ライフサイエンスコーパス: Th2

1 asmablasts and CD21(low) B cells, as well as TH2 and regulatory T cells, indicating a common disease

2 While Th2 and Tc2 clustered with disease severity, IFN-gamma p

3 er virus exposure by a marked innate, but no Th2 and Th1 response subsequently followed by enhanced n

4 ediator performance (T-helper Type 17 [Th17]/Th2 and Th1/Th2 cell levels) were performed according to

5 of dendritic cells (DCs) is crucial for both TH2 and TH17 cell differentiation and is mediated throug

6 essential to suppress Th1 differentiation in Th2 and Th17 conditions in vitro and also to control IFN

7 numbers, and forkhead box protein 3 (Foxp3), TH2 and TH17 cytokine, and Tgfbeta expression in mesente

8 stant to steroids and characterized by mixed TH2 and TH17 responses, including IL-13(+)IL-17(+)CD4(+)

9 re, we found that many CSF-c cells coexpress TH2 and TPH1 and contain both DA and 5-HT, a dual neurot

10 RGC-32(-/-) mice have normal Th1, Th2, and regulatory T cell differentiation but show defe

11 bsets of effector T cells (T helper 1 (TH1), TH2, and TH17) defined by expression of the key transcri

12 entiation of Th cell subsets, including Th1, Th2, and Th9 cells, but it impairs the development of Th

13 gnature cytokine production, but it promoted Th2- and Th9-associated cytokine expression.

14 velopments include improved understanding of Th2 antibodies, intratumoral innate allergy effector cel

15 D4(+) T cells, reduced expression of Th1 and Th2 associated transcription factors, Tbet and GATA3, an

16 way inflammation, immunoglobulin production, TH2-associated cytokine synthesis, and pulmonary dendrit

17 y, Pak2-deficient Tregs gained expression of Th2-associated cytokines and the transcription factor, G

18 - and Th17-associated responses and enhanced Th2-associated responses.

19 -deficient naive CD4(+) T cells revealed the TH2 bias and TH17 defect to be T-cell intrinsic.

20 the clinical features of this disorder: the TH2 bias is likely to contribute to atopic disease, wher

21 a potent allergen of S aureus and induces a TH2-biased inflammatory response in the airways in an IL

22 ers and that Th1 immunity can be imparted to Th2-biased offspring; in some instances, it can be great

23 ated the role of recombinant SplD in driving TH2-biased responses and IgE formation in a murine model

24 With the renewed interest in anti-TH2 biologics, we propose a rationale for why they are p

25 the role of Cav1.2 alpha1 in mouse and human TH2 but not TH1 cell functions and showed that knocking

26 ithelial cells to reprogram them and promote Th2, but not Th17, development in lymph nodes.

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

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

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

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

31 1beta, IL-6, and IL-23, whereas HDM-specific TH2 cell differentiation was hampered by increased IL-12

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

56 Th2 cells contribute to the development of disease throu

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

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

59 Ex-Foxp3 Th2 cells exhibit characteristic Th2 effector functions

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

98 cultures identified CD200R as upregulated on Th2 cells.

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

100 h preferential suppression of Th1 cells over Th2 cells.

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

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

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

104 ote effector differentiation of HDM-specific TH2 cells.

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

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

107 Salmonella independently of T regulatory or Th2 cells.

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

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

110 r functional profile with that of autologous TH2 cells.

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

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

113 ted mice from anaphylaxis, without affecting Th2 cells.

114 about how TH2 cells are differentiated, the TH2 checkpoint mechanisms remain elusive.

115 Th22 cells also displayed plasticity under Th2 conditions in vitro by upregulating IL-13 expression

116 sis of in vitro-differentiated Th0, Th1, and Th2 cultures identified CD200R as upregulated on Th2 cel

117 d to induce our model of FA, whereas any pro-TH2 cytokine can maintain established FA.

