ライフサイエンスコーパス: Th2 cell

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

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

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

4 and IL-3 regulates the effector functions of Th2 cells.

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

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

7 ted mice from anaphylaxis, without affecting Th2 cells.

8 cultures identified CD200R as upregulated on Th2 cells.

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

10 h preferential suppression of Th1 cells over Th2 cells.

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

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

13 and is downregulated in Malat1(-/-) Th1 and Th2 cells.

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

15 ote effector differentiation of HDM-specific TH2 cells.

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

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

18 Salmonella independently of T regulatory or Th2 cells.

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

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

21 n allergic patients control the viability of TH2 cells.

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

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

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

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

26 -1 sites surrounding type-2 cytokine loci in Th2 cells.

27 and M2 macrophages in myeloma elimination by Th2 cells.

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

29 numbers of T follicular helper and effector Th2 cells.

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

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

32 eading to increased GATA3 expression in lung Th2 cells.

33 HPGDS+ CRTH2+IL-17RB+FFAR3+CD4+ T8 effector Th2 cells.

34 cells that were unable to suppress extrinsic Th2 cells.

35 type 2 lymphocytes, NKT, and CD4(+) CRTH2(+) Th2 cells.

36 FAR3 was found to be highly expressed in EoE Th2 cells.

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

38 r functional profile with that of autologous TH2 cells.

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

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

41 ection, ASC depletion impaired lung ILC2 and Th2 cell accumulation and function, which are in part de

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

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

44 Efficient TH2 cell activation required both an increased stability

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

46 popolysaccharide (LPS) prevented T helper 2 (Th2) cell allergic responses in adult, but not infant, m

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

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

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

50 creased numbers of intestinal Th17 cells and Th2 cells and decreased numbers of RORgammat(+) Treg cel

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

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

53 Activated TH2 cells and eosinophils are hallmarks of the allergic

54 ls but increases in interleukin 5-expressing Th2 cells and eosinophils in perigonadal and inguinal AT

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

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

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

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

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

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

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

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

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

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

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

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

67 TH2 cells and their cytokines are associated with allerg

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

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

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

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

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

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

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

75 ukin (IL)-4, IL-5 and IL-13 from T helper 2 (Th2) cells and innate lymphoid cells type 2 (ILCs), and

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

77 e in inhibiting the Th1 program in committed Th2 cells, and mechanistically, its role might relate to

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

79 Differentiation of T-helper (Th1) cells, Th2 cells, and T-regulatory cells was determined by nucl

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

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

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

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

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

85 3 expression in an antigen-primed developing Th2 cell are not well understood.

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

87 te that Th2 Trm cells and circulating memory Th2 cells are functionally and transcriptionally distinc

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

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

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

91 T helper type 2 (Th2) cells are important regulators of mammalian adaptiv

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

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

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

95 t, upregulation of T helper type 1 (Th1) and Th2 cell-associated pathways, including interferon respo

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

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

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

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

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

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

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

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

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

105 from mice with pancreatitis had increases in Th2 cells but not in Th1 cells.

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

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

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

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

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

111 whole blood flow cytometry: CD4(+) T cells, Th2 cells (CD4(+) CRTh2(+) T cells and % of CD4(+) T cel

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

113 y Th2 (Th2 Trm) cells and circulating memory Th2 cells collaborate in vivo remain unclear.

114 pecific enrichment of CD4+ Treg and effector Th2 cells, confinement of type 2 cytokine production to

115 Th2 cells contribute to the development of disease throu

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

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

118 nt receptor-homologous molecule expressed on Th2 cells (CRTH2), a receptor for the bioactive lipid pr

119 hemoattractant receptor homolog expressed on Th2 cells (CRTH2)-expressing CD4(+) and CD8(+) T cells d

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

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

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

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

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

125 TFH and TH2 cells demonstrated unique phenotypes, tissue localiz

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

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

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

129 uced interleukin-12 (IL-12), which prevented Th2 cell development by promoting T-bet upregulation in

130 ter of GATA3 expression that is critical for Th2 cell development in the lung to inhaled but not syst

131 ctivation to up-regulate Blimp-1 and promote Th2 cell development.

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 at TRIM32 deficiency contributes to enhanced Th2 cell differentiation in vitro.

138 ming of integrin alpha(V)beta(3) expression: Th2 cell differentiation led to high alpha(V)beta(3) exp

139 1beta, IL-6, and IL-23, whereas HDM-specific TH2 cell differentiation was hampered by increased IL-12

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

141 lls uncovered multiple miRNAs that inhibited Th2 cell differentiation.

142 amine receptor (DRD4) to promote T helper 2 (Th2) cell differentiation.

