ライフサイエンスコーパス: Th1

1 inducing Th17 polarization at the expense of Th1.

2 tients with multiple sclerosis, we find that TH1/17 cells have elevated expression of CXCR3 and reduc

3 Compared to TH17 cells, TH1/17 cells have gene signatures with marked similarity

4 human peripheral blood IFN-gamma(+)IL-17(+) (TH1/17) and IFN-gamma(-)IL-17(+) (TH17) CD4(+) T cells d

5 s of CpG loci within the promoter regions of Th1/2 lineage commitment genes (GATA3, IL-4, IL-4R, STAT

6 proteins and helminths induce IgG1, whereas Th1 Ags, such as Salmonella Typhimurium, predominantly i

7 cell responses shift toward IL-6-independent Th1 and CD4 cytotoxic Th cell responses.

8 aining T-bet(+) cells specifically inhibited TH1 and CD8 T cell activation consistent with their co-l

9 rom the affected patient displayed increased TH1 and follicular T helper cell and suppressed TH17 cel

10 ess to type I and II interferons, normalized TH1 and follicular T helper cell responses, improved TH1

11 In addition, more Th1 and less Th2 cytokine production in exposed splenocy

12 Furthermore, formation of memory TH1 and memory TFH cells strongly depended on Tcf1 long

13 CXCL10 and contained mainly CXCR3-expressing TH1 and TH1/TH17 subsets.

14 ribute to atopic disease, whereas defects in TH1 and TH17 cells compromise antiviral and antifungal i

15 Th1 and Th17 cells have an established role in protectiv

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

17 ssociated with reduced donor proinflammatory Th1 and Th17 cells, accumulation of donor myeloid-derive

18 n increased disease severity, populations of Th1 and Th17 cells, and inflammatory markers (IFN-gamma,

19 In contrast with Th1 and Th17 cells, ex-Th17 cells were highly resistant

20 -cell proliferation and differentiation into Th1 and Th17 cells, increased T-cell apoptosis, reduced

21 t with the TLR7 ligand imiquimod can inhibit Th1 and Th17 cells, resulting in the prevention of, and

22 r antigen uptake but were impaired to induce Th1 and Th17 cells.

23 nd TRBV16/(TRBD1/2)TRBJ1-7 (CGGKRRLESIFR) in Th1 and Th17 cells.

24 d promoted sustained upregulation of OX40 by Th1 and Th17 cells.

25 d a TH2 type, and this was at the expense of TH1 and TH17 cells.

26 roportion of activated CD4(+)-T cells with a Th1 and Th17 cytokine profile was increased in cMy-mOVA-

27 ive potential yet preferentially secrete the Th1 and Th17 cytokines interferon-gamma and interleukin

28 ependently and in combination with classical Th1 and Th17 cytokines.

29 CA2a 971-990-sensitized T cells produce both Th1 and Th17 cytokines.

30 o, testosterone treatment not only decreased Th1 and Th17 differentiation in an aromatase-independent

31 In addition, enhanced TH1 and TH17 immune responses are seen in experimental a

32 Finally, they were found to induce strong Th1 and Th17 immune responses in vivo in immunization ex

33 iption factor known for its role in limiting Th1 and Th17 immunity.

34 Citrobacter rodentium, which induces a mixed Th1 and Th17 response.

35 local draining iliac lymph nodes, yet robust Th1 and Th17 responses were prominent in the FRT.

36 like other family members, actually promotes Th1 and Th17 responses.

37 highlighted their unexpected role in priming TH1 and TH17 responses.

38 r T-cell activation and differentiation into Th1 and Th17 subsets in vivo.

39 +) T-cells and CD4(+) T-cells including TH0, TH1 and TH17).

40 ducing CD4(+) T cells, reduced expression of Th1 and Th2 associated transcription factors, Tbet and G

41 Supernatant of activated TH1 and TH2 cells impaired epithelial integrity, while t

42 ibition of inosine on the differentiation of Th1 and Th2 cells in vitro depended on adenosine A2A rec

43 Exploring the interplay of Th1 and Th2 cells through co-culture, Th2-derived IL-4 p

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

45 ype, contributing to the cross-regulation of Th1 and Th2 cells.

