ライフサイエンスコーパス: Th17 cell

1 equal amount as CD4(+)RORgammat(+) T cells (TH17 cells).

2 s with marked similarity to mouse pathogenic TH17 cells.

3 naive CD4(+) T cells and IL-17A secretion by Th17 cells.

4 elated with profound increases in intestinal Th17 cells.

5 6/(TRBD1/2)TRBJ1-7 (CGGKRRLESIFR) in Th1 and Th17 cells.

6 (APC) types that sustain the self-renewal of TH17 cells.

7 e specifically induced in the spinal cord by Th17 cells.

8 ) T cells in vitro, downregulating levels of Th17 cells.

9 nd salt-sensitive hypertension by modulating TH17 cells.

10 ges, defined as T helper (Th)22 and IL-22(+) Th17 cells.

11 lating the differentiation of Treg cells and TH17 cells.

12 d miR-466i orchestrates GM-CSF expression in Th17 cells.

13 ed sustained upregulation of OX40 by Th1 and Th17 cells.

14 e essential for the generation of pathogenic TH17 cells.

15 restricts the frequency and pathogenicity of Th17 cells.

16 T cells and IL-17 production in established Th17 cells.

17 ompare pure populations of cultured Th22 and Th17 cells.

18 lls preferentially secreted IL-6 and induced Th17 cells.

19 nhibitors had no effect on already polarized Th17 cells.

20 t (RORgammat) directs the differentiation of Th17 cells.

21 mediates the CD172alpha(+)LPDC induction of Th17 cells.

22 ory macrophage population, and a decrease in Th17 cells.

23 ion of inflammatory skin disorders involving Th17 cells.

24 nd miR-182, can enhance the pathogenicity of Th17 cells.

25 in favor of Foxp3(+) Tregs while decreasing Th17 cells.

26 a marked absence of Th1-like IFNgamma(+) ex-Th17 cells.

27 rostaglandin E2 (PGE2) secretion to generate Th17 cells.

28 eage distinct from cTregs, Treg17 cells, and Th17 cells.

29 d expansion of IL-10-producing T cells among Th17 cells.

30 els of 2-hydroxyglutarate in differentiating TH17 cells.

31 om the gene expression profile of pathogenic Th17 cells.

32 is essential for fate determination towards TH17 cells.

33 type, and this was at the expense of TH1 and TH17 cells.

34 n uptake but were impaired to induce Th1 and Th17 cells.

35 because these may not inhibit pathogenic ex-Th17 cells.

36 diseases alter glucocorticoid sensitivity of Th17 cells.

37 AE and were more prone to differentiate into Th17 cells.

38 oduction of the proinflammatory cytokines in Th17 cells.

39 in both TCRgammadelta(+) T cells and CD4(+) Th17 cells.

40 o 3-BrPa than is the production of IL-17A by Th17 cells.

41 Finally, we showed that ex-Th17 cells accumulated in the joints of rheumatoid arthr

42 esting an alternative mechanism of promoting Th17 cell accumulation.

43 d with reduced donor proinflammatory Th1 and Th17 cells, accumulation of donor myeloid-derived suppre

44 because ex-Th17 cells proliferated more than Th17 cells after stimulation.

45 ase to naive recipients as effectively as do Th17 cells alone.

46 Baseline CXCR5(+)Th17 cells also correlated with numbers of swollen joint

47 ed arthritis specifically reduced intestinal Th17 cells and attenuated arthritis.

48 sferring in vitro generated, highly purified Th17 cells and by using IL-17A fate reporter mice, we de

49 ORgammat is a master transcription factor of Th17 cells and considered as a promising drug target for

50 STAT3 drives development of Th17 cells and cytokine production by Th2 and Th17 cells

51 expression profile in CT-induced intestinal Th17 cells and endogenous intestinal Th17 cells at homeo

52 Increased hepatic Th17 cells and IL-17 expression were observed in NASH mi

53 knock-out of HuR reduced CCR6 expression on Th17 cells and impaired their migration to CNS compared

54 al survival of Lactobacillus spp., increased TH17 cells and increased blood pressure.

55 ons, but its role in regulating autoreactive Th17 cells and organ-specific autoimmunity remains large

56 ire TGF-beta signals to appropriately dampen Th17 cells and regulate responses in the gastrointestina

57 hritis (CAIA), via targeting IL-17 secreting Th17 cells and regulatory T cells (Treg).

