ライフサイエンスコーパス: Th1 cell

1 d TRBV23/(TRBD2)TRBJ2-2 (CRKLHSCATCALNFL) in Th1 cells.

2 TH17CM cells but also blocked virus-specific TH1 cells.

3 of microbiota Ag-specific Th17 cells but not Th1 cells.

4 ction cases, correlating with an increase in Th1 cells.

5 lted in a significantly reduced frequency of Th1 cells.

6 atitis had increases in Th2 cells but not in Th1 cells.

7 h CTH522-specific interferon gamma-producing Th1 cells.

8 mouse and human TH2 cells with no effect on TH1 cells.

9 ion of CXCR3 downregulation and crippling of Th1 cells.

10 st tested the pathogenic contribution of CD4 Th1 cells.

11 model and is not compensated by Ag-specific Th1 cells.

12 f miR-150, compared with IFN-gamma-secreting Th1 cells.

13 D11c(+) cells and IFN-gamma-expressing donor Th1 cells.

14 al CNS activation of myelin antigen-specific Th1 cells.

15 ress high levels of IL-7Ralpha compared with Th1 cells.

16 T-bet knockout mice (T-bet(-/-)), which lack Th1 cells.

17 tal naive T cells toward IFN-gamma-producing TH1 cells.

18 D4(+) T cells, resulting in proliferation of Th1 cells.

19 is is mediated by IFN-gamma-secreting CD4(+) Th1 cells.

20 lls that had lower tumoricidal activity than Th1 cells.

21 lls, and to a lesser extent, on NK cells and Th1 cells.

22 ay from Tfh cells, instead promoting that of Th1 cells.

23 and by supporting the development of classic Th1 cells.

24 teractions are required to generate Th2 than Th1 cells.

25 BLIMP-1 is required for IL-10 expression by Th1 cells.

26 MHCII) leads to activation of proatherogenic Th1 cells.

27 cells in AIH seem to be aberrantly activated Th1 cells.

28 high alpha(V)beta(3) expression relative to Th1 cells.

29 and increases interferon gamma production by Th1 cells.

30 t represent a pathogenic activation state of Th1 cells.

31 that are distinct from conventional Th17 and Th1 cells.

32 hed regions of IFNG and TBX21 (TH1 genes) in TH1 cells.

33 g CD4(+) T cells to transition directly into Th1 cells.

34 ntigen-specific population of differentiated Th1 cells.

35 ient for maintaining IFN-gamma production by Th1 cells.

36 However, Th17 cells are generated before Th1 cells.

37 and chemoattractant for CXCR3(+) T-helper 1 (Th1) cells.

38 of T follicular helper (TFH) and T helper 1 (TH1) cells.

39 ty in chronically activated T-helper type 1 (Th1) cells.

40 esting and restimulated effector T helper 1 (Th1) cells.

41 uberculosis growth, while CX3CR1(+) KLRG1(+) Th1 cells accumulate in the lung vasculature and are non

42 CR3(Tg) mice showed enhanced Th2 and reduced Th1 cell accumulation associated with increased neutroph

43 Therefore, Th1 cells act to restrict bacteria within IFN-gamma-depe

44 are differentially expressed within 24 h of Th1 cell activation.

45 rafficking properties of pathogenic CXCR3(+) TH1 cells, allowing Treg localization and control of exc

46 gs reveal an important function for DAP12 in Th1 cells and a new mechanism to recruit effector T cell

47 ly, Il18r1(-/-) mice display lower levels of Th1 cells and are highly susceptible to infection, but c

48 ng cells (APCs), CD4(+)IFN-gamma(+) effector Th1 cells and CD4(+)Foxp3(+) regulatory T cells (Tregs)

49 s, but that was distinct from that of CD4(+) TH1 cells and CD8(+) terminal effectors.

50 work governing maintenance and plasticity of Th1 cells and defines a new pathway for the development

51 (-/-) mice had reduced ability to convert to Th1 cells and displayed reduced sensitivity to suppressi

52 Thus Th1 cells and IFN-gamma are the dominant contributors in

53 as significantly reduced in peripheral blood Th1 cells and in the skin of MPE patients vs controls.