46 g as a previously unappreciated regulator of Th1 and Th2 immunity and an important element of antifun

47 yte recruitment, and simultaneously impaired Th1 and Th2 responses.

48 Combining the TLR4 and TLR7 ligands balances Th1 and Th2-type immune responses for long-lived cellula

49 d genetic studies suggest the involvement of TH1 and type 2 interferon pathways.

50 al autoimmune uveitis (EAU), in which CD4(+) Th1 and/or Th17 cells are immunopathogenic, mimics vario

51 MV infection, where balanced CD4 T helper 1 (Th1) and T follicular helper (Tfh) responses were induce

52 ted in chronic ischemic HF, with Th2 (versus Th1) and Th17 (versus Treg) predominance in failing hear

53 typic and functional features of human Th17, Th1, and ex-Th17 cell populations.

54 mulas varied regarding the induction of Th2, Th1, and proinflammatory cytokines.

55 es and chemokines, representative of innate, TH1, and TH17 immune responses, were assessed by Luminex

56 s had significantly higher levels of innate, TH1, and TH17-associated mediators (P </= .05) in serum.

57 the differentiation and expansion of T reg, Th1, and Th2 cells.

58 nal analysis of in vitro-differentiated Th0, Th1, and Th2 cultures identified CD200R as upregulated o

59 associated with diminished antigen-specific Th1- and Th17-associated responses and enhanced Th2-asso

60 L-4Ralpha monoclonal antibodies restored the TH1- and TH2-induced epithelial barrier dysfunction, res

61 , while demonstrating plasticity toward both Th1- and Th2-type cells.

62 Treg cells, thereby enhancing suppression of Th1 anti-tumour immunity.

63 for suppressing the expression of Blimp1 and TH1-associated genes and for positively regulating Id3 t

64 the disease, in patients with LA, innate and TH1-associated mediators were often >10-fold higher in s

65 (4)-fold boost in antibody titers, increased Th1-associated responses, and expanded germinal center B

66 Here we demonstrate that expression of the TH1-associated transcription factor T-bet in mouse Treg

67 larisation, we predict that promotion of the Th1-associated transcription factor T-bet, rather than i

68 expression in Treg cells-resulted in severe TH1 autoimmunity.

69 to pp65, IE1, IE2, and gB was predominantly Th1 biased, with neither the loss nor the accumulation o

70 iruses also had higher antibody titers and a Th1-biased T cell memory response at 75 days p.i.

71 antigen-specific gamma interferon-dominated Th1-biased T cell response.

72 n the ratio of CD4 Foxp3(+) Treg to effector Th1 CD4 T cells in ocular lesions and lymphoid tissues,

73 ant for differentiation of cytotoxic CD8 and Th1 CD4 T cells.

74 SL3261/sec strain generated large numbers of Th1 CD4(+) ESAT-6(+) splenic T cells compared to those o

75 se could be related to a loss of circulating Th1* CD4(+) T cells rather than major changes in the num

76 strong type 1 immune response that involves Th1, CD8, and B cell entry across the blood-brain barrie

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

98 5, and CCR7 and to suppress proliferation of Th1 cells in the pancreas.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

116 that are distinct from conventional Th17 and Th1 cells.

117 ntigen-specific population of differentiated Th1 cells.

118 However, Th17 cells are generated before Th1 cells.

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

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

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

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

123 lted in a significantly reduced frequency of Th1 cells.

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

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

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

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

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

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

130 eficient Treg cells lacked expression of the Th1-characteristic trafficking receptor CXCR3, which cor

131 ntly, it was proposed that activation of the Th1-characteristic transcription factor T-bet optimizes

132 Furthermore, under Th1 culture conditions in vitro, as well as in an IFN-ga

133 nhibited while addition of exogenous IL-4 to Th1 cultures enhanced IL-10 production.