143 Memory CD4+ T helper type 2 (Th2) cells drive allergic asthma, yet the mechanisms whe

144 -4 and IL-13, released from T-helper type 2 (Th2) cells, drive macrophage polarization toward an alte

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

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

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

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

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

150 vealed that while Notch-deficient lymph node Th2 cells established competence for lung migration, the

151 Ex-Foxp3 Th2 cells exhibit characteristic Th2 effector functions

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

153 This is because Malat1(-/-) Th1 and Th2 cells express lower levels of the immunosuppressive

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

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

156 ion of the Gata3 promoter detectable only in Th2 cells for EPIT from the 4th week and a significant h

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

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

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

160 Th2 cells from asthmatic subjects expressed higher level

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

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

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

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

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

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

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

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

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

170 complex, expressed primarily on mast cells, Th2 cells, group 2 innate lymphoid cells and regulatory

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

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

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

174 Th2 cells have long been considered responsible for the

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

176 urden of SCNAs have high levels of Tregs and Th2 cells, highlighting the importance of evaluating evo

177 cing Th1 cells, interleukin-(IL)-4-producing Th2 cells, IL-17-producing Th17 cells, follicular T help

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

179 o its receptor ST2 on targets such as CD4(+) Th2 cells, ILC2, and mast cells.

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

181 PKCzeta that controls the differentiation of Th2 cells important for AD pathogenesis.

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

183 Raif Geha, they studied the role of Th2 cells in allergic responses and he began work in Kaw

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

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

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

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

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

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

190 These data suggest that Th2 cells in peripheral blood may be a sensitive measure

191 Moreover, Th2 cells in presence of IL-3 show increased expression

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

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

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

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

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

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

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

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

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

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

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

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

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

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

206 on of naive CD4(+) T cells to Th17, Th1, and Th2 cells led to significant increase in Lcn2 expression

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

208 Interestingly, IL-3R(+) cells exhibit a Th2 cell-like phenotype and show high GATA-3 expression.

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

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

211 ophil-rich pulmonary type 2 immune response (Th2 cells, M2 macrophages, type 2 innate lymphoid cells,

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

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

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

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

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

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

218 critically contributes to the development of Th2 cell-mediated disorders, most likely by influencing

219 Supported by a mixed Th1/Th2 cell-mediated immunity, P27A induced a marked specif

220 Specifically, IL18 induced a Th2 cell-mediated response in the absence of IL12.

221 ote inflammation and simultaneously induce a Th2 cell-mediated response via IL18.

222 ced activation of T cells and no increase in Th2 cell-mediated responses compared with control mice.

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

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

225 Th1 and Th2 cell modes of motility could be switched simply by m

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

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

228 te motility gene programs that shape Th1 and Th2 cell navigation of the inflamed dermis.

229 ith EoE convtained a prominent population of Th2 cells not seen in controls.

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

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

232 During exacerbation, peripheral blood Th2 cell numbers correlated with ACQ6 and AQLQ scores, w

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

234 ly infect Th17 cells, compared to Th1 cells, Th2 cells, or Tregs.

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

236 Although T-helper type 2 (Th2) cell pathology is implicated in severe disease, the

237 te that Th2 Trm cells and circulating memory Th2 cells perform nonredundant functions.

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

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

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

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

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

243 roles in host protection against TB, whereas Th2 cells producing IL-4 and regulatory T cells (Tregs)

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

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

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

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

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

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

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

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

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

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

254 regulate T-bet and did not secrete IL-12 and Th2 cell responses normally developed in infant mice.

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

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

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

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

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

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

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

262 hether cDC1s also control CD4(+) T helper 2 (Th2) cell responses, since suppressive and activating ro

263 bility of CD11b(+) mDCs to suppress allergic Th2-cell responses upon dose-dependent endotoxin sensiti

264 GPCR) and chemokine-dependent fashion, while Th2 cells scanned a larger tissue area independent of GP

265 ed that Th2 Trm cells and circulating memory Th2 cells share a core Th2 gene signature but also exhib

266 Instead, Notch-deficient in vitro-polarized Th2 cells showed reduced accumulation in the lungs upon

267 eover, a MRTF signature is correlated with a Th2 cell signature in human PDA tumors.

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

269 CXCR5IFN-gammaCD8 T cell to combined CD4 Th1/Th2 cell subsets (IFN-gammaCD4 and IL-4CD4 cells; P = 0.

270 Recent identification of memory Th2 cell subsets that are characterized by high receptor

271 itro-polarized Th1 and Th17 cells but low in Th2 cells, suggesting that this lncRNA may regulate infl

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

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

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

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

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

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

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

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

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

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

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

283 Upon HDM rechallenge, circulating memory Th2 cells trafficked into the lung parenchyma and ignite

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

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

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

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

288 It acts by attracting regulatory T cells and Th2 cells via their receptor CCR type 4 (CCR4).

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

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

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

292 r and allergen challenge, as Notch-deficient Th2 cells were retained in the lung-draining lymph nodes

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

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 PKCzeta stability tended to be increased in Th2 cells with a Trim32 null background.

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

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

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