54 that Th17.1 cells could be misclassified as Th1 cells and may be the predominant producer of IFN-gam

55 TH2 cells in asthmatic patients, the role of TH1 cells and other non-TH2 types in asthmatic patients,

56 TNF locus and other related genes in resting Th1 cells and released in a myosin VI-dependent manner f

57 king bias of CD4 T cell differentiation into Th1 cells and substantially impaired formation of follic

58 aive CD4 T cells into two distinct lineages, Th1 cells and T follicular helper (TFH) cells.

59 Id2 expression and reciprocal development of TH1 cells and TFH cells.

60 s an enhanced capacity to differentiate into Th1 cells and Th17 cells upon stimulation in vitro.

61 roles in the normal differentiation of human TH1 cells and TH2 cells.

62 is needed for sustained IL-10 production by Th1 cells and that the transcription factor BLIMP-1 is r

63 ion may be associated with the prevention of Th1 cells and the maintenance of Tregs migration into th

64 dal CD3(+)CD4(+)Tbet(+)RORgammaT(-) effector Th1 cells and the systemic levels of TNF-alpha were decr

65 he HR and influence Th17 cells to convert to Th1 cells and to acquire increased sensitivity to suppre

66 RAV8/TRAJ52 (CATDLNTGANTGKLTFG) TCR genes in Th1 cells and TRBV16/(TRBD1/2)TRBJ1-7 (CGGKRRLESIFR) in

67 Type 1 helper T (Th1) cells and Type 17 helper T (Th17) cells increased i

68 ility to repression of type 1 helper T cell (TH1 cell) and follicular helper T cell (TFH cell) respon

69 ovel tool for their distinction from classic Th1 cells, and 2) they demonstrate that RORC2-expressing

70 and tumor necrosis factor alpha secretion by Th1 cells, and 3) increased monocyte-mediated IL-1beta s

71 PDHK1 was expressed in Th17 cells, but not Th1 cells, and at low levels in Tregs, and inhibition or

72 to promote responses by cytotoxic NK cells, Th1 cells, and CD8(+) T cells.

73 is and diminished renal-infiltrating Tfh and Th1 cells, and improved overall survival.

74 atory infiltrates and spinal infiltration of Th1 cells, and increased differentiation of regulatory T

75 ed by gamma interferon (IFN-gamma)-secreting Th1 cells, and regulatory T cells play a protective role

76 ionship of Tact (CD4CD45ROCD25-CD127) cells, Th1 cells, and thymus-derived regulatory (Treg) (CD4CD45

77 hese mice also lacked intestinal T helper 1 (Th1) cells, and failed to support Th1 cell differentiati

78 t of follicular helper (Tfh) and T helper 1 (Th1) cells, and short-lived effector and memory precurso

79 to inflammatory diseases, we used the murine Th1 cell- and Th17 cell-driven model of experimental aut

80 Th1 cells are central pathogenic mediators of crescentic

81 Here, we demonstrate that differentiated TH1 cells are responsive to trans-presented IL-15.

82 identify a previously unrecognized role for Th1 cells as integrators of perivascular CF and cardiac

83 vement of virus-specific, joint-infiltrating Th1 cells as one of the main pathogenic mediators of CHI

84 we observed induction of IFN-gamma-producing Th1 cells as reported earlier.

85 TH1 cells as well as CD8(+) T cells express a subset-spe

86 T helper 1 (Th1) cell-associated immunity exacerbates ileitis induce

87 naive CD4(+) T cells into type-1 effector T (TH1) cells at the expense of TH2.

88 However, an inability to generate Th1 cells because of Stat4, Ifngr, and Ifng deficiencies

89 ytes, termed nonclassic, differ from classic Th1 cells because of the presence of retinoic acid orpha

90 e ex-Th17 cells are also called nonclassical Th1 cells because of their ability to produce IFN-gamma,

91 nly a transient increase in activated CD4(+) Th1 cells but also a persistent decrease in the size of

92 d a reduced capability to differentiate into Th1 cells but were poised to differentiate better into i

93 notypic differences compared to HIV-specific Th1 cells but with similarities to CD8+ T cells.