134 IL-10 production and that Th2 cells modulate Th1 cultures towards a self-regulatory phenotype, contri

135 h2-derived IL-4 promoted IL-10 expression by Th1 cultures, reducing their pathogenicity in vivo.

136 lso reduced the encephalitogenic capacity of Th1 cultures.

137 CCL17, eotaxin-1/CCL11, CCL13, CCL4, IL-10), Th1 (CXCL10, CXCL11) and Th1/Th17/Th22 (IL-12/IL-23p40)

138 Th subsets Th1 (CXCR3(+)), Th17 (CCR6(+)), and particularly those e

139 type of myeloid cells, increased NK cell and Th1 cytokine levels, and reduced immature myeloid cell i

140 ng adaptive T-cell cytokines, an increase of TH1 cytokines and, in particular, TH17 cytokines IL-17A,

141 and greater stimulated production of TH2 and TH1 cytokines by PBMCs (Ps < .05).

142 M-CSF, stimulates ATM proliferation, whereas Th1 cytokines, such as TNF-alpha, inhibit local ATM prol

143 e responses by DCs and natural killer cells, Th1 development, phagocytic receptor expression, and pha

144 the transcription factor T-bet, a driver of Th1 differentiation and cytotoxic effector cell maturati

145 Egr2 and 3 were essential to suppress Th1 differentiation in Th2 and Th17 conditions in vitro

146 how that CD4(+) T(Pam3) cells are capable of Th1 differentiation in the presence of TGF-beta, suggest

147 is a serine-threonine kinase that regulates Th1 differentiation, secretion of the inflammatory cytok

148 a novel mechanism by which mTORC1 regulates Th1 differentiation, through control of T-bet phosphoryl

149 Pam3Cys4 (CD4(+) T(Pam3)) become primed for Th1 differentiation.

150 ese findings are important in the context of Th1 driven diseases since they reveal how the Th1 phenot

151 ased differentiation of T lymphocytes toward Th1 during infection.

152 Th1 effector cells selectively drive CF both in vitro an

153 Thus, in addition to promoting Th1 effector commitment, T-bet acts as a repressor in di

154 Polyfunctional Tg Th1 effectors demonstrated enhanced IFN-gamma production

155 of T follicular helper (TFH) cells, but not TH1 effectors, elicited by viral infection.

156 deed, the results show that fluorinated ITIC-Th1 exhibits redshifted absorption, smaller optical band

157 le to serve as an immunophenotype capable of Th1, follicular Th, and CTL functionalities, yet they ar

158 PD-1:28 engineering reinstated Th1 function in tumor-infiltrating lymphocytes that had

159 t R-loop-enriched regions of IFNG and TBX21 (TH1 genes) in TH1 cells.

160 new fluorinated nonfullerene acceptor, ITIC-Th1, has been designed and synthesized by introducing fl

161 creased in serum of both diseases, including Th1 (IFN-gamma, CXCL9, TNF-beta) and Th17 (CCL20) marker

162 However, alum hardly induces T helper 1 (Th1) immune responses that are required for anti-tumor i

163 th low doses of gp96 primes T helper type 1 (Th1) immune responses, whereas high-dose immunization pr

164 ntly to innate and adaptive T-helper 1 cell (TH1) immune responses, whereas the role of T-helper 17 c

165 missive for parasite growth even in a strong Th1-immune environment, and the preferential infection o

166 nity can cross MHC class I barriers and that Th1 immunity can be imparted to Th2-biased offspring; in

167 Initiation of TH1 immunity to dietary antigen was dependent on interfe

168 tory T cell (pTreg) conversion and promoting TH1 immunity to dietary antigen.

169 eg1 cells, showed spontaneous skewing toward Th1 immunity.

170 ses leading to the initiation of T helper 1 (TH1) immunity against dietary gluten and celiac disease

171 nce is a novel molecular defect causative in TH1 immunodeficiency and genomic instability in patients

172 , but Egr2 and 3 expression was inhibited by Th1-inducing cytokines.