58 TH17 cells and the consequent neutrophilic inflammation

59 ction, proliferation, and differentiation of Th17 cells and the expression of transcription factors i

60 tion to CNS compared with the response of WT Th17 cells and thereby ameliorated EAE.

61 hich can be used to both identify pathogenic TH17 cells and to measure the effect of treatment on TH1

62 ly due to mastication, promotes induction of Th17 cells and tones homeostatic immunity at the gingiva

63 oteins, our data highlight the importance of Th17 cells and Wnt/beta-catenin signaling in HIV control

64 10-related cytokine produced by T helper 17 (Th17) cells and other immune cells that signals via IL-2

65 r-promoting T helper type 2 cell (Th2 cell), Th17 cell, and regulatory T cell populations while suppr

66 sed disease severity, populations of Th1 and Th17 cells, and inflammatory markers (IFN-gamma, TNF-alp

67 kine production than either Th1 or bona fide Th17 cells, and produced increased amounts of proinflamm

68 cells are functionally distinct from Th1 and Th17 cells, and suggest that they may play a pathogenic

69 M-CSF mRNA in comparison with wild-type (WT) Th17 cells, and that HuR binds directly to GM-CSF mRNA 3

70 ice lacking Ndfip1 have increased numbers of Th17 cells, and this increase is cell intrinsic.

71 s; and (3) significantly increased Th1, Th2, Th17 cells, and Tregs, in the spleen and mediastinal lym

72 icial effect of AM80, targeting both Tfh and Th17 cells, and warrant strict safety monitoring of gut-

73 The proliferative brake on Th17 cells appeared to be lifted because ex-Th17 cells p

74 Here we show that Th17 cells are a source of tumour-induced Foxp3(+) cells

75 These ex-Th17 cells are also called nonclassical Th1 cells becaus

76 Th17 cells are an important therapeutic target in autoim

77 Th1, Th2, Th9 and Th17 cells are conventional CD4(+) effector T cells iden

78 Th17 cells are critical effectors mediating the ocular s

79 together, these data indicate that human ex-Th17 cells are functionally distinct from Th1 and Th17 c

80 However, Th17 cells are generated before Th1 cells.

81 itions and increasing evidence supports that Th17 cells are glucocorticoid resistant.

82 ne uveitis (EAU), in which CD4(+) Th1 and/or Th17 cells are immunopathogenic, mimics various clinical

83 T follicular helper (Tfh) and Th17 cells are known to promote inflammation and autoant

84 The Th17/Treg axis and maturation of Th17 cells are major contributing factors to the pathoge

85 Th17 cells are major players in multiple autoimmune dise

86 SFB-induced gut Th17 cells are preferentially recruited to lung over spl

87 However, Th17 cells are present in the normal intestine and show

88 T helper 17 (TH17) cells are critically involved in host defence, inf

89 type 2-regulated disease, type 17 helper T (Th17) cells are known to be influential in asthma pathog

90 sing interleukin (IL)-17-producing T helper (Th17) cells are widely reported, the effect of these mol

91 We also found gammadelta T and Th17 cells as the main IL-17A(+) cells during VL infecti

92 f Rac1 that suppresses both murine and human Th17 cells as well as EAE.

93 ly higher percentage of circulating Treg and Th17 cells as well as their dominantly secreting cytokin

94 ity between Th1-Th2-Tfh cell populations and Th17 cells, as well as similarity of Th2 cells with Treg

95 estinal Th17 cells and endogenous intestinal Th17 cells at homeostasis, with upregulated expression o

96 Accumulation of Th17 cells at the gingiva was driven in response to the

97 hts unique requirements for the induction of Th17 cells at the oral/gingival mucosal barrier.

98 in situ and revived the clonal expansion of TH17 cells both ex vivo and in vivo, whereas lung macrop

99 M cells were closely related to conventional TH17 cells but had more pathogenic features.

100 quired for the pathogenicity of T helper 17 (Th17) cells but the molecular mechanisms governing this

101 ntribute to the generation and plasticity of Th17 cells, but rather promoted the expansion of a GM-CS

102 consequently blocked the differentiation of TH17 cells by antagonizing the function of transcription

103 Based on evidence that Th17 cells can be polarized to Th17.1 cells to produce o

104 in and gastrointestinal tract, we found that Th17 cells can develop at the gingiva independently of c

105 While Th17 cells can protect against colonization by pathogeni

106 Th17 cells can switch to become ex-Th17 cells that no lo

107 4 T cells that differentiate into pathogenic Th17 cells can trigger autoimmune diseases.

108 ), are sufficient to induce the expansion of Th17 cells (CD4(+) T helper cells producing IL-17).