94 interferon-gamma-expressing T-helper type 1 (Th1) cells but increases in interleukin 5-expressing Th2

95 hanced the proliferation of CXCR3-expressing Th1 cells, but did not impact Th17 cells and EAE develop

96 Interestingly, only the proliferation of Th1 cells, but not of Th2 or Th17 cells, was affected.

97 Further, maximal stimulation of Th1 cells by lipopolysaccharide (LPS) did not require T-

98 all ILC1 subsets shared characteristics with Th1 cells, CD4(+) ILC1 also demonstrated significant phe

99 Thus, M1 macrophages, IFN-gamma-secreting Th1 cells, CD8+ T cells, and B cells promote IR, in part

100 ron (IFN-gamma) production and activation of Th1 cells characterize resistance to subcutaneous infect

101 h superantigen and to present CMV antigen to TH1 cells, co-opting MC secretory granules for antigen p

102 n the absence of cDCs, pI:C failed to induce Th1 cell commitment and IgG2c production.

103 o of both monofunctional and dual-functional Th1 cells compared with UN.

104 Adoptive transfer of Th17/1, but not Th1, cells confers the disease to naive recipients as ef

105 dentified an enrichment of clonally expanded Th1 cells containing intact HIV-1 proviruses, suggesting

106 ; however, it remains unclear to what extent Th1 cells contribute to DED pathogenesis.

107 ediated transfer of Let-7d from Treg cell to Th1 cells contributed to suppression and prevention of s

108 RA signaling is essential for limiting Th1-cell conversion into Th17 effectors and for preventi

109 Here, we show that CD4(+) T helper 1 (Th1) cells could be rapidly stimulated by microbe-associ

110 ed toward DCs driving the differentiation of TH1 cells (DC1s), DC2s, or DCs driving the differentiati

111 a dichotomy between Th1 and Th2 cells, with Th1 cells deemed culpable for autoimmune islet destructi

112 ST2 expression on virus-specific Th1 cells depended on the Th1-associated transcription f

113 expression of both innate and subsequent T (Th1) cell-dependent acquired resistance, including the s

114 on, we show that TLR7 signaling can suppress Th1 cell development and function through a mechanism di

115 terolemic Ldlr(-/-) mice led to intrahepatic Th1 cell differentiation and CD11b(+)CD11c(+) leukocyte

116 ialized gene program required for pathogenic Th1 cell differentiation and development of neuroinflamm

117 we demonstrate a role for DOT1L in limiting Th1 cell differentiation and maintaining lineage integri

118 helper 1 (Th1) cells, and failed to support Th1 cell differentiation in MLN and mount Th1 cell respo

119 sion of T cell proliferation and T helper-1 (Th1) cell differentiation.

120 thway and promoted T(REG) or T(H)17, but not Th1, cell differentiation in vitro and in vivo, an effec

121 as a reduced capacity to drive Th17, but not Th1, cell differentiation.

122 In contrast, lack of CCR7 on Th1 cells diminished their tissue egress while enhancing

123 Mechanisms responsible for Th1 cell downregulation, however, remain widely unknown.

124 Both in steady and in T helper type 1 (Th1) cell-driven inflammatory states, the MR(hi) dermal

125 which will serve as a death marker for these Th1 cells during rechallenge with Ag.

126 Delta5G, deplete CXCR3(+) CCR5(+) CD4(+) T (Th1) cells during the primary infection, thereby comprom

127 /IL-23R and IL-7/IL-7R signaling in Th17 and Th1 cell dynamics during CNS autoimmunity.

128 Expansion and acquisition of Th1 cell effector function requires metabolic reprogramm

129 gs were necessary and sufficient to suppress Th1 cell effector function.

130 t used by the TCR, except that unexpectedly, Th1 cells employed the ITAM-bearing protein DAP12, which

131 We previously showed in mice that CXCR3(+) Th1 cells enter the lung parenchyma and suppress M. tube

132 CR3 deficiency decreases the average rate of Th1 cell entry into the lung parenchyma by half, while C

133 RC2 and IL17A demethylation, whereas classic Th1 cells exhibit a complete methylation of these genes.

134 P2, IL-1beta) are paradoxically increased in TH1 cells expressing SUMOylation-deficient WASp.

135 nd its resident pomc(+), ff1b(+) and otpb(+) Th1(+) cells fail to differentiate.