118 No single mAb to a pro-TH2 cytokine could suppress established FA, and optimal

119 We conclude that IL-6 acts as a Th2 cytokine in obesity by stimulating M2 polarization a

120 We sought to determine whether anti-pro-TH2 cytokine mAbs can block both FA maintenance and indu

121 sion of ST2(+) regulatory T cells, increased Th2 cytokine milieu, and induced alternatively activated

122 ro-TH2 cytokines or with an inhibitor of pro-TH2 cytokine production might be able to suppress establ

123 f HC subjects, were not anergic and had high TH2 cytokine production upon peanut-specific restimulati

124 antigen-driven T-cell proliferation and TH1/TH2 cytokine production were suppressed (P < 0.05).

125 onstrate increased AHR, airway inflammation, TH2 cytokine production, and immunoglobulin levels and a

126 airway inflammation, allergic sensitization, TH2 cytokine production, and mucous cell metaplasia.

127 diated facilitated allergen presentation and Th2 cytokine production.

128 well as diarrhea, mast cell activation, and TH2 cytokine responses and serum allergen-specific IgE/I

129 of mature lymphocytes or of Stat6-dependent Th2 cytokine signaling.

130 an epigenetic hotspot regulated by IL-13, a TH2 cytokine with increased levels in patients with EoE

131 Expression of TH2 cytokines (IL-13 and IL-31) was similar to that seen

132 panied by increased mRNA expression of other Th2 cytokines (IL-4 or IL-13).

133 MNs-CIT regulated Th2 cytokines (IL-4, IL-5 & IL-13) and anti-inflammatory

134 Other biologics similarly inhibit TH2 cytokines (thymic stromal lymphopoietin, IL-4, IL-5,

135 inophil counts, lower protein expressions of Th2 cytokines and associated transcription factors.

136 were evaluated by checking the expression of TH2 cytokines and transcription factors in vivo and in v

137 All of the pro-TH2 cytokines are required to induce our model of FA, wh

138 The pro-TH2 cytokines IL-25, IL-33, and thymic stromal lymphopoi

139 s (ILC2s) resemble TH2 cells and produce the TH2 cytokines IL-5 and IL-13 but lack antigen-specific r

140 on TH2 cells and decreases the production of TH2 cytokines in the skin.

141 oma environment without unleashing undesired Th2 cytokines or IL10.

142 ined treatment with antagonists to all 3 pro-TH2 cytokines or with an inhibitor of pro-TH2 cytokine p

143 Pro-TH2 cytokines prevent oral tolerance.

144 igh CD4(+) T cell-proliferative response and TH2 cytokines production after casein stimulation in chi

145 Despite low TH2 numbers, TH2 cytokines were detected, and TH2 skewing correlated

146 mice, led to synergistic increases in airway Th2 cytokines, eosinophilia, and peribronchial inflammat

147 ively, this study strongly suggests that the Th2 cytokines, not only IL-4 but also IL-13, are involve

148 We show that exposure of AT to Th2 cytokines, such as IL-4, IL-13, and GM-CSF, stimulat

149 eosinophilic lung infiltrates and increased Th2 cytokines.

150 ll as depressed levels of CCL2 chemokine and Th2 cytokines.

151 uced basophil activation and peanut-specific TH2 cytokines.

152 duced markers on DCs and effectively blunted Th2 development.

153 roteins in direct transcriptional control of Th2 development.

154 ecular pathways that govern the induction of TH2 differentiation and the critical role of GATA-3 in t

155 though the mechanisms by which they instruct TH2 differentiation are still poorly understood, express

156 of the Treg cell master TF Foxp3 and induced TH2 differentiation even under iTreg-cell-differentiatio

157 whether staphylococcal enterotoxins promote TH2 differentiation of allergen-specific CD4 conventiona

158 mediator of the enhanced susceptibility for TH2-driven allergic asthma.

159 cytes that contribute to the pathogenesis of Th2-driven asthma and allergic lung diseases.

160 TH2-driven eosinophilic inflammation and neutrophil-asso

161 Ex-Foxp3 Th2 cells exhibit characteristic Th2 effector functions and provide immunity to H. polygy

162 y to uptake allergen and stimulate naive and TH2 effector responses on allergen stimulation in vivo a

163 High IL-5 levels may reflect a Th2 environment associated with impaired clearance of cr

164 1 and alpha2delta2, to test their effects on TH2 functions and their capacity to reduce allergic airw

165 spliced mRNA of IFNG and TBX21 but not IL13 (TH2 gene).

166 of B cells in a house dust mite (HDM)-driven TH2-high asthma mouse model.