109 leukin-17a (IL-17a) produced by T helper 17 (TH17) cells (CD4(+) T helper effector cells involved in

110 o atopic disease, whereas defects in TH1 and TH17 cells compromise antiviral and antifungal immunity,

111 Deletion of S1P1 in Th17 cells conferred resistance to experimental autoimmu

112 Th17 cells contribute to several inflammatory conditions

113 Thus the selective targeting of TH1/TH17 cells could inhibit relapses without causing John C

114 ceptor antagonist protein, inhibited BAL TH2/TH17 cell counts.

115 Induction of TH17 cells depends on gut microbiota; however, the effec

116 Thus, the balance between Treg cells and TH17 cells determines the severity of a TH17 cell-driven

117 However, the means by which Th17 cells develop in response to microbiota is still no

118 monstrate that gingiva-resident T helper 17 (Th17) cells developed via a commensal colonization-indep

119 otentiating the genetic program required for Th17 cell development and adaptive immunity.

120 CK2 inhibition or genetic ablation prevents TH17 cell development and promotes the generation of Tre

121 t the influence of anaphylatoxins on Th2 and Th17 cell development during allergic asthma with a part

122 aling that controlled dysbiosis, constrained Th17 cell development, and regulated the susceptibility

123 itic cells (LPDC) have been shown to promote Th17 cell development, it is still unclear whether TLR5

124 Although dispensable for homeostatic Th17 cell development, JunB is required for induction an

125 In Th1 and Th17 cells differentiated in vitro, ORAI1 was required f

126 unodeficiency and autoimmunity with impaired TH17 cell differentiation and exaggerated responsiveness

127 reated microglia significantly inhibited Th1/Th17 cell differentiation and increased the number of IL

128 itic cells (DCs) is crucial for both TH2 and TH17 cell differentiation and is mediated through nuclea

129 ly of adaptor proteins, negatively regulates Th17 cell differentiation and lupus autoimmunity.

130 critical mechanism by which TGFbeta controls TH17 cell differentiation and uncovers the SKI-SMAD4 axi

131 wth factor beta (TGFbeta) is instrumental in TH17 cell differentiation by cooperating with interleuki

132 treatment in ovariectomized mice suppressed Th17 cell differentiation by inhibiting transcription fa

133 Here we reveal that TGFbeta enables TH17 cell differentiation by reversing SKI-SMAD4-mediate

134 ion of TLR7 signaling in T cells can inhibit Th17 cell differentiation from naive T cells and IL-17 p

135 Transcriptional regulation of Th17 cell differentiation has been extensively studied,

136 died, but post-transcriptional regulation of Th17 cell differentiation has remained less well charact

137 tion of the Rorc locus, Rorc expression, and TH17 cell differentiation in a SMAD4-dependent manner.

138 ults identify RGC-32 as a novel regulator of Th17 cell differentiation in vitro and in vivo and sugge

139 ) RAR-related orphan receptor (ROR)gammat(+) Th17 cell differentiation in vitro and increased the num

140 pression suppresses RORgammat expression and TH17 cell differentiation of SMAD4-deficient T cells.

141 Yet, the mechanism by which TGFbeta enables TH17 cell differentiation remains elusive.

142 TNFAIP3-deficient DCs induced HDM-specific TH17 cell differentiation through increased expression o

143 tion and deacetylation of the Rorc locus and TH17 cell differentiation via SMAD4: ectopic SKI express

144 y and specifically inhibited mouse and human Th17 cell differentiation while promoting the generation

145 ell-specific deletion of genes that regulate TH17 cell differentiation, including Il6ra and RAR-relat

146 beta activation of Smad2, therefore limiting Th17 cell differentiation.

147 RGC-32 is preferentially upregulated during Th17 cell differentiation.

148 re maternal intestinal bacteria that promote TH17 cell differentiation.

149 ct and critical role for miR-18a in limiting Th17 cell differentiation.

150 nt of TNFAIP3 expression in DCs controls TH2/TH17 cell differentiation.

151 e encoding TAZ or activation of TAZ directed TH17 cell differentiation.

152 -mediated suppression of RORgammat to enable TH17 cell differentiation.

153 n they co-regulate during mouse T helper 17 (Th17) cell differentiation.

154 TLR7-mediated suppression of Th17 cells does not require dendritic cell involvement.

155 with vitamin D reduces frequency of Th1 and Th17 cells, down-regulates genes in key signaling pathwa

156 t CK2 could be targeted for the treatment of Th17 cell-driven autoimmune disorders.