136 Thus, cDCs are required for the pI:C-driven Th1 cell fate commitment but have no crucial accessory f

137 work governing maintenance and plasticity of Th1-cell fate and defines an additional pathway for the

138 or of the reciprocal balance between Tfh and Th1 cell fates and their respective metabolic activities

139 tion and severely impaired the generation of TH1 cells following infection with Toxoplasma gondii.

140 use CD43 requires cooperation with PSGL-1 in Th1 cells for binding to E-selectin.

141 Concomitantly, IT induced Th1 cells, Foxp3(+), and IL-10-producing Treg cells.

142 creased graft lymphangiogenesis and lymphoid Th1 cell frequencies as compared to control.

143 ces, here we analyze in vitro differentiated Th1 cells from 16 inbred mouse strains.

144 Th1 cells from dnRARalpha mice showed enhanced plasticit

145 ide "help" for the development of pathogenic Th1 cells from naive precursors.

146 ine receptor CXCR3 and prevents diabetogenic Th1 cells from reaching the pancreas, leading to suppres

147 he epigenetic level the origin of nonclassic Th1 cells from Th17 cells, also identifying in the RORC2

148 enhanced lymphatic egress of Ag-sequestered Th1 cells from the inflamed site and alleviated inflamma

149 e of TLR-2 in rescuing chronically activated Th1 cells from undergoing exhaustion.

150 to treat chronic diseases involving loss of Th1 cell function.

151 Cav1.2 alpha1 in mouse and human TH2 but not TH1 cell functions and showed that knocking down Cav1 al

152 nd HDAC2-deficient T helper type 0 (TH0) and TH1 cells further upregulated CD8-lineage genes and acqu

153 ecrease APC maturation and suppress effector Th1 cell generation relative to saline-treated control.

154 BEC secretome did not promote Th1 cell generation.

155 eir ability to produce IFN-gamma, similar to Th1 cells; however, it is unclear whether they resemble

156 icted recruitment of cytotoxic CD8+ T cells, Th1 cells, IgM+ B cells, and plasma cells.

157 IL-12-polarized Th1 cells, IL-23-polarized Th17 cells, and Th17 cells th

158 irae and B. intestinihominis specific-memory Th1 cell immune responses selectively predicted longer p

159 reduced the tissue egress of proinflammatory Th1 cells in a mouse model of delayed hypersensitivity.

160 uces allosensitization and the generation of Th1 cells in draining lymphoid tissues; (c) decreases gr

161 One of the mechanisms of control of Th1 cells in homeostasis is the interaction between the

162 t further assessment of the pathogenicity of TH1 cells in patients with severe asthma.

163 The frequencies of Th1 cells in regional lymphoid tissue and graft-infiltra

164 Our protocol permits the detection of Th1 cells in single LNs and enables temporal in vivo mon

165 cells, reduced frequencies of Th9, Th17 and Th1 cells in spleen, and suppressed expression of IL-9,

166 Fibrinogen depletion reduces Th1 cells in the multiple sclerosis model, experimental

167 5, and CCR7 and to suppress proliferation of Th1 cells in the pancreas.

168 ficant reduction in numbers of both Th17 and Th1 cells in their lungs after Coccidioides infection.

169 ence of an MK2 inhibitor strongly accumulate Th1 cells in their lymph nodes.

170 While a high frequency of Th1 cells in tumors is associated with improved cancer p

171 Our findings elucidate an unexpected role of TH1 cells in vasculature and immune reprogramming.

172 d increased propensity to differentiate into Th1 cells in vitro, and this was significantly inhibited

173 Finally, glucosamine treatment inhibited Th1 cells in vivo, prolonged the survival of islet graft

174 The high amount of Th1 cells in VL was dependent on the NOD2-RIP2 signaling

175 mTOR kinase activity compared to T helper 1 (Th1) cells in response to acute viral infection.