173 ent formulations in combination with several Th1-inducing Toll-like receptor (TLR) agonists in vivo I

174 and especially the DI domain, drive a local Th1 inflammatory response, with subsequent plaque instab

175 reaction (T1R) is an acute T-helper type 1 (Th1) inflammatory episode in patients with leprosy.

176 ammatory (IL-2), innate (IL-1beta), and some TH1/interferon (IFN-gamma) markers in patients with icht

177 ad significantly reduced percentages of CD4+ Th1 (interleukin2, tumor necrosis factor alpha) and Th17

178 Bet v 1-nonreactive TCC were mainly Th1-like and showed a higher expression of the integrin

179 i-CTLA-4 induces the expansion of an ICOS(+) Th1-like CD4 effector population in addition to engaging

180 ts with LRBA deficiency were biased toward a TH1-like cell phenotype, which was partially reversed by

181 ve CD4(+) T cells to proliferate and secrete Th1-like cytokines.

182 A Th1-like response was also detected in Dau c 1-reactive

183 ollowing Ad5 immunization exhibited impaired Th1 lineage commitment, generating significantly decreas

184 by Ad5 vectors expressed decreased levels of Th1 markers, such as Tim3, SLAM, T-bet, and Ly6C, had sm

185 r associated with significant enhancement of Th1-mediated and cytotoxic T-cell-mediated antitumor imm

186 cellular immune responses that result in the Th1-mediated pathology of T1R.

187 d ones it enhanced the expression of the pro-Th1 mediators Fizz-1 and arginase 1, indicating that it

188 site Toxoplasma gondii causes a nonresolving Th1 myositis with prolonged tissue damage associated wit

189 in terms of cytokine production than either Th1 or bona fide Th17 cells, and produced increased amou

190 however, it is unclear whether they resemble Th1 or Th17 cells in terms of their function and regulat

191 Additionally, CGS treatment did not inhibit Th1 or Th17 differentiation.

192 the key effector molecules while a shift to Th1 or Treg cells mainly contributes to the efficacy of

193 gh conversion of Tregs into T helper type 1 (Th1) or type 17 (Th17) effector lymphocytes.

194 IL-2 feedback had no effect on Th1- or Th17-signature cytokine production, but it promo

195 In human TH1- or TH2-skewing cell culture systems, cotranscriptio

196 h1 driven diseases since they reveal how the Th1 phenotype and function can be modulated by IL-4.

197 nfected tissue, and acquire a polyfunctional Th1 phenotype in infected mice.

198 otherapy leading to a chronically stimulated Th1 phenotype, lack of IL-4Ralpha inhibited the inductio

199 s predominantly of a CXCR3(+)CCR6(+)CCR4(-) (Th1*) phenotype, aTB or HIV infection was associated wit

200 atio together support a role of CDC42 in the TH1 polarization and pulmonary function deficits found i

201 metabolomic changes may link HCA exposure to TH1 polarization of the neonatal adaptive immune respons

202 ericidal capacity and the ability to promote Th1 polarization over Th2 responses.

203 t RIG-I and MDA5 triggering by DENV leads to TH1 polarization, which is characterized by high levels

204 gs in the CNS during T. gondii infection are Th1 polarized, as exemplified by their T-bet, CXCR3, and

205 se data suggest that clonal proliferation of Th1-polarized CD4+ T cells encoding for intact HIV-1 rep

206 CD4 T cells, were preferentially observed in Th1-polarized cells, were longitudinally detected over a

207 4+ and CD8+ T cells are capable of producing Th1-polarized effector cytokines and killing PIV3-expres

208 esponse, while the dual combination promoted Th1-polarized IgG responses.

209 fferentially expressed genes associated with TH1-polarized inflammation.

210 me-wide transcriptome analyses revealed that Th1-polarized inflammatory responses, defined by express

211 infection with Toxoplasma gondii leads to a Th1-polarized parasite-specific effector T cell response

212 c children, suggesting its role in nonatopic TH1-polarized systemic inflammation and pulmonary functi

213 The TH1-polarizing activity of L lactis G121-treated human D

214 reated murine BMDCs and human moDCs released TH1-polarizing cytokines and induced TH1 T cells.

