ライフサイエンスコーパス: Th1

1 itment to IL4/5/13 (Th2) and away from IFNg (Th1).

2 Persistence of VZV-Th1 1 year after vaccination was independently predicted

3 MHC-II/CD40 expression leading to diminished Th1/17 but unchanged Th2 differentiation.

4 erentiation, polarization toward the Th1 and Th1/17 states, and overproduction of the autoimmunity-re

5 ponses elicited by FHA and Prn, resulting in Th1/17-skewed responses in inherently Th2-skewed BALB/c

6 K18 ACE2 transgenic mice produced a modest TH1/2/17 cytokine storm in the lung and spleen that peak

7 tion of Kdm6a showed upregulation of Th2 and Th1 activation pathways and downregulation of neuroinfla

8 ined mTOR activity than effector T-bet- (non-Th1) Ag-expT cells throughout the course of malaria.

9 Th1 and antibody responses are associated with prolonged

10 (CRC), which can be attributed to defective Th1 and CD8+ T cell responses.

11 The frequencies of Th1 and CXCR3+ CD8+ T cells were increased and negativel

12 ells also contained IFN-gamma, they had both Th1 and cytotoxic characteristics.

13 tuate an amplification loop for CXCR3-driven Th1 and effector CD8+ T cells recruitment to the gut, wh

14 erferon gamma, the main cytokine produced by Th1 and effector CD8+ T cells, downregulates the express

15 to a lesser extent, RV-C induced predominant Th1 and inflammatory cytokine expression.

16 s study, we demonstrate that NKG2D modulates Th1 and proinflammatory T-bet+ Th17 cell effector functi

17 n IL-2R signaling, which is known to promote Th1 and suppress Tfh cell differentiation.

18 r production of proinflammatory cytokines by Th1 and T-bet+ Th17 cells and reinforces their transcrip

19 sed differentiation, polarization toward the Th1 and Th1/17 states, and overproduction of the autoimm

20 protected regulatory T cells, and suppressed Th1 and Th17 biasness.

21 dulators that promote T(CM) responses of the Th1 and Th17 cell lineages may improve BCG vaccine effic

22 al memory cell (CMC) response with increased Th1 and Th17 cells at the time of a relapse.

23 n of AW112010 was high in in vitro-polarized Th1 and Th17 cells but low in Th2 cells, suggesting that

24 competent regulatory T (Treg) cells, whereas Th1 and Th17 cells decreased significantly.

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

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

27 regulate the osteoclast number by inhibiting Th1 and Th17 cells, which governed the new bone formatio

28 CNS infiltration of activated myeloid cells, Th1 and Th17 cells.

29 iraglutide showed decreased proliferation of TH1 and TH17 cells.

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

31 ls was required for increasing expression of Th1 and Th17 cytokines and reducing expression of Th2 cy

32 of casein-specific Th2 immunity and induced Th1 and Th17 cytokines as well as induction of IL-10.

33 , intestinal tissues increased production of Th1 and Th17 cytokines, and bacteria were reduced.

34 These results indicate that inhibition of Th1 and Th17 development provides effective suppression

35 Cytokines and chemokines shape Th1 and Th17 effector responses as well as regulate migr

36 e immune regulatory mechanisms that modulate Th1 and Th17 immune responses are altered in multiple sc

37 rects allergen-specific Th2 responses toward Th1 and Th17 immunity, and protects from allergen challe

38 nd Th17-type of cytokine expression, reduced Th1 and Th17 lymphocyte detection, and low osteoclast fi

39 Cytokines that induce and maintain Th1 and Th17 polarization were higher in CD than in NCSR

40 n of important pro-inflammatory cytokines of Th1 and Th17 profiles, while increasing Treg cells.

41 CP-rCpa1 vaccine has shown to elicit a mixed Th1 and Th17 response and confers protection against pul

42 Loss of NLRC3 promotes pathogenic Th1 and Th17 responses and enhanced experimental autoimm

43 ed by the downmodulation of antigen-specific Th1 and Th17 responses and the upregulation of Th2 and T

44 ells in the CNS and enhanced myelin-specific Th1 and Th17 responses in the periphery.

45 i-infected IL-21(-/-) mice exhibited limited Th1 and Th17 responses in their gastric mucosa.

46 eukocidin-neutralizing antibodies and robust Th1 and Th17 responses, which collectively protect again

47 disease progression by inhibiting protective Th1 and Th17 responses.

48 X-13 in vitro decreases differentiation into Th1 and Th17 subsets with increased oxidative phosphoryl

49 shifting the iTreg polarization in favor of Th1 and Th17 subsets.

50 to activate and polarize CD4(+) T cells into Th1 and Th17 subsets.