176 Our data show that Th1 cells included in a hematopoietic allograft can nega

177 ApoA-I reduced Th1 cells independently of changes in CD4(+)Foxp3(+) reg

178 nocytes and that local activation of Th2 and Th1 cells induces keratinocyte TSLP expression.

179 ficient patients, characterized by defective Th1 cell induction, failed to upregulate the molecular c

180 Thus, the fraction of Th1 cell input into the lungs during M. tuberculosis inf

181 s differentiation of naive CD4(+) T cells to Th1 cells, interfere with peptide processing and present

182 ntiate into interferon-(IFN)-gamma-producing Th1 cells, interleukin-(IL)-4-producing Th2 cells, IL-17

183 receptors to the migration and entry rate of Th1 cells into M. tuberculosis-infected lungs using comp

184 ee, CCR5 and CXCR6 also promote the entry of Th1 cells into the lungs of infected mice.

185 he production of IFN-gamma by differentiated Th1 cells is more sensitive to 3-BrPa than is the produc

186 he abundance of lamina propria Th17, but not Th1, cells is highly correlated with the severity of art

187 have demonstrated its use in mouse T helper (TH1) cells, it should be applicable to any cell type or

188 demonstrate in this article that nonclassic Th1 cells, like Th17 cells, have a marked RORC2 and IL17

189 lled by stable expression differences of the Th1 cell lineage-specifying transcription factor T-bet.

190 Our data demonstrate that Th1 cells lose their capacity to produce IFN-gamma when

191 KLRG1 blockade has no effect on Th1 cell lung migration.

192 n interferon-gamma (IFN-gamma) expression by Th1 cells, mathematical modeling predicted that this beh

193 TH1 cells may be a marker and a determinant of both immu

194 regulatory mechanism by which post-effector TH1 cells may contribute to long-term cell-mediated and

195 ch as LL-CFA/I, may be harnessed to restrict Th1 cell-mediated immunity and protect against T1D.

196 ; both cytokines are essential in regulating Th1 cell-mediated immunity.

197 Recently, populations of natural Th17 and Th1 cells (nTh17 and nTh1) with innate-like phenotype ha

198 ro and in vivo, whereas adoptive transfer of Th1 cells, opposite to activated IFN-gamma(-/-) Th cells

199 ice resisted fibrosis, transfer of polarized Th1 cells or inhibition of MMP activity reversed this ou

200 ) pre-ASCs following stimulation with either Th1 cells or with IFNgamma, IL-2, anti-Ig and TLR7/8 lig

201 hout affecting cytotoxic T lymphocyte (CTL), Th1 cell, or Th17 cell responses to herpes simplex virus

202 expansion, with preferential suppression of Th1 cells over Th2 cells.

203 h17.1-cell percentages were also higher than Th1-cell percentages, and approximately 60% of Th17.1-en

204 er bystander recruitment to the CNS, whereas TH1 cells perform immune surveillance.

205 Here we show that type 1 T helper (TH1) cells play a crucial role in vessel normalization.

206 ulatory T cell populations while suppressing Th1 cell polarization and cytotoxic CD8(+) T cell activa

207 pe is mediated by increased T helper type 1 (Th1) cell polarization, which in turn results from the d

208 onconventional (but not classical antiviral) Th1 cell polarizations were induced.

209 s associated with nonatopic T-helper type 1 (Th1) cell polarized inflammation that correlates with pu

210 E), expansion of pathogenic, myelin-specific Th1 cell populations drives active disease; selectively

211 T helper 1 (Th1) cells producing interferon gamma (IFN-gamma) and Th

212 CD4(+) T helper 1 (Th1) cells producing interferon gamma (IFN-gamma) are cr

213 CD4(+) T cells toward pathogenic T helper 1 (Th1) cells producing interferon-gamma (IFN-gamma) and gr

214 ncluding T helper 1 (Th1) cells, suppressing Th1 cell proliferation and cytokine secretion.