215 on in BMDCs or moDCs impaired the release of TH1-polarizing cytokines, costimulatory molecule express

216 massive T cell activation and a predominant Th1 profile of cytokine production.

217 ed with CMV antigens, induce a recall CD4(+) TH1 proliferation response only in CMV-seropositive dono

218 e a surrogate of lack of protection, whereas TH1-related responses may be involved in protective mech

219 mphysematous destruction COPD is driven by a Th1 response activated by infiltrating ILC1, NK, and LTi

220 pathway involved in the establishment of the Th1 response against an in vivo infection, a presently c

221 ully understood, but a shift from a TH2 to a TH1 response has been suggested as a possible explanatio

222 exposure by a marked innate, but no Th2 and Th1 response subsequently followed by enhanced numbers o

223 trating neutrophils and elicits a mixed TH17/TH1 response.

224 s a crucial element for induction of cognate Th1 responses against an important human pathogen.

225 dulate the immune system to support enhanced TH1 responses and decreased IL-5 responses.

226 overexpression of miR-27 harbor dysregulated Th1 responses and develop autoimmune pathology, these di

227 production of IFN-gamma, and polyfunctional Th1 responses are associated with enhanced protection.

228 ced distinctly higher levels of inflammatory Th1 responses than Delta5G.

229 mmitment, generating significantly decreased Th1 responses than those induced by LCMV infection.

230 cosylation of Env modulates the inflammatory/Th1 responses through the monocyte/macrophage subsets an

231 selectively dysregulated renal and systemic Th1 responses.

232 formation of IgG2b/c, which is indicative of Th1 responses.

233 biting Th2 immunity and promoting pathogenic Th1 responses.

234 wing Ad5 immunization partially restored CD4 Th1 responses.

235 ory T cells; or immune deviation in favor of TH1 responses.

236 ion of an overexpressed phospho-null mutant, TH1-S31A, was restricted to the soma of neuroblastoma ce

237 clein A53T, a PD-associated mutation, caused TH1-S31E accumulation in the cell soma.

238 TH1-S31E associated with vesicular monoamine transporter

239 al fraction, whereas a phospho-mimic mutant, TH1-S31E, was distributed throughout the soma and neurit

240 s more pronounced after high-thoracic level (Th1) SCI disconnecting adrenal gland innervation, compar

241 Among innovative adjuvants conferring a Th1-shift, RNAdjuvant is a promising candidate.

242 Moreover, the OSCs based on FTAZ:ITIC-Th1 show much better efficiency and better stability tha

243 ildren with severe asthma display a dominant TH1 signature and atypical cytokine profiles that link t

244 In this regard, NFAT5 upregulated the Th1-stimulatory cytokine IL-12 in classically activated

245 eleased TH1-polarizing cytokines and induced TH1 T cells.

246 ted in significantly enhanced frequencies of Th1/Tc1, Th2/Tc2, Th17/Tc17, Th9, and Th22 cells with pa

247 To this end, we examined the frequency of Th1/Tc1, Th2/Tc2, Th9/Tc9, Th17/Tc17, and Th22/Tc22 cell

248 TH1, TH17, and CD8(+) memory T-cell differentiation was

249 te differentiation into the effector subsets Th1, Th17, and induced regulatory T cells.

250 upon in vitro T cell receptor stimulation of Th1, Th17, and T regulatory (Treg) cells.

251 mixed T helper cell population comprised of Th1, Th17, and Th22 cells, which was abrogated by the ad

252 10-treated microglia significantly inhibited Th1/Th17 cell differentiation and increased the number o

253 Thus the selective targeting of TH1/TH17 cells could inhibit relapses without causing Jo

254 TH1/TH17 central memory (TH1/TH17CM) cells were selectiv

255 In contrast, TH1/TH17 cytokines, which dominated the response to S au

256 (+) CD127(+) CD25(high) cells that display a Th1/Th17 phenotypic profile, as reflected by heightened

257 TLR4 mutant) mice reversed M1 macrophage and TH1/TH17 polarization after TBI compared with C3H/OuJ (w

258 timulators of T lymphocyte proliferation and TH1/TH17 polarization compared with C3H/OuJ monocytes.

259 nd contained mainly CXCR3-expressing TH1 and TH1/TH17 subsets.

260 e CD103(+)alpha4beta7(high) subsets enhanced Th1/Th17 T cell generation and accumulation in the intes

261 At functional level, Treg-derived (but not Th1/Th17-derived) EVs inhibited CD4(+) T cell proliferat

262 Cortistatin reduced Th1/Th17-driven inflammatory responses and increased reg

263 nstrates that these CD4(+) T cells display a Th1/Th17-like phenotype with an enrichment of gene targe

264 CL13, CCL4, IL-10), Th1 (CXCL10, CXCL11) and Th1/Th17/Th22 (IL-12/IL-23p40) responses.

265 therapies efficiently targeted autoreactive TH1/TH17CM cells but also blocked virus-specific TH1 cel

266 We propose that autoreactive TH1/TH17CM cells expand in patients with MS and promote

267 TH1 cells responded consistently to viruses, TH1/TH17CM cells reacted strongly with John Cunningham v

268 TH1/TH17CM cells were closely related to conventional TH

269 TH1/TH17 central memory (TH1/TH17CM) cells were selectively increased in peripher

270 nct subsets of effector T cells (T helper 1 (TH1), TH2, and TH17) defined by expression of the key tr

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

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

273 2 cytokines; and (3) significantly increased Th1, Th2, Th17 cells, and Tregs, in the spleen and media

274 (Th) T lymphocytes, together with increased Th1, Th2, Th17, and regulatory T-cell (Treg) CD4(+) subs

275 previously thought to be selective for Treg, Th1, Th2, Th17, and Tfh cells, including CD194 (CCR4)(+)

276 cells in failing myocardium, with increased Th1, Th2, Th17, and Treg CD4(+) subsets, marked reductio

277 pendent functional characterization of human Th1, Th2, Th17, T follicular helper (Tfh), Treg, and Tr1

278 Th1, Th2, Th9 and Th17 cells are conventional CD4(+) eff

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

280 sed in patients group versus controls, while Th1, Th2, Treg, and eosinophil gene signatures were incr

281 ferent subsets, including similarity between Th1-Th2-Tfh cell populations and Th17 cells, as well as

282 for disease progression and illustrates that Th1/Th2 (IFN-gamma/ELISA antibodies) assays are importan

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

284 nhibited multiorgan inflammation by reducing Th1/Th2 cells and their associated cytokines.

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

286 Treg CD4(+) subsets, marked reduction of the Th1/Th2 ratio, augmentation of the Th17/Treg ratio, and

287 ific antibody titer with an overall balanced Th1/Th2 response, while the dual combination promoted Th

288 We quantified TH1/TH2/TH17 CD4 memory T cells in blood and lymph nodes

289 mRNA expression of Th1/Th2/Th17-associated cell markers decreased between 4

290 mRNA expression of Treg/Th1/Th2/Th17-associated cell markers was measured ex viv

291 ced T-cell proliferation and a switch from a Th1 to a Th2 phenotype.

292 llary disease, no shift in T cell genes from Th1 to Th2 pattern but rather an incremental decline int

293 ue to defects in regulation of the canonical Th1 transcription factor T-bet at the level of protein p

294 Mice deficient in the Th1 transcription factor T-bet did not gain any survival

295 humans, and hypoxia was reduced by adoptive TH1 transfer.

296 (LdCen(-/-) ) parasites through induction of Th1 type immune response in mice, hamsters, and dogs.

297 d a shift in cytokine expression from Th2 to Th1 type while remodeling the tumor-associated fibroblas

298 us disorder characterized by accumulation of TH1-type CD4(+) T cells and immune effector cells within

299 3(+) regulatory T (Treg) cells to counteract Th1-type inflammation.

300 (+) and CD8(+) T cells in type 1 conditions (Th1) were regulated by glutamine and alpha-ketoglutarate