157 and TH17 cells determines the severity of a TH17 cell-driven disease and therefore is a promising ta

158 responsible for TLR7-mediated inhibition of Th17 cells due to induction of suppressor of cytokine si

159 merulonephritis induction, and we found that Th17 cells egress from the gut in a S1P-receptor-1-depen

160 In contrast with Th1 and Th17 cells, ex-Th17 cells were highly resistant to suppr

161 However, it is known that Th17 cells exhibit considerable plasticity, particularly

162 TH2/TH17 cells expressed higher levels of the IL-1 receptor

163 Th17 cells expressing a constitutively activated form of

164 in vitro and increased the number of tissue Th17 cells expressing CCR6, RORgammat, and IL-17A in air

165 -17A fate reporter mice, we demonstrate that Th17 cells fail to acquire substantial expression of the

166 es of CD8(+) T-helper type 1 (Th1), Th2, and Th17 cells following stimulation by M. tuberculosis anti

167 the levels of certain microRNA expression in Th17 cells; for example, miR-466i functioned to mediate

168 Moreover, Th17 cells from 13R(-/-) mice had reduced ability to con

169 The beta7 blockade prevented both Tfh and Th17 cells from entering the non-immunopathogenic site,

170 ansforming growth factor beta) restored CD4+ Th17 cell function in cells from IP children to levels m

171 romodomain extraterminal (BET) inhibitors on Th17 cell function was studied in a mouse model of EAU i

172 proinflammatory and anti-inflammatory human TH17 cell functions based on the differential expression

173 itzler syndrome were analyzed for changes in TH17 cell functions before and during therapy with IL-1b

174 inct TH17 phenotypes translate into distinct TH17 cell functions with implications for human health o

175 uce proinflammatory versus anti-inflammatory TH17 cell functions.

176 d Rora, all key transcription factors in the Th17 cell gene-expression program.

177 ernatively, antigen-specific effector/memory TH17 cells, generated in culture with CD4(+) T cells fro

178 IL17-producing Th17 cells, generated through a STAT3-dependent mechanis

179 inase Mink1 as a novel negative regulator of Th17 cell generation.

180 croscopy studies demonstrated that CD43(-/-) Th17 cells had impaired rolling on TNF-alpha-treated mic

181 , whether HuR regulates GM-CSF expression in Th17 cells has not been fully investigated.

182 Th1 and Th17 cells have an established role in protective immuni

183 Two distinct types of TH17 cells have been described recently, which differed

184 we showed that HuR conditional knockout (KO) Th17 cells have decreased GM-CSF mRNA in comparison with

185 Like the story of Jekyll and Hyde, Th17 cells have two guises.

186 tor of transcriptional programs that support Th17 cell identity and restrain alternative Th1 and Treg

187 global transcriptional programs that promote Th17 cell identity and restrict alternative CD4(+) T-cel

188 JunB supports Th17 cell identity by regulating key AP-1 complex consti

189 -1) factor JunB is an essential regulator of Th17 cell identity.

190 hed in LTBI; in contrast to pro-inflammatory Th17 cells (IFNgamma(+)IL17A(+)/IL10(-)) in the blood an

191 onal profiles identified regulatory IL10 (+) Th17 cells (IL10(+)IL17A(+)IL17F(+)IL22(+)) to be signif

192 influences the function of effector Th1 and Th17 cells in a Treg-dependent fashion.

193 ls and to measure the effect of treatment on TH17 cells in human autoimmune diseases.

194 PEG decreased the number of pro-inflammatory Th17 cells in inflamed arthritic joints through TRAIL-in

195 g evidence supports the role of IL-23-driven Th17 cells in inflammation.

196 study, we specifically explored the role of Th17 cells in LdCen(-/-) -induced host protection in mic

197 However, Th17 cells in psoriasis and related diseases are glucoco

198 We investigated CXCR5(+)Th17 cells in RA subjects with stable or active disease

199 nal dendritic cells interacted directly with TH17 cells in situ and revived the clonal expansion of T

200 r data suggest that therapeutic targeting of TH17 cells in susceptible pregnant mothers may reduce th

201 , it is unclear whether they resemble Th1 or Th17 cells in terms of their function and regulation, an

202 , SMAD4-deficient T cells differentiate into TH17 cells in the absence of TGFbeta signalling in a ROR

203 ncy of pathogenic IFN-gamma(+) and GM-CSF(+) Th17 cells in the CNS.