215 perative selectin and chemokine signaling in Th1 cells promoted alphaLbeta2-dependent slow rolling an

216 NG pathway in the mechanism of action of the Th1 cell-promoting polysaccharide adjuvant chitosan.

217 ce was associated with reduced production of Th1-cell-promoting IL-18.

218 owever, of preferential interactions between Th1 cell-prone, high-affinity T cells and XCR1(+) DCs or

219 dies demonstrate that myelin-specific CD4(+) Th1 cells provoke microglia to release glutamate via the

220 TDLNs correlated significantly with the Th2/Th1 cell ratio in tumors, where they served as an indepe

221 ing to the downregulation of IP-10 and other Th1 cell-recruiting chemokines (e.g., CXCL9 and CXCL11).

222 l superantigen SEE induced the production of Th1 cell-recruiting chemokines, including IP-10, through

223 ated into inhibition of superantigen-induced Th1 cell recruitment.

224 ncreased R-loops and R-loop-mediated DSBs in TH1 cells relative to TH2 cells.

225 CD4 Th1 cells represent the main lymphocyte population that

226 Th17) cells, along with IFN-gamma-expressing Th1 cells, represent two major pathogenic T cell subsets

227 However, while TH1 cells responded consistently to viruses, TH1/TH17CM

228 romotes Tregs differentiation and suppresses Th1 cell response, and ameliorates experimental colitis.

229 cytokine secretion profile more typical of a TH1-cell response.

230 revious studies have implicated dysregulated Th1 cell responses in AIG pathogenesis, eosinophils have

231 R-induced IL-1, which became dispensable for Th1 cell responses in the absence of T regulatory (Treg)

232 et al. show one way that Treg cells suppress Th1 cell responses is through nonautonomous gene silenci

233 protection against cutaneous infection while Th1 cell responses provided protection against systemic

234 sive cytokine IL-10 has been shown to dampen Th1 cell responses to M. tuberculosis infection impairin

235 aliva of Crohn's disease patients can induce Th1 cell responses to promote colitis.

236 rt Th1 cell differentiation in MLN and mount Th1 cell responses to Trichuris muris infection.

237 dent cDCs promote anti-viral and T-helper 1 (Th1) cell responses, whereas IRF4-expressing cDCs have b

238 Abrogation of retinoic acid signalling in Th1 cells resulted in loss of T-bet expression and STAT4

239 tion of microglial cells and infiltration of Th1 cells resulted in white matter injury, characterized

240 ss and present the secreted tumor antigen to Th1 cells, resulting in induction of macrophage cytotoxi

241 We found that mouse Th1 cells rolling on P- or E-selectin triggered signals

242 Th1 cells scanned a smaller tissue area in a G protein-c

243 Tregs levels and high expansion of antitumor Th1 cells showed better clinical responses.

244 Here, TH1 cells showed more robust Id2 expression than that of

245 In vivo, Th1 cells sort purified by secreted IFN-gamma amounts pr

246 Th1 cells specific for the 3 proteins can be selected wi

247 l function of IRF-1 in the death of neonatal Th1 cells stems from the ability of its gene to bind STA

248 nged IFN-gamma production by IL-10-deficient Th1 cells stimulated in hypoxic conditions.

249 se, followed by polyclonal expansion of Th17/Th1 cell subsets with release of inflammatory cytokines

250 eart allografts compared with Abs induced by Th1 cells, suggesting a requirement for IFN-gamma during

251 various immune cells, including T helper 1 (Th1) cells, suppressing Th1 cell proliferation and cytok

252 , we elaborated the role of T-bet-expressing Th1 cells, T cell-derived IL-10, and Ag-specific thymic

253 We found that like Th1 cells, Th17 are a distinct population throughout the

254 referentially infect Th17 cells, compared to Th1 cells, Th2 cells, or Tregs.

255 Differentiation of T-helper (Th1) cells, Th2 cells, and T-regulatory cells was determ

256 ter numbers of T follicular helper (TFH) and Th1 cells than alum, the SE alone, or GLA without SE.

257 ion of Leishmania-specific CD4(+) T cells to Th1 cells than their wild-type counterpart cells.

258 Induction of TH1 cells that coexpress IFN-gamma and TNF is not a requ

259 ) functional Tregs may lose Foxp3 and become Th1 cells that could contribute to lesion expression.