167 Although new therapies are emerging for Th2-high disease, identifying molecular pathways in Th2-

168 Claudin-18 levels were lowest among TH2-high patients with asthma.

169 t could be a useful additional indicator of "TH2-high" asthma.

170 disease progression and illustrates that Th1/Th2 (IFN-gamma/ELISA antibodies) assays are important fo

171 expression, AD serum showed up-regulation of Th2 (IL-13, CCL17, eotaxin-1/CCL11, CCL13, CCL4, IL-10),

172 or Hox5 genes as developmental regulators of Th2 immune cell function that demonstrates a redeploymen

173 The Th2 immune gene IL13 is a highly plausible genetic candi

174 reflecting the diverse environments in which Th2 immune responses are initiated.

175 erial contact early in life induces allergic TH2 immune responses.

176 ed to the induction of regulatory or type 2 (Th2) immune responses.

177 Th2 immunity and allergic immune surveillance play criti

178 facilitate disease progression by inhibiting Th2 immunity and promoting pathogenic Th1 responses.

179 Suppression of TH2 immunity can occur as a consequence of either deleti

180 on, suggesting miR-24-mediated inhibition of Th2 immunity cannot be attributed to TCF1 repression by

181 Th2 immunity is a primary host defence against metazoan

182 ly 24 was recently implicated in restricting Th2 immunity, as well as the differentiation and functio

183 monoclonal antibodies restored the TH1- and TH2-induced epithelial barrier dysfunction, respectively

184 Multiple exposure to type 2 helper T cell (Th2)-inducing stimuli further enhances both the diversit

185 The TH2-inducing capacity of sorted skin-derived DC subsets

186 ient strategy to interfere with SplD-induced TH2 inflammation but does not prevent the allergic sensi

187 SAHM1 treatment dampened TH2 inflammation during ongoing HDM challenge and enhanc

188 Allergic asthma is a chronic Th2 inflammation in the lungs that constricts the airway

189 ) or house dust mite (HDM), and accessed for TH2 inflammation.

190 re compared with a three-gene-mean marker of TH2 inflammation.

191 IL-4 level was the highest, and Th17/Th2 levels were the lowest in RESV-treated rats compared

192 nctioning as regulatory T (Treg)/T helper 2 (Th2)-like cells; (iii) interfering with dendritic cell (

193 nd the transcription factor, Gata3, becoming Th2-like cells, explaining their inability to regulate i

194 h disease, identifying molecular pathways in Th2-low disease remains an important goal.

195 unclear what role airway basophils play in "TH2-low" asthma phenotypes.

196 Allergic asthma is a CD4 TH2-lymphocyte driven disease characterized by airway hy

197 uxiliary subunits on Cav1 alpha1 function in TH2 lymphocytes and on the development of acute allergic

198 ability and activation of Cav1.2 channels in TH2 lymphocytes both in vitro and in vivo, as demonstrat

199 t receptor-homologous molecules expressed on TH2 lymphocytes, PDE4, the histamine 4 receptor, and Jan

200 treatment with a cocktail of all 3 anti-pro-TH2 mAbs.

201 tible to the development of severe, enhanced Th2-mediated AAD, which can be regulated by CD8(+) T cel

202 y in T cells is crucial for the induction of TH2-mediated AAI in an HDM-driven asthma model but that

203 s induced by the cytokine activin-A suppress TH2-mediated allergic responses and linked airway diseas

204 target for the treatment of asthma and other TH2-mediated diseases.

205 tissue homeostasis and wound healing during Th2-mediated immune responses, such as parasitic infecti

206 IL-5-producing TH2 cell differentiation and TH2-mediated inflammation.

207 ve regulation between innate interferons and TH2 mediators.

208 Despite low TH2 numbers, TH2 cytokines were detected, and TH2 skewin

209 y the proliferation of Th1 cells, but not of Th2 or Th17 cells, was affected.

210 AA patients had increased CLA(+) /CLA(-) Th2 (P < .007), CLA(+) Tc2 (P = .04), and CLA(+) Th22 (P

211 t CD200R expression strongly correlates with Th2 pathology; though, the mechanism is as yet elusive.

