulatory T cell populations

263 In addition to conventional TH2 cells, TH2/TH17 and TH17 cells were also detected in

264 ntiated into IL-4 and IL-13 double-producing Th2 cells that accumulated in the lung and recruited eos

265 are likely to confer pathogenic features to Th2 cells that are either unique or common to both asthm

266 mors inhibited Th1 and favored generation of Th2 cells that had lower tumoricidal activity than Th1 c

267 Ectopic Etv5 expression in Th2 cells that lack Etv5 restored IL-10 production and t

268 Here, we show that in reactivated Th2 cells, the transcription factors NFATc2, NF-kB p65,

269 IL-13 released from IL-13(+)Th2 cells then promotes the production of DOX-MDSC and M

270 Exploring the interplay of Th1 and Th2 cells through co-culture, Th2-derived IL-4 promoted

271 PGD2 and LTE4 activate TH2 cells through different pathways but act synergistic

272 disease through ablation of allergic memory TH2 cells through SERPINB3 and SERPINB4 mRNA downregulat

273 e development and function of IL-5-producing TH2 cells through the Notch/Gata3 pathway.

274 nnate lymphoid cells (ILC2s) and T helper 2 (Th2) cells, thus underpinning its association with helmi

275 ells and how such activation might allow the TH2 cells to engage downstream effectors, such as neutro

276 tion results in a substantial convergence of Th2 cells toward ILC2 regulomes.

277 t cell metaplasia, accumulation of ILC2s and TH2 cells, type 2 cytokine production, and airway hyperr

278 by the cytokines IL-5 and IL-13 coming from Th2 cells, type 2 innate lymphoid cells, and probably ma

279 Allergic asthma is caused by Th2-cell-type cytokines in response to allergen exposure

280 lls and prevented differentiation of TH1 and TH2 cells under respective TH1- and TH2-skewing conditio

281 regulatory T (Treg) cells in suppression of Th2 cells using a mouse model of experimental cryptococc

282 med in isolated CD4+T cells and in polarized TH2 cells using skin-derived native RNase 7 and a recomb

283 ced Fo of monofunctional and dual-functional Th2 cells was significantly increased in INF compared wi

284 EGFR expression on Th2 cells was TCR-signaling dependent, and therefore, ou

285 unidentified putative targets in pathogenic TH2 cells, we performed in silico analyses of recently p

286 I than WT littermates, whereby both ILC2 and Th2 cells were important cellular sources of IL-5 and IL

287 Circulating ILC2s and TH2 cells were isolated by means of fluorescence-activat

288 ral load and downregulation of IL-4Ralpha on Th2 cells were observed in IFN-alpha-treated neonatal mi

289 Spi2A-deficient TH2 cells were studied in in vitro culture or in vivo af

290 However, once polarized, TH2 cells were unaffected by the inhibitor.

291 ells, which are unable to differentiate into Th2 cells, were transplanted.

292 further increase of lung OVA-specific CD4(+) Th2 cells, whereas CD4(+) Th17 and ILC2 cell numbers rem

293 potently inhibits the release of IL-31 from Th2 cells, whereas IL-33, a cytokine associated with Th2

294 to low doses of inhaled CS, indicating that Th2 cells, which are dominant in MMA, do not solely orch

295 a significant increase in numbers of CD4(+) TH2 cells, which enhance IL-25-stimulated IL-13 producti

296 y triggers an increase of Ag-specific CD4(+) Th2 cells, which facilitates the collaborative interacti

297 s and cytokine production by mouse and human TH2 cells with no effect on TH1 cells.

298 Treatment of activated human CD4+T cells and TH2 cells with RNase 7 selectively reduced the expressio

299 ons and Th17 cells, as well as similarity of Th2 cells with Treg cells.

300 y was considered a dichotomy between Th1 and Th2 cells, with Th1 cells deemed culpable for autoimmune