ライフサイエンスコーパス: Th1 cell

1 that are distinct from conventional Th17 and Th1 cells.

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

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

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

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

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

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

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

9 lls that had lower tumoricidal activity than Th1 cells.

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

11 and by supporting the development of classic Th1 cells.

12 ntigen-specific population of differentiated Th1 cells.

13 teractions are required to generate Th2 than Th1 cells.

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

15 epigenetically silenced in anergic effector TH1 cells.

16 ntly greater amounts of CTLA-4 compared with Th1 cells.

17 s dependent on IFN-gamma derived from CD4(+) Th1 cells.

18 in order to allow their differentiation into Th1 cells.

19 the conversion of Th2, Th17 or Treg cells to Th1 cells.

20 -Th1 reprogramming that could be elicited by Th1 cells.

21 However, Th17 cells are generated before Th1 cells.

22 ory response leading to the proliferation of Th1 cells.

23 ability of cDCs to prime IFN-gamma-producing Th1 cells.

24 pecific IFN-gamma secretion from pluripotent Th1 cells.

25 and CXCL11 coordinate migration of CXCR3(+) Th1 cells.

26 contributing to the bioactivity of NKG2D(+) Th1 cells.

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

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

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

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

31 lted in a significantly reduced frequency of Th1 cells.

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

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

34 ion of CXCR3 downregulation and crippling of Th1 cells.

35 st tested the pathogenic contribution of CD4 Th1 cells.

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

37 f miR-150, compared with IFN-gamma-secreting 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 a(2+) and cytokine responses in TH2, but not TH1, cells.

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

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

44 As expected, (64)Cu-OVA-Th1 cells also accumulated significantly in the pulmonar

45 Innate stimulation of Th1 cells also required host expression of TLR4 and infl

46 tified a predominance of IFN-gamma-producing Th1 cells and an absence of IL-17-producing Th17 cells,

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

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

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

50 of IL-17-producing neutrophils and Th17 and Th1 cells and dependent on production of IL-17 but not I

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 hereas intranasal inoculation produces fewer Th1 cells and instead many Th17 cells.

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 ements, relationship with "classic" Th17 and Th1 cells and physiological role in normal immune respon

57 alytic partner Cdk9, impaired development of Th1 cells and protective short-lived effector CTL and en

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

75 on was detectable in CD4(+) T cells, ex vivo TH1 cells, and TH17 cells, whereas Cav1.2 channels predo

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 nfants cannot readily mount T helper type 1 (TH1) cell antibacterial and antiviral responses.

81 Th1 cells are central pathogenic mediators of crescentic

82 Th1 cells are critical for containment of Mycobacterium

83 Although Th1 cells are key orchestrators of T1D, the function(s)

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

85 Whereas the costimulation properties of Th1 cells are well studied, relatively little is known a

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

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

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

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

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

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

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

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

94 Moreover, macrophages and Th1 cells (both of which mediate atherosclerotic plaque

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

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

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

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

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

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

101 ivation of MyD88 promotes the development of Th1 cells by rendering them impervious to T(reg) cell-me

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

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

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

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

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

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

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

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

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

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

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

113 ired in the absence of Bcl-3, differentiated Th1 cells converted to less-pathogenic Th17-like cells,

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

115 We show that primarily Th1 cells cross the ependymal layer of the ventricle and

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

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

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

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

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

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

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

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

124 catenin in DCs programmed them to drive Th17/Th1 cell differentiation in response to zymosan.

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

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

127 ell differentiation, whereas IL-17 inhibited Th1-cell differentiation.