204 n vivo, and by reduced numbers of endogenous Th17 cells in the intestinal mucosa.

205 implicated in glucocorticoid sensitivity of Th17 cells in the literature, as this information is use

206 T helper type 2 (Th2) and psoriasis-specific Th17 cells in the skin, and impaired expression of disea

207 Here, we identified GAS-specific Th17 cells in tonsils of humans naturally exposed to GAS

208 te that NAD(+) promotes Treg conversion into Th17 cells in vitro and in vivo via CD25 cell surface ma

209 model of EAU in vivo and in mouse and human Th17 cells in vitro.

210 tory T cells, while decreasing the levels of Th17 cells in vivo, indicating that CCR2 regulates the i

211 ession in T cells and to generate pathogenic TH17 cells in vivo.

212 educed and do not support the development of Th17 cells in vivo.

213 ation of intrahepatic, but not intrasplenic, Th17 cells in wild-type mice, whereas the disrupted live

214 n of Ag-specific T lymphocytes, specifically TH17 cells, in vivo.

215 bolic program is observed in mouse and human Th17 cells, including those isolated from Crohn disease

216 oliferation and differentiation into Th1 and Th17 cells, increased T-cell apoptosis, reduced severity

217 phenotype and functions of T helper type 17 (Th17) cells induced by healthy (PH) versus acne (PA) ski

218 tors of Hippo signaling, was expressed under TH17 cell-inducing conditions and was required for TH17

219 esenchymal transition, IL-17 production, and Th17 cell infiltration in response to dialysis fluid tre

220 CX-4945 treatment inhibits the maturation of Th17 cells into inflammatory IFN-gamma-coproducing effec

221 However, how did circulating Treg/Th17 cells involve in MMD patients remains unclear.

222 We conclude that BET targeting of Th17 cells is a potential therapeutic opportunity for a

223 Moreover, higher expression of IL10 in TH17 cells is found in clinically stable vs. active pati

224 ssion is post-transcriptionally regulated in Th17 cells is unknown.

225 When transferred in vivo, Th17 cells lacking Ndfip1 were more likely to maintain t

226 Lack of expansion of GM-CSF-producing Th17 cells led to ameliorated disease in mice deficient

227 CK2 as a regulator of the Th17/Treg axis and Th17 cell maturation and suggest that CK2 could be targe

228 regulate the differentiation of Tregs versus Th17 cells may depend on miR signature profile.

229 mmensal bacteria with a propensity to induce TH17 cells may increase the risk of neurodevelopmental d

230 infections caused by impaired generation of TH17 cells; meanwhile, some patients with chronic mucocu

231 These results clearly demonstrate that Th17 cells mediate ocular surface autoimmunity through b

232 Th17 cells mediate pathological immune responses respons

233 yeloid cells for the development of TH2- and TH17-cell mediated asthma.

234 se findings highlight how HuR contributes to Th17 cell-mediated autoimmune neuroinflammation and supp

235 opment of treatments that selectively target TH17 cell-mediated autoimmunity but do not affect thymoc

236 kocyte numbers in the CNS and attenuated Th1/Th17 cell-mediated cytokine production.

237 Although elimination of RORgammat prevents TH17 cell-mediated experimental autoimmune encephalomyel

238 nd was required for TH17 differentiation and TH17 cell-mediated inflammatory diseases.

239 therapeutic approaches for the treatment of TH17-cell-mediated autoimmune diseases.

240 CR6) is critical for pathogenic T helper 17 (Th17) cell migration to the central nervous system (CNS)

241 ll function, promoting increases in gingival Th17 cell numbers.

242 clones and show that P. acnes strains induce Th17 cells of varied phenotype and function that are sta

243 ressive regulatory T cells, pro-inflammatory Th17 cells, or their ability to express IL-17.

244 These findings indicated that the IL23 and Th17 cell pathways might be promising targets for the tr

245 ed to target distinct levels of the IL23 and Th17 cell pathways, and the results are providing insigh

246 T helper 17 (Th17) cell plasticity contributes to both immunity and a

247 hypotheses regarding the mechanisms by which Th17-cell plasticity may be controlled in vivo.

248 Th17 cells play a critical role in autoimmune diseases,

249 Th17 cells play a role as an inflammation mediator in a

250 ing factor (GM-CSF) produced by T helper 17 (Th17) cells plays an essential role in autoimmune diseas

251 ASPASIA in conjunction with an SBML model of Th17-cell polarisation, we predict that promotion of the

252 nctional features of human Th17, Th1, and ex-Th17 cell populations.