51 oduction and MHC-II expression by microglia, Th1 and Th17 T cell infiltrates, and VCAM-1+ endothelial

52 responsible for T helper type 1 and type 17 (Th1 and Th17) development and macrophage responses durin

53 ssue accumulation of other Th subsets (e.g., Th1 and Th17), highlighting that GM-CSF expression not o

54 ed with lymphocyte activation, including the Th1 and Th17-related cytokines Ifngamma and Il17a and th

55 okine-driven polarization and maintenance of Th1 and Th17/Th 22, and anti-inflammatory/profibrogenic

56 Th1 and Th2 cell modes of motility could be switched sim

57 s discrete motility gene programs that shape Th1 and Th2 cell navigation of the inflamed dermis.

58 This is because Malat1(-/-) Th1 and Th2 cells express lower levels of the immunosupp

59 ted mice and is downregulated in Malat1(-/-) Th1 and Th2 cells.

60 s study provides evidence for the ability of Th1 and Th2 cytokines to determine PTB status in AFB mic

61 E, mast cell protease 1 (Mcpt-1) and Mcpt-4, Th1 and Th2 cytokines, and patterns of ileal mastocytosi

62 he production of main cytokines that promote Th1 and Th2 differentiation, and the induction of allerg

63 control the differentiation of T cells into Th1 and Th2 helper cells that mediate cell-based and hum

64 s to infection regimes that promote distinct Th1 and Th2 responses in C57BL/6 mice.

65 n and more balanced IgG1:IgG2a/IgG2b-derived Th1 and Th2 responses than LcrV-immunized mice.

66 ry T (Treg) cell differentiation and inhibit Th1 and Th2 responses.

67 tivity is integral to human T helper type 1 (Th1) and cytotoxic T cell responses.

68 tment and a higher percentage of T helper 1 (Th1) and NK cells.

69 enrichment, upregulation of T helper type 1 (Th1) and Th2 cell-associated pathways, including interfe

70 differentiated DC to activate invariant NKT, Th1, and FOXP3(+) regulatory T cells.

71 reases in CD4(+) and CD8(+) effector memory, Th1, and regulatory T cell percentages, and stable naive

72 However, roles for IL-33 in promoting CD8, Th1, and T regulatory cell responses have also emerged.

73 erentiation of naive CD4(+) T cells to Th17, Th1, and Th2 cells led to significant increase in Lcn2 e

74 ibited significantly decreased levels of the TH1- and TH17- associated cytokines in comparison to UN

75 an important target for the amelioration of Th1- and Th17-mediated chronic inflammatory diseases.

76 tis, and this bone loss is associated with a Th1- and Th17-pattern of immune response triggered in th

77 with a dismissed RANKL expression, decreased Th1- and Th17-type of cytokine expression, reduced Th1 a

78 In this study, we show in various Th1- and/or Th17-polarized settings of acute and chronic

79 d hepatosplenomegaly; and early induction of Th1-associated cytokine gene expression.

80 HIP-reactive T-cell clones produced Th1-associated cytokines and proliferated in response to

81 mice produced significantly lower levels of Th1-associated IFN-gamma than controls.

82 Typhimurium (STm) requires IFN-gamma and the Th1-associated transcription factor T-bet.

83 Vaccination induced type 1 helper T-cell (Th1)-biased CD4 T-cell responses and low or undetectable

84 stable and induced high levels of effective Th1-biased antibody and T cell responses in mice after t

85 A-SE was able to elicit robust and sustained Th1-biased antigen-specific multifunctional CD4(+) T-cel

86 of viral replication and in the context of a Th1-biased immune response.

87 ratio, indicative of augmented OVA-specific Th1-biased immunity.

88 this trial, demonstrating an induction of a Th1-biased response characterized by interferon-gamma an

89 saRNA LNP immunizations induce a Th1-biased response in mice, and there is no antibody-de

90 Our data indicate a Th1-biased response to Cb, consistent with previous repo

91 nicity studies in our labs have shown that a Th1-biased seroconversion to both rabies virus and MARV

92 usion conformation, and in the presence of a Th1-biasing adjuvant, unexpectedly led to ERD in the cot

93 calation in BALB/c mice in the presence of a Th1-biasing adjuvant.

94 vaccine-induced immunopathology, CpG 1018, a Th1-biasing synthetic toll-like receptor 9 (TLR9) agonis

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

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

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

98 BEC secretome did not promote Th1 cell generation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

125 CD4 Th1 cells represent the main lymphocyte population that

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

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

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

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

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

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

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

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

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

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

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

137 MHCII) leads to activation of proatherogenic Th1 cells.

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

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

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

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

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

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

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

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

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

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

148 endent production of protective IL-12p40 and Th1 chemokines by alveolar macrophages, leading to activ

149 er individuals had reduced expression of the Th1 chemokines CXCL9/10/11 and their cognate receptor CX

150 h as OAS1-3 and IFIT1-3 and T helper type 1 (Th1) chemokines CXCL9/10/11, as well as a reduction in t

151 In cells differentiated under Th1 conditions in vitro, p73 negatively regulates IFNgam

152 , IFN-gamma expression recovers in polarized TH1 cultures following removal of JQ1.