212 isease, no shift in T cell genes from Th1 to Th2 pattern but rather an incremental decline into immun

213 ented antigen to 1-DER T cells and induced a TH2 phenotype.

214 l proliferation and a switch from a Th1 to a Th2 phenotype.

215 al deletion of PD-L1 on ILC2s impaired early Th2 polarization and cytokine production, leading to del

216 fects in T follicular helper development and TH2 polarization, as seen in a house dust mite exposure

217 strong eosinophilic infiltration, excessive Th2 polarization, marked airway hyperresponsiveness, alv

218 ng a cytokine milieu rich in IL-23 to favour Th2 polarization.

219 Examination of T cells grown in Th2 polarizing conditions showed increased proliferation

220 ells were analyzed for the expression of the TH2-polarizing cytokine IL-4 and the T-cell activation m

221 ecific regulatory T (Treg) cells to create a TH2-polarizing cytokine milieu.

222 with patients with TH2/TH17-predominant and TH2-predominant asthma, which included neutrophilic asth

223 hances migration to draining lymph nodes and Th2 priming capacity.

224 R, and CD83 expressions in DC induced by the Th2-promoting cytokine TSLP, as well as the production o

225 tions suggest that ACh polarizes DC toward a Th2-promoting profile.

226 ILC2 activation and eosinophil recruitment, TH2-related cytokine and chemokine production, lung hist

227 FN-gamma during HDM challenge to support the TH2 response and exacerbate asthma.

228 a chronic allergen model, with an increased Th2 response and exacerbated lung tissue pathology.

229 ll-derived IL-4 was required to maintain the Th2 response in the mesenteric lymph nodes of infected m

230 Allergic asthma is characterized by a TH2 response induced by dendritic cells (DCs) that prese

231 antibody titer with an overall balanced Th1/Th2 response, while the dual combination promoted Th1-po

232 ay hyperresponsiveness, lung resistance, and TH2 responses after allergic sensitization to ovalbumin.

233 Here we show that intestinal Th2 responses against Trichuris muris worms and Schistos

234 TH2 responses are implicated in asthma pathobiology.

235 Protease activity of Per a 10 favours Th2 responses by differential regulation of IL-12p70 and

236 in is a key player involved in prevention of TH2 responses by flagellin A conjugate vaccines.

237 rFlaA:Betv1 suppressed TH2 responses from Bet v 1-specific CD4(+) T cells and p

238 Target cells of TSLP in Th2 responses include CD4 T cells and dendritic cells (D

239 Thus, the priming of Th2 responses is associated with distinct transcriptiona

240 ment of disease as well as allergen-specific Th2 responses occurs despite deficiencies in several IL-

241 SEA promoted TH2 responses of allergen-specific T cells and asthma pa

242 whereas TCF1 was previously shown to promote Th2 responses through inducing GATA3, enforced TCF1 expr

243 g and gut regulatory T cells, decreased lung TH2 responses, and ameliorated allergic airway inflammat

244 ng changes in airway inflammatory responses, Th2 responses, and lung histopathology.

245 nd assisting early T helper dichotomy toward Th2 responses, which are detrimental in cutaneous leishm

246 uitment, and simultaneously impaired Th1 and Th2 responses.

247 the ability to promote Th1 polarization over Th2 responses.

248 ial role during allergy and helminth-induced Th2 responses.

249 ting the role of B cells in amplification of TH2 responses.

250 s also effectively prime S. mansoni-specific Th2 responses.

251 It was proposed that TH2 sensitization through the skin occurs when skin barr

252 ype 2 conventional DCs as crucial players in TH2 sensitization to common inhaled allergens that enter

253 asthma was associated with an IL-13-induced TH2 signature and IL-1 receptor-like 1 (IL1RL1) mRNA exp

254 H2 numbers, TH2 cytokines were detected, and TH2 skewing correlated with total IgE levels.

255 rom skin LN of mice exposed to two different Th2 stimuli: the helminth parasite Nippostrongylus brasi

256 rly responses of the bronchial epithelium to Th2-stimuli.

257 significantly, whereas the anti-inflammatory Th2 subset (CCR3(+)) was increased after DMF treatment.