253 Th17 cells appeared to be lifted because ex-Th17 cells proliferated more than Th17 cells after stimu

254 Induced regulatory T (iTreg) and Th17 cells promote mucosal homeostasis.

255 as a mitogenic mediator of encephalitogenic Th17 cells rather than qualitative inducer of their gene

256 expand dual T cell receptor (TCR)-expressing Th17 cells recognizing both an SFB epitope and self-anti

257 In vivo, Th17 cell recruitment into the air pouch was reduced in

258 Targeting the intestinal Th17 cell "reservoir" may present a therapeutic strategy

259 ect of curcumin on: 1) systemic T helper 17 (Th17) cell response; 2) gingival expressions of interleu

260 ssue-specific mechanisms govern education of Th17 cell responses and demonstrate that mechanical dama

261 Mechanisms that elicit mucosal TH17 cell responses have been described, yet how these c

262 Th17 cell responses orchestrate immunity against extrace

263 and follicular T helper cell and suppressed TH17 cell responses.

264 he TLR7 ligand imiquimod can inhibit Th1 and Th17 cells, resulting in the prevention of, and an immun

265 anistically, the essential role of OXPHOS in Th17 cells results from their limited capacity to increa

266 Donor Th22 and IL-22(+) Th17 cells share a similar IL-6-dependent developmental

267 responsible for promoting differentiation of Th17 cells specific to P. gingivalis.

268 T cells towards a pro-inflammatory T helper (TH17) cell state and away from a regulatory T cell state

269 Th17 cells stimulated with cl-CD95L produced sphingosine

270 rather promoted the expansion of a GM-CSF(+) Th17 cell subset, thereby enhancing its encephalitogenic

271 +)FOXP3(+) Treg and CD183 (CXCR3)(+)T-bet(+) Th17 cell subsets.

272 function through a mechanism different from Th17 cell suppression.

273 Compared to TH17 cells, TH1/17 cells have gene signatures with marke

274 nfection was disproportionately higher among Th17 cells than among IL-17(-) or gamma interferon-posit

275 However, expansion of Th17 cells that do not induce IDO1-mediated suppression

276 the molecular signature of murine pathogenic TH17 cells that induce experimental autoimmune encephalo

277 cell responses, leading to the generation of Th17 cells that may contribute to either homeostasis or

278 Th17 cells can switch to become ex-Th17 cells that no longer produce IL-17 but produce IFN-

279 likely operate through the HR and influence Th17 cells to convert to Th1 cells and to acquire increa

280 equired for in vivo transition of pathogenic Th17 cells to IFN-gamma producers.

281 ndly impaired the ability of myelin-reactive TH17 cells to invade central nervous system (CNS) tissue

282 Additionally, the uveitogenic capacity of Th17 cells to transfer EAU was abrogated by BET inhibito

283 Rgammat, is sufficient to drive switching of Th17 cells towards an IFN-gamma-producing phenotype.

284 programs the differentiation of T helper 17 (TH17) cells towards induced regulatory T (iTreg) cells,

285 are potentially a distinct cell lineage from Th17 cells under in vitro culture conditions.

286 The induction of Th17 cells was dependent on bacterial dihydrolipoamide a

287 As expected, differentiation of Th17 cells was impaired in both cohorts.

288 roliferation of Th1 cells, but not of Th2 or Th17 cells, was affected.

289 Furthermore, using IFN-gamma-deficient Th17 cells, we demonstrate the disease-amplifying role o

290 spleen-to-pancreas dynamics of both Th1 and Th17 cells were affected in 13R(-/-) mice.

291 TH17 cells were also cocultured with lung APC subsets to

292 In contrast with Th1 and Th17 cells, ex-Th17 cells were highly resistant to suppression of proli

293 an commensal bacteria that induce intestinal TH17 cells were more likely to produce offspring with MI

294 t despite their loss of IL-17 expression, ex-Th17 cells were more polyfunctional in terms of cytokine

295 Th9 and Th17 cells were quantified in chronic hepatitis B (CHB)

296 thogenic signature of intestinal homeostatic Th17 cells, which are actively regulated by the commensa

297 olecular signature of human pro-inflammatory TH17 cells, which can be used to both identify pathogeni

298 h17 cells and cytokine production by Th2 and Th17 cells, which contribute to asthma.

299 drive autoimmunity by inducing T helper 17 (TH17) cells, which can also contribute to hypertension.

300 in splenic IL-17-producing gammadeltaT- and Th17-cells; yet in the CNV eye, only elevated levels of