153 d (fl/fl) counterparts; the effects of DC on Th1 cytokine production were mediated through production

154 d activate NK cells concurrently producing a Th1 cytokine response resulting in potent antitumor func

155 Splenocyte proliferation and TH1 cytokine transcription were increased in spleen and

156 Overall, there was an up-regulation of Th1 cytokines (IL-2 and IFN-gamma) as compared to Th2 cy

157 sulfasalazine resulted in the suppression of Th1 cytokines and a marked increase in lung macrophages

158 ly on TLR7 or TLR9 signals in the context of Th1 cytokines for their formation and activation.

159 t genetics, age, cellular tropisms, elevated Th1 cytokines, and loss of surfactant expression and pul

160 This was associated with lower levels of Th1 cytokines, decreased T cell infiltration, increased

161 In a Th1-dependent and Th17-associated scleroderma model, GS-

162 lternatively activated phenotype despite the Th1 dermal environment required for their recruitment.

163 Finally, Th1 differentiation after UV-HSV inoculation was rescued

164 s mitigates renal fibrogenesis by inhibiting Th1 differentiation and renal accumulation of profibroti

165 hus, the transcription factor T-bet controls Th1 differentiation program, while the development of Th

166 nt include Ag-specific T cell activation and Th1 differentiation, followed by T cell and macrophage m

167 upstream of, and modulates the expression of Th1 differentiation-related genes such as Ifng and Il12r

168 es that the p53 family protein, p73, affects Th1 differentiation.

169 ells in vitro but failed to induce antitumor Th1 differentiation.

170 A marked Th1 dominant response was noted from cytokines secreted

171 in vitro; they recruit and activate DCs with Th1-dominant cytokine profiles at the injection site in

172 Chronic Th1-driven colitis was induced in AKR/J mice using a par

173 t effector response in Aire (-/-) retinas is Th1-driven, 2) a subset of monocytes convert to either a

174 eting of endogenous retroviruses adjacent to Th1 enhancers.

175 after HCV antigen stimulation, demonstrating Th1 functionality.

176 CD40L vector had a blunting effect on CD4(+) Th1 helper responses and instead favored the induction o

177 ed by GA, the T cell proliferation and their Th1 IFN-gamma production are further inhibited, whereas

178 tory molecule upregulation, and secretion of Th1 (IL-12)- and Th17 (IL-23, IL-1beta, and IL-6)-condit

179 expression in OVA-sensitized skin, and lower Th1 immune response, including lower serum IgG2a and IFN

180 identify p73 as a negative regulator of the Th1 immune response, suggesting that p73 dysregulation m

181 e and adaptive immune synergy which biases a Th1 immune response.

182 us, we have demonstrated a critical role for Th1 immunity in clearing Chlamydia from the small intest

183 unostimulants in cancer because they promote Th1 immunity in mammals.

184 is a negative regulator of protective CD4(+) Th1 immunity in mice infected with L. major and suggest

185 e deficient in developing Chlamydia-specific Th1 immunity showed chlamydial persistence in the small

186 of cytokines important for the generation of Th1 immunity such as intereukin-18.

187 AIT redirect the Th2 immune response towards Th1 immunity.

188 Furthermore, Th1-independent roles for Tbet were suggested by signifi

189 farnesol, there is reduced secretion of the Th1-inducing cytokine, IL-12, and increased release of p

190 Intranasal delivery of CXCL10 siRNA blocked Th1 infiltration but did not fully rescue microglial act

191 lial polarization to M2 phenotype, prevented Th1 infiltration, and increased Th2 and Treg levels.

192 +)Ly6C(hi) myeloid cells, and mRNA levels of Th1 inflammatory cytokines are elevated in obstructed TK

193 ther increased frequency of T helper type 1 (Th1)-like CD4 effector T cells even though anti-PD-1 mon

194 ed a cDC population and increased Bhlhe40(+) Th1-like cells and CD8(+) memory T cells.

195 bet(low), and T-bet(-) subsets, with innate, Th1-like effector activity exclusively associated with T

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

197 Early life immune responses are deficient in Th1 lymphocytes that compromise neonatal vaccination.

198 milk sensitization through the induction of Th1-mediated immunity and induction of blocking IgG.

199 of beta-thalassemia intermedia in the Hbbth1/th1 murine model.

200 gher-affinity TCRs promoted the formation of Th1 or Th17 cells.

201 (+) T cells expanded and differentiated into Th1 or Th2 cytokine-producing effectors in a manner simi

202 However, Tfh, Th1, or Th17 cell-deficient mice produced as many PE-spe

203 edles promoted immune modulation towards the Th1 pathway.

204 y to reduce HBV-induced pathology during the TH1 phase and chronic phase of schistosomiasis.

205 Although cells with a Th1 phenotype were the predominant subset at baseline, c

206 BPZE1-specific T cells showed a Th1 phenotype, and the IgG exclusively consisted of IgG1

207 + T-cell responses that were biased toward a Th1 phenotype.

208 