258 We compared the expression of genes in the TH2 subset of helper T cells to enhancer occupancy by th

259 Conversely, eosinophils, Th2 T cells, type 2 innate lymphoid cells, and possibly

260 Alopecia areata is accompanied by Th2/Tc2 activation in skin-homing and systemic subsets,

261 gnificantly enhanced frequencies of Th1/Tc1, Th2/Tc2, Th17/Tc17, Th9, and Th22 cells with parasite an

262 s end, we examined the frequency of Th1/Tc1, Th2/Tc2, Th9/Tc9, Th17/Tc17, and Th22/Tc22 cells in 15 S

263 nt subsets, including similarity between Th1-Th2-Tfh cell populations and Th17 cells, as well as simi

264 g formulas varied regarding the induction of Th2, Th1, and proinflammatory cytokines.

265 ously thought to be selective for Treg, Th1, Th2, Th17, and Tfh cells, including CD194 (CCR4)(+)FOXP3

266 extent of TNFAIP3 expression in DCs controls TH2/TH17 cell differentiation.

267 TH2/TH17 cells expressed higher levels of the IL-1 recep

268 recipients increases house dust mite-induced Th2/Th17 inflammation in the airway.

269 cus overproduction, collagen deposition, and Th2/Th17 inflammation.

270 mRNA expression of Th1/Th2/Th17-associated cell markers decreased between 4.5 a

271 mRNA expression of Treg/Th1/Th2/Th17-associated cell markers was measured ex vivo.

272 A subgroup of patients with TH2/TH17-low asthma had neutrophilic asthma and increase

273 The mechanism of TH2/TH17-predominant and TH2/TH17-low asthma is unknown.

274 immune mechanism of TH2/TH17-predominant and TH2/TH17-low asthma.

275 TH17-predominant asthma and 22 patients with TH2/TH17-low asthma.

276 le for the IL-1beta pathway in patients with TH2/TH17-predminant asthma.

277 This contrasted with patients with TH2/TH17-predominant and TH2-predominant asthma, which i

278 The mechanism of TH2/TH17-predominant and TH2/TH17-low asthma is unknown.

279 We sought to study the immune mechanism of TH2/TH17-predominant and TH2/TH17-low asthma.

280 ents, 16 patients were immunophenotyped with TH2/TH17-predominant asthma and 22 patients with TH2/TH1

281 Patients with TH2/TH17-predominant asthma had increased IL-1beta, IL-6

282 Various T-cell subsets, including Th2/Th22 cells, are increased in lesional and nonlesiona

283 Th1, Th2, Th9 and Th17 cells are conventional CD4(+) effector

284 y rate < 0.05), with increased expression of Th2, Th9, Th17/Th22 polar cytokines (i.e. IL-5, IL-13, I

285 are not fully understood, but a shift from a TH2 to a TH1 response has been suggested as a possible e

286 lammation from eosinophilic T helper cell 2 (TH2) to neutrophilic TH17 polarity.

287 n to most allergens clustered with age, TH1, TH2, total IgE levels, and B-cell memory subsets.

288 s, SAHM1 downregulated expression of the key TH2 transcription factor GATA3 and intracellular IL-4 in

289 pregulated their expression of the canonical TH2 transcription factor GATA3, as well as ST2, and prod

290 cells) by repression of the T helper type 2 (TH2) transcriptional program.

291 n patients group versus controls, while Th1, Th2, Treg, and eosinophil gene signatures were increased

292 ne response is muted and not yet skewed to a Th2 type response that is associated with chronic diseas

293 t memory CD4(+) T cells were biased toward a TH2 type, and this was at the expense of TH1 and TH17 ce

294 emonstrating plasticity toward both Th1- and Th2-type cells.

295 cells with the potent capability to produce Th2-type cytokines such as interleukin (IL)-5 and IL-13.

296 g the TLR4 and TLR7 ligands balances Th1 and Th2-type immune responses for long-lived cellular and ne

297 cripts and correlated with serum IgE and the Th2-type mRNA profile to establish an IGHE score for tis

298 with impaired BEC properties showed a skewed Th2-type secretion profile (high IL-4/IFN-gamma ratio).

299 lammatory disease characterized by excessive TH2-type-dominant responses.

300 d and activated in chronic ischemic HF, with Th2 (versus Th1) and Th17 (versus Treg) predominance in