260 T (Th) cells into distinct fates, including Th1 cells that preferentially produce interferon-gamma (

261 istence of high-frequency RV-specific memory Th1 cells that recognize a limited set of conserved epit

262 e when compared to terminally differentiated Th1 cells that reside preferentially in the lung-associa

263 TH1 cells that secrete interferon-gamma are a major popu

264 cells as an independent subset distinct from Th1 cells that show combined activity with CD8+ T cells

265 multifunctional activity of T-helper type 1 (TH1) cells that simultaneously produce IFN-gamma and TNF

266 s identify a new strategy to manipulate Th17/Th1 cells through TLR7 signaling, with important implica

267 -viral humoral immunity, the contribution of TH1 cells to a protective antibody response remains unkn

268 stered the ability of chronically stimulated Th1 cells to activate B cells.

269 The specific chemokine receptors utilized by Th1 cells to migrate into the lung during Mycobacterium

270 T-bet acts as a repressor in differentiated Th1 cells to prevent abberant autocrine type I IFN and d

271 mapping and the ability for RV-A16-specific Th1 cells to proliferate in response to their RV-A39 pep

272 show that Th17 cells are more effective than Th1 cells to provide B cell help.

273 The reduced expression of Tim3 in Th1 cells together with the impaired expression of Gal9

274 ation of lineage stability using T helper 1 (Th1) cells, traditionally considered the most phenotypic

275 tudy, we show that the T helper type 1 cell (Th1 cell) transcriptional regulators T-bet and STAT4 are

276 , similarly to Th17 cells and in contrast to Th1 cells, Tregs depend on LFA-1 for their entry into th

277 s have been reported with IFNgamma-producing Th1 cells, tumor-specific Th2 cells have been largely ne

278 ne, can sometimes promote rather than impair Th1 cell-type immune responses.

279 on, and inhibits T-cell differentiation into Th1 cells under different cytokine-polarizing conditions

280 ingly, STAT3 phosphorylation is increased in Th1 cells under hypoxia, leading to enhanced HIF-1alpha

281 Under these circumstances, differentiating Th1 cells upregulate IL-13Ralpha1, leading to an unusual

282 se to decreased IL-2 signalling, T helper 1 (TH1) cells upregulate Bcl-6 and co-initiate TFH- and TCM

283 Mechanistically, Th1 cells use integrin alpha4 to adhere to and induce TG

284 of both Th1 and TFH cells, the expansion of Th1 cells was more affected.

285 The expression of ST2 on Th1 cells was transient, in contrast to constitutive ST2

286 In summary, ex vivo ACT of AdV-specific Th1 cells was well tolerated and led to successful and s

287 e concurrent development of Tfh and effector Th1 cells, we performed high-dose Ag immunization in con

288 Memory CCR5(+) TH1 cells were enriched in BAL fluid versus blood, and p

289 In this model, Th17 and Treg but not Th1 cells were found enriched at the tumor tissues.

290 HIF-1alpha(-/-) Th1 cells were insensitive to hypoxia, underlining a cri

291 nd interferon-gamma, which are secreted from TH1 cells, were essential for the observed greater persi

292 pression of Smad7 in in vitro differentiated Th1 cells when cultured in presence of 1,25(OH)2D3.

293 icrobiota are strong inducers of T helper 1 (TH1) cells when they colonize in the gut.

294 for sustaining T-bet expression in activated Th1 cells, whereas mTOR was necessary but not sufficient

295 via Itk controls the development of natural Th1 cells, which are expanded by the presence of IL4.

296 ignaling can selectively inhibit Th17 and/or Th1 cells, which are important for controlling excessive

297 a lineage-defining transcription factor for Th1 cells, which in turn supports IFN-gamma production i

298 , CD8(+) cytotoxic T cells (TC1), and CD4(+) TH1 cells, which protect against intracellular microbes

299 Functionally, Th1 cells with graded IFN-gamma production competence di

300 populations revealed an increased amount of Th1 cells within the CD4(+) population of Grb2(fl/fl) CD