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

129 reduced inflammatory function, particularly Th1 cells, display elevated and sustained IL-10 expressi

130 interactions, required to generate Th2 over Th1 cells, does not involve CD40, OX40, or ICOS costimul

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

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

133 test the functional capacities of (64)Cu-OVA-Th1 cells during experimental OVA-induced airway hyperre

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

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

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

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

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

139 flammation induced IL-6-mediated T helper 1 (Th1) cell effector commitment and the emergence of STAT1

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

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

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

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

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

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

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

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

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

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

150 Th1 cells from dnRARalpha mice showed enhanced plasticit

151 Restimulation of Th1 cells from LCMV-infected mice promoted BLIMP-1 and s

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

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

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

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

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

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

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

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

160 ingly, intravenously administered (64)Cu-OVA-Th1 cells homed predominantly into the lung and spleen b

161 To elucidate the fate of Th1 cell homing by PET, 10(7 64)Cu-OVA-Th1 cells were in

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

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

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

165 ough BCG induces host-protective T helper 1 (Th1) cell immune responses, which play a central role in

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

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

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

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

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

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

172 producing Th17 cells and IFN-gamma-producing Th1 cells in the pancreas as well as in the serum levels

173 5, and CCR7 and to suppress proliferation of Th1 cells in the pancreas.

174 The accumulation of (64)Cu-OVA-Th1 cells in the pulmonary LNs (6.8 +/- 1.1 percentage i

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

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

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

178 xogenous IL-1beta to reactivate Th17 but not Th1 cells in vitro.

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

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

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

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

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

184 f SFB-colonized mice also harboured a strong TH1 cell inducer, Listeria monocytogenes, in their intes

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

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

187 Similarly, reactivation of Th1 cells infiltrating the CNS was selectively impaired

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

189 hyperreactivity, we injected 10(7 64)Cu-OVA-Th1 cells intraperitoneally into OVA-immunized or nonimm

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

191 Thus, the in vivo bactericidal capacity of Th1 cells is regulated by the response to noncognate sti

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

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

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

195 T-bet synthesis, thus adopting a T helper 1 (Th1) cell-like effector phenotype.

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

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

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

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

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

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

202 Th1 cell numbers were elevated in MPE from IL-17(-/-) mi

203 ed antigen concentration, adjuvants inducing Th1 cells operated by affecting DC costimulation that am

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

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

206 igations into treatments for DLE that target Th1 cells or the IFN-gamma signaling pathway.

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

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

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

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

211 Thus, Bcl-3 constrained Th1 cell plasticity and promoted pathogenicity by blocki

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

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

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

215 Importantly, we showed that Th17, but not Th1 cells, preferentially produce these two oxysterols.

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

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

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

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

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

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

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

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

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

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

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

227 presence of memory IFN-gamma-producing CD4+ Th1 cells requires the administration of live bacteria a

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

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

230 ronic profibrotic state through induction of Th1 cell responses as a consequence of recurrent inflamm

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

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

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

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

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

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

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

238 T helper 17 (Th17) cell responses, but also Th1 cell responses.

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

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

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

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

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

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

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

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

247 Finally, the elimination of noncognate Th1 cell stimulation hindered the resolution of primary

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

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

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

251 mer's disease, amyloid-beta (Abeta)-specific Th1 cells target Abeta plaques, increase Abeta uptake, a

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

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

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

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

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

257 gainst disease correlated with a decrease in Th1 cells that produced the cytokines IFN-gamma and GM-C

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

280 Although differentiation into Th1 cells was not impaired in the absence of Bcl-3, diff

281 ation, but CX3CR1 expression by both Th2 and Th1 cells was required to induce AD.

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

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

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

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

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

287 Primary virus-specific CD4(+) Th1 cells were generated in B cell-depleted mice; howeve

288 te of Th1 cell homing by PET, 10(7 64)Cu-OVA-Th1 cells were injected intraperitoneally or intravenous

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

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

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

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

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

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

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

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

297 iting pathogenic T helper type 17 (TH17) and TH1 cells while promoting Treg cell expansion.

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

299 c interferon (IFN)-gamma-producing CD4(+) T (Th1) cells with 0.7-2.2 MBq of (64)Cu-PTSM and analyzed

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