ライフサイエンスコーパス: Th17 cell

1 o limits their differentiation to pathogenic Th17 cells.

2 proliferation of MOG(35-55)-specific Th1 and Th17 cells.

3 ly affecting homeostatic microbiota-specific Th17 cells.

4 es the levels of intestinal pro-inflammatory Th17 cells.

5 ity by metabolic reprogramming of pathogenic Th17 cells.

6 ion, associated with decreased activation of Th17 cells.

7 been associated with increased signaling of Th17 cells.

8 ells, CD1d(hi)CD5(+) regulatory B cells, and Th17 cells.

9 were similar, PTCs had higher frequencies of Th17 cells.

10 polarize naive CD4(+) T cells from Tregs to Th17 cells.

11 oimmune encephalomyelitis, often mediated by Th17 cells.

12 reprogramming and proliferative capacity of Th17 cells.

13 nature and the encephalitogenic functions of Th17 cells.

14 beta promoted IL-17 production by intestinal Th17 cells.

15 essor that antagonizes RORgammat function in Th17 cells.

16 finity TCRs promoted the formation of Th1 or Th17 cells.

17 s sufficient to stimulate IL-26 release from Th17 cells.

18 ltration of activated myeloid cells, Th1 and Th17 cells.

19 Th17 phenotype and supports the survival of Th17 cells.

20 remarkably distinct from cytokine-polarized Th17 cells.

21 ferentiation and non-pathogenic functions of Th17 cells.

22 inflammatory monocytes and macrophages, and Th17 cells.

23 une disease sustained by proinflammatory Th1/Th17 cells.

24 gulatory CD4(+) T cells (Tregs) and effector Th17 cells.

25 ta linked to a reduction in pro-inflammatory Th17 cells.

26 d with vaccinated wild-type mice, especially Th17 cells.

27 haustion as well as increased skewing toward Th17 cells.

28 is regulatory pathway also operated in human Th17 cells.

29 PI3K signaling promotes IL-22 production in Th17 cells.

30 SLT patients have an increased ratio of Th2:Th17 cells.

31 de showed decreased proliferation of TH1 and TH17 cells.

32 fied a specific strain that potently induces Th17 cells.

33 FN-I) and acts as autoantigen for pathogenic Th17-cells.

34 henotypes, characterized by abundant mucosal Th17 cells, a deficit in the tolerogenic RORgammat(+) re

35 Noteworthy, T helper 17 (Th17) cells, a proinflammatory subset of CD4(+) T cells,

36 Overproportionate Th17 cell abundance is associated with the pathogenesis

37 al SAA1 and SAA2 production, and hippocampal Th17 cell accumulation.

38 ry in concert with gut microbes that enhance Th17 cells act synergistically to worsen CNS autoimmunit

39 critical illness in COVID-19 with increased Th17 cell activation and IL-17 signaling that may lead t

40 s expression of IL23 correlated with stromal Th17 cells, advanced tumor stage, lymph node metastasis,

41 licates IL6 in promoting durable immunity of Th17 cells against large, established solid tumors.

42 T helper 17 (Th17) cells, an important subset of CD4(+) T cells, help

43 ceptor Il12rb1 expression, in turn promoting Th17 cell and Th1-like Th17 cell differentiation in C57B

44 inhibits the generation of small-intestinal Th17 cells and ameliorates SFB-promoted inflammation in

45 g CD30 RNA aptamers to down-regulate CD30(+) Th17 cells and can be developed as a targeted therapy fo

46 It instead caused enhanced infiltration of TH17 cells and CX3CR1(+) monocytes into the injured tiss

47 oral contraceptive pills (COCPs) on cervical Th17 cells and cytokines were compared.

48 oral contraceptive pills (COCPs) on cervical Th17 cells and cytokines were compared.

49 ue gene up-regulated only in pathogen-primed Th17 cells and discovered a critical role for T cell-int

50 elated with increased hepatic recruitment of TH17 cells and enhanced IL-17 production in the injured

51 numbers of group 3 innate lymphoid cells and Th17 cells and enhanced transcription of IL-22, Ab-media

52 llular immune responses, such as survival of Th17 cells and homeostasis of NK cells among others.

53 ockout donors (AlloTbet) have increased lung Th17 cells and IL-17A and develop fibrosis resembling hu

54 l use of therapies directed at modulation of Th17 cells and IL-17A signaling in the treatment of COVI

55 nabled PTH to expand intestinal TNF(+) T and Th17 cells and increase their S1P-receptor-1 mediated eg

56 el, Orai1, participates in the activation of Th17 cells and influences renal injury.

57 pha binds to ROR response elements (RORE) in Th17 cells and inhibits the expression of RORgammat-depe

58 nduces differentiation of naive T cells into Th17 cells and loss of STAT3 in T cell prevents developm

59 icantly reduced conjunctival infiltration of Th17 cells and lower corneal fluorescein staining scores

60 produce chemokines mediating recruitment of Th17 cells and more monocytes into portal tracts.

61 cells upon direct cell-cell contact between Th17 cells and neurons.

62 In contrast, Treg cells arrive after Th17 cells and persist during the chronic phase.

63 ute to inflammation through the induction of Th17 cells and production of inflammatory cytokines; the

64 on profiles in non-pathogenic and pathogenic Th17 cells and promotes the pathogenic effector program

65 ta, which was correlated with a reduction in Th17 cells and protection from colitis.

66 proinflammatory cytokines by Th1 and T-bet+ Th17 cells and reinforces their transcription of type 1

67 The role of IL-21, produced mainly by Th17 cells and T follicular helper cells, has been inten

68 rm-free mice increased numbers of intestinal Th17 cells and Th2 cells and decreased numbers of RORgam

69 Although Th17 cells and the Aryl hydrocarbon receptor (AhR) have

70 take an intricate look at the involvement of Th17 cells and their affiliated cytokines (interleukin-1

71 s) promotes the emergence of IL-22-producing Th17 cells and thereby tumorigenesis in mice.

72 L2 was associated with downregulation of Th1/Th17 cells and upregulation of TGF-beta and induction of

73 rols the pathogenic inflammation mediated by Th17 cells, and IL-9R(-/-) mice develop more severe EAE

74 Consequently, gammadelta and Th17 cells are attractive targets for immunotherapy in t

75 In multiple sclerosis (MS), Th17 cells are critical drivers of autoimmune central ne

76 Th17 cells are critical drivers of autoimmune diseases a

77 IL-17-producing Th17 cells are implicated in the pathogenesis of rheumat

78 Oral pathobiont-reactive Th17 cells are imprinted with gut tropism and migrate to

79 re equally infected by the virus in vivo and Th17 cells are not preferentially infected.IMPORTANCE Fu

80 analogous to T helper type 1 (Th1), Th2, and Th17 cells are well characterized, an ILC subset strictl

81 T helper 17 (Th17) cells are pathogenic in many inflammatory diseases

82 l inflammation, particularly HIV-susceptible Th17 cells, are unknown.

83 n, particularly HIV-susceptible T-helper 17 (Th17) cells, are unknown.

84 Th17 cells arrive before the onset of clinical symptoms,

85 ssues, decreases in CD4(+) T cells producing Th17 cell-associated cytokines, CD8(+) T cell dysfunctio

86 y cell (CMC) response with increased Th1 and Th17 cells at the time of a relapse.

87 y intake and to promote autoimmunity via the Th17 cell axis.

88 trast to its function as a pioneer factor in Th17 cells, BATF is neither sufficient nor required for

89 However, Th17 cell behaviors vary markedly according to their env

90 of immune homeostasis, including intestinal Th17 cells, both before and after ART, were shown to be

91 c signaling indeed induces the generation of Th17 cells but at the same time highly immunosuppressive

92 12010 was high in in vitro-polarized Th1 and Th17 cells but low in Th2 cells, suggesting that this ln

93 that mouse SRC3 interacts with RORgammat in Th17 cells but not in thymocytes.

94 ice after transfer of microbiota Ag-specific Th17 cells but not Th1 cells.

95 s impaired the generation of proinflammatory Th17 cells, but surprisingly did not ameliorate the cour

96 Thus, IL-17A limits pathogenicity of Th17 cells by inducing IL-24.

97 hogenic effector program of encephalitogenic Th17 cells by regulating GM-CSF via Bhlhe40 and inhibiti

98 Th17 cells from accessing APCs and suppress Th17 cell Ca(2+) signaling by a mechanism that is upstre

99 As Th17 cells can be proinflammatory in nature, the equilib

100 nism by which human IL-1RI(+) "antimicrobial Th17 cells" can be rapidly activated by IL-1beta as part

101 sociated with increased local frequencies of Th17 cells (CD4(+)IL-17A(+)).

102 Memory T helper 17 (Th17) cells (CD4(+)IL-17A(+)CD44(+)) drive the chronic a

103 Knockout of HuR altered the transcriptome of Th17 cells characterized by reducing the levels of RORga

104 CD4+ T helper 17 (Th17) cells, characterized by IL-17 production, play imp

105 found that SIV did not preferentially infect Th17 cells, compared to Th1 cells, Th2 cells, or Tregs.

106 Moreover, Th17 cells contributed proportionately to the total pool

107 ritic cells (DCs) and conversion of Tregs to Th17 cells could be modulated with antibiotics (AB) as p

108 t regulatory T (Treg) cells, whereas Th1 and Th17 cells decreased significantly.

109 However, Tfh, Th1, or Th17 cell-deficient mice produced as many PE-specific, i

110 T helper 17 (Th17) cells, defined by RORgammat-dependent production o

111 elated dry eye disease, and evaluated memory Th17 cell depletion with anti-IL-15 antibody as a strate

112 Loss of IL-17A in autopathogenic Th17 cells did not reduce their pathogenicity and instea

113 Here, we compared the characteristics of Th17 cells differentiating in response to commensal bact

114 wever, T cell-specific PKM2 deletion impairs Th17 cell differentiation and ameliorates symptoms of EA

115 tumor progression, is a key factor mediating Th17 cell differentiation and autoimmune inflammation.

116 tical nonmetabolic regulator that fine-tunes Th17 cell differentiation and function in autoimmune-med

117 Consistently, silence of Th17 cell differentiation and IL-17A and IL-17F synthesi

118 Th17 cell differentiation and pathogenicity depend on me

119 -dependent mechanism that selectively drives Th17 cell differentiation and pathogenicity in autoimmun

120 HuR by its inhibitor DHTS inhibited splenic Th17 cell differentiation and reduced experimental autoi

121 on, in turn promoting Th17 cell and Th1-like Th17 cell differentiation in C57BL/6J mice.

122 nst C. rodentium infection due to suboptimal Th17 cell differentiation in vivo.

123 Dysregulated Th17 cell differentiation is associated with autoimmune

124 poral precision within cells and to modulate Th17 cell differentiation on demand using UV light illum

125 tivatable immune modulator (PIM) to increase Th17 cell differentiation on demand with spatial and tem

126 thway, increased aerobic glycolysis, favored Th17 cell differentiation over that of Treg cells, and p

127 ionally direct a pathogenic pro-inflammatory Th17 cell differentiation program, acting directly on T

128 Th17 cell differentiation was downregulated in galectin-

129 nding the molecular mechanisms of regulating Th17 cell differentiation will help find a novel therape

130 P mount defective immune responses, impaired Th17 cell differentiation, and higher fungal burden.

131 otal to various cellular processes including Th17 cell differentiation, has been implicated in MS.

132 verity, reduced Th17 program and inefficient Th17 cell differentiation.

133 ancing its activation and thereby increasing Th17 cell differentiation.

134 carbon receptor (AhR) and ultimately induces Th17 cell differentiation.

135 IL-1beta and IL-6, cytokines known to drive Th17 cell differentiation.

136 f glucose specifically promoted T helper-17 (Th17) cell differentiation by activating transforming gr

137 T helper 17 (Th17)-cell differentiation triggered by interleukin-6 (I

138 cytokine, restricts inflammation by blocking Th17-cell differentiation via an unknown mechanism.

139 ture therapies directed against inflammatory Th17 cells do not inadvertently damage the resident gut

140 autoimmune encephalomyelitis (EAE) model of Th17 cell-driven pathology.

141 manner, thereby supporting the expansion of Th17 cells during cancer progression.

142 ce with the known role of SAAs in regulating Th17 cell effector function, epithelial RARbeta promoted

143 G2D modulates Th1 and proinflammatory T-bet+ Th17 cell effector functions in vitro and in vivo.

144 ular mechanisms by which Treg cells regulate Th17 cell effector functions: reduction of APC density,

145 by pathogens and tissue-resident homeostatic Th17 cells elicited by commensals.

146 t is unclear what distinguishes inflammatory Th17 cells elicited by pathogens and tissue-resident hom

147 Day 4 Th17 cells engrafted, induced release of multiple cytoki

148 7-induced EAU, whereas silencing of IL-24 in Th17 cells enhanced disease.

149 Th17 cells exhibit functional heterogeneity fostering bo

150 Homeostatic Th17 cells exhibited little plasticity towards expressio

151 we describe a streamlined ACT protocol using Th17 cells expanded only 4 days ex vivo.

152 r-instructed mDCs, which mediated subsequent Th17 cell expansion.

153 In contrast, inflammatory Th17 cells experience a hypoxic microenvironment known t

154 y which RNA-binding protein HuR orchestrates Th17 cell fate decisions by posttranscriptionally regula

155 stable, pathogen-specific, antiinflammatory Th17 cell fate in human T cells in vitro.

156 l-induced acquisition of an antiinflammatory Th17 cell fate was confirmed in vivo in an experimental

157 -(IL)-4-producing Th2 cells, IL-17-producing Th17 cells, follicular T helper (Tfh) cells, or regulato

158 ed to develop therapies targeting pathogenic Th17 cells for the treatment of autoimmune disorders.

159 Th17 cells form from naive precursors when signals from

160 ents BCOR and KDM2B work together to enhance Th17 cell formation by repressing Th17 fate suppressors.

161 ed CpG DNA islands, are required for optimal Th17 cell formation in mice after Streptococcus pyogenes

162 enous hormone levels and associated cervical Th17 cell frequencies to a greater extent than use of NE

163 enous hormone levels and associated cervical Th17 cell frequencies to greater extent than NET-EN/COCP

164 confined but highly motile Treg cells limit Th17 cells from accessing APCs and suppress Th17 cell Ca

165 (-) conventional T and CD4(+)RORgammat(+) T (Th17) cells from RRMS subjects that associated with an i

166 tion and RORgammat expression, to pathogenic Th17 cell function in EAE.

167 p between SRC1 and SRC3 in the regulation of Th17 cell function remains unknown.

168 Malt1, critical for NF-kappaB activation and Th17 cell function, is reduced.

169 ed the molecular mechanism of HuR regulating Th17 cell functions, underscoring the therapeutic value

170 in ligase Hectd3 is necessary for pathogenic Th17 cell generation in experimental autoimmune encephal

171 high glucose-induced TGF-beta activation and Th17 cell generation.

172 In mature Th17 cells, GSK-J4 induces an altered transcriptional pr

173 In the absence of VHL, Th17 cells had decreased activation of STAT3 and SMAD2,

174 Compared with wild-type, VHL-deficient Th17 cells had elevated glycolysis and glycolytic capaci

175 ells recruitment to the gut, while impairing Th17 cells homing through the CCR6-CCL20 axis in treated

176 to IL-17A and IL-17F, which are expressed in Th17 cells, IL-17D is expressed broadly in nonimmune cel

177 ve for successful IL-17-based gammadelta and Th17 cell immunotherapy.

178 increases in Bacteroides ovatus and Th1 and Th17 cells in ATG16L1 T300A mice.

179 -ERBalpha activity may be used to manipulate Th17 cells in autoimmune diseases.

180 Due to the role of Th17 cells in autoimmune pathogenesis, it is important t

181 ty, proliferation and cytokine production of Th17 cells in BALB/c mice was associated with higher pro

182 (+), TNF-alpha(+), and IL4(+)), whereas most Th17 cells in blood and RM were single IL-17A producers

183 These findings establish a central role for Th17 cells in CDI pathogenesis following colitis and ide

184 .05), and the proliferation of both Treg and Th17 cells in cervical lymph nodes.

185 nse, suggesting an important role for memory Th17 cells in driving chronic inflammation in autoimmune

186 Despite the critical roles of Th17 cells in immunity, how the immune system regulates

187 Microbiota transplant reduced gut Th17 cells in mice colonized with a microbiota from a do

188 atory genes, and control their expression in Th17 cells in response to activin-A.

189 Cre(-) mice despite a selective reduction in Th17 cells in the colon of Cre(+) mice and a continued r

190 mice maintained higher frequencies of memory Th17 cells in the draining lymph nodes relative to young

191 ts in generation of oral pathobiont-reactive Th17 cells in the oral cavity.

192 that microRNA-132 is specifically induced in Th17 cells in the presence of either AhR agonist or CS-e

193 draining lymph node and Ag-specific Th1 and Th17 cells in the spleen.

194 fic gene expression and function of effector Th17 cells in tissue inflammation.

195 expressed throughout the differentiation of Th17 cells in vitro and during experimental autoimmune e

196 nhibits differentiation and pathogenicity of Th17 cells in vitro and in vivo using the experimental a

197 ts led to potent protumorigenic expansion of Th17 cells in vitro but failed to induce antitumor Th1 d

198 ng of the dynamic functions and behaviors of Th17 cells in vivo during immune responses and in mouse

199 ties of colonic mast cells, eosinophils, and TH17 cells in youth with IBS; and, (2) explore relations

200 Ts contribute to increased T helper type 17 (Th17) cells in psoriasis.

201 higher percentages of CD3(+)CD4(+)IL-17(+) (Th17) cells in the presence versus absence of NETs, as a

202 (hi)IL-17(+)IFN-gamma(-) memory T-helper 17 (Th17) cells in the retina, cervical lymph nodes, inguina

203 1 helper T (Th1) cells and Type 17 helper T (Th17) cells increased initially and promoted osteoclasto

204 r hand, interleukin-17 (IL-17) production by Th17 cells increases CDI-associated mortality.

205 sis, blockade of IL-17A, or depletion of the Th17 cell-inducing gut microbiota markedly reduces stres

206 in mice whose microbiota was enriched by the Th17 cell-inducing taxa segmented filamentous bacteria (

207 ivers of Tnfr1(-/-)/Mdr2(-/-) mice indicated TH17 cell infiltration.

208 STAT5 and BATF convert Th17 cells into cells that mediate IL-9-dependent effect

209 Mechanistic in vitro studies revealed a Th17 cell-intrinsic autocrine loop triggered by binding

210 roduction and the polarity of gammadelta and Th17 cells is critical.

211 The differentiation of Th17 cells is dependent on the retinoic acid receptor-re

212 The role of VHL in Th17 cells is not known.

213 ved antiinflammatory phenotype in stimulated Th17 cells is reduced expression of key metabolic transc

214 and IL-17 double-positive T helper type 17 (Th17) cells is a leading feature of refractory rejection

215 dings suggest that RORgammat, in addition to Th17 cells, is also expressed in peripherally induced, c

216 the abundance of adhesion molecule VLA-4 on Th17 cells, knockout of HuR impaired splenic Th17 cell m

217 ort hairpin RNA targeting USF2 in pathogenic Th17 cells led to reduced expression of proinflammatory

218 that promote T(CM) responses of the Th1 and Th17 cell lineages may improve BCG vaccine efficacy.

219 Selectively targeting memory Th17 cells may be a viable therapeutic approach in the t

220 Th17 cells meander widely, interact with APCs, and exhib

221 developed as a targeted therapy for treating Th17 cell mediated conditions.

222 find a novel therapeutic target for treating Th17 cell-mediated diseases.

223 nd ameliorates symptoms of EAE by decreasing Th17 cell-mediated inflammation and demyelination.

224 Th17 cells, knockout of HuR impaired splenic Th17 cell migration to the CNS and abolished the disease

225 When in the gut, Th17 cells of oral origin can be activated by translocat

226 kin-17A (IL-17A) secretion from T helper 17 (Th17) cells of the lamina propria, followed by the expan

227 -specific antisense is increased in Treg and Th17-cells of Crohn's disease patients over controls.

228 Although the impact of Th17 cells on autoimmunity is undisputable, their pathog

229 ic HSC (pHSC) by incorporating polarized Th1/Th17 cells or CCR6+CLA+ T cells derived from psoriasis p

230 Coculturing lung cancer cells with Th9/Th17 cells or exposing them to the respective CM induced

231 In homeostatic Th17 cells, partial blockade of glycolysis upon Gpi1 ina

232 ncover activin-A as a critical controller of Th17 cell pathogenicity that can be targeted for the sup

233 NaCl was coopted to promote murine and human Th17 cell pathogenicity, if T cell stimulation occurred

234 endent, dichotomous role for NaCl in shaping Th17 cell pathogenicity.

235 n naive CD4(+) T-lymphocyte and T helper 17 (Th17) cell percentages, increases in CD4(+) and CD8(+) e

236 Th17 cells play a critical role in the adaptive immune r

237 re inflammatory diseases of the CNS in which Th17 cells play a major role in the disease pathogenesis

238 alternatively activated (M2) macrophages and Th17 cells play a role in the progression of chronic kid

239 us aureus and, by licensing encephalitogenic Th17 cells, played a key role in the development of auto

240 ed tumors IL-17 production by gammadelta and Th17 cells potentiates antitumor immunity.

241 odentium-primed Th17 cells resembled that of Th17 cells primed following infection in vivo but was re

242 T helper 17 (Th17) cells produce interleukin-17 (IL-17) cytokines and

243 s producing interferon gamma (IFN-gamma) and Th17 cells producing interleukin-17 (IL-17) play key rol

244 Th17 cells (producing IL-17) and Th9 cells (producing IL

245 effector over regulatory cells for the Day 4 Th17 cell product relative to cell products expanded lon

246 A2 by the host, which increases T helper 17 (Th17) cell production.

247 beta signaling in CD4+ T cells (specifically Th17 cells) promotes the emergence of IL-22-producing Th

248 neutrophil-recruiting genes and T helper 17 (Th17)-cell-promoting genes.

249 CD4(+) T helper 17 (Th17) cells protect vertebrate hosts from extracellular

250 ted that cervical cancer cells contribute to Th17 cell recruitment, a cell type with protumorigenic p

251 f CD4+ T cells, especially T-helper type 17 (Th17) cells, remains incomplete in the gut mucosa of mos

252 ranscriptome of in vitro C. rodentium-primed Th17 cells resembled that of Th17 cells primed following

253 determined for mast cells, eosinophils, and TH17 cells, respectively, in 37 youth with IBS and 10 co

254 Only IL-1RI(+) Th17 cells responded to IL-1beta, inducing an NF-kappaB-

255 e mice, and demonstrate a predominant memory Th17 cell response, suggesting an important role for mem

256 Dysregulated Th17 cell responses underlie multiple inflammatory and a

257 S of individuals with MS and restrains human Th17 cell responses.

258 Th17 cells secrete IL-17A and are important for clearing

259 a mice with B. ovatus specifically increased Th17 cells selectively in ATG16L1 T300A knock-in mice.

260 Therefore, IL-17-producing Th17 cells show promise as a target for development of n

261 y inflammatory proteins linked to pathogenic Th17 cell states.

262 However, Th17 cells that are crossreactive to Aspergillus fumigat

263 achment receptor (SNARE) complex proteins in Th17 cells that enable a vesicular glutamate release pat

264 n inducer of differentiation of human CD4(+) Th17 cells that harbor heterologous specificity for othe

265 f the antimicrobial peptide IL-26 from human Th17 cells that is independent of and more rapid than cl

266 instead were driven by a metabolic switch in Th17 cells that led to the induction of the amino acid s

267 transcription factor for the development of Th17 cells that produce proinflammatory cytokines such a

268 Th17 cells that secrete GM-CSF are pathogenic and drive

269 y enhancing IL-10 production and suppressing Th17 cells, the SCFA pentanoate might be of therapeutic

270 In contrast to psoriatic Th17-cells, these LL37-specific SLE T-cells displayed a

271 , we investigated the contribution of memory Th17 cells to age-related dry eye disease, and evaluated

272 reduction of APC density, limiting access of Th17 cells to APCs, and suppression of Th17 Ca(2+) signa

273 ted, 4-day ex vivo expansion method licenses Th17 cells to confer long-lived immunity against solid m

274 compromised cell yield, this method licensed Th17 cells to eradicate large tumors to a greater extent

275 Adoptive transfer of Th17 cells to naive mice is sufficient to increase CDI-a

276 Th17 chemoattractant CCL20, which recruited Th17 cells to the BM.

277 ics, and interactions of endogenous Treg and Th17 cells together with antigen-presenting cells (APCs)

278 RORgammat, the key Thelper17 (Th17) cell transcriptional regulator, is also expressed

279 signaling stimulates glutamate release from Th17 cells upon direct cell-cell contact between Th17 ce

280 capacity to differentiate into Th1 cells and Th17 cells upon stimulation in vitro.

281 Gene expression analysis revealed that in Th17 cells, VHL regulates many cellular pathways, includ

282 rrespondingly, major accumulation of Th9 and Th17 cells was detected in human lung cancer tissue and

283 Th17 cells were defined as CCR6+ and CCR10-.

284 Th17 cells were defined as CCR6+CCR10-.

285 cantly elevated by approximately 10-fold and Th17 cells were elevated by approximately 4-fold in AKI

286 s, densities of mast cells, eosinophils, and TH17 cells were higher in IBS patients as compared to co

287 o greater extent than NET-EN/COCPs, although Th17 cells were more activated and Th17-related cytokine

288 extent than use of NET-EN or COCPs, although Th17 cells were more activated and Th17-related cytokine

289 Here, we report that Th17 cells were regulated by their own signature cytokin

290 Th17 cells were required to promote depressive-like beha

291 in T cells in mice results in global loss of Th17 cells, whereas deficiency of the glycolytic enzyme

292 TGF-beta1 promotes the differentiation of Th17 cells, which are known to be a major source of IL-2

293 the osteoclast number by inhibiting Th1 and Th17 cells, which governed the new bone formation.

294 e, IL-23, is critical for the development of Th17 cells, which produce IL-17.

295 Increased extracellular sodium activates Th17 cells, which provide protection from bacterial and

296 Levels of CD4(+) T helper 17 (Th17) cells, which secrete interleukin 17A (IL-17A), are

297 y cytokines, resulting in differentiation of Th17 cells with a phenotype that has been associated wit

298 search, Knochelmann and colleagues show that Th17 cells with less in vitro expansion in IL6-driven Th

299 Coinjection of Th9/Th17 cells with tumor cells in WT, Rag1-/-, Il9r-/-, and

300 nflammatory encephalitogenic and colitogenic Th17 cells, without substantially affecting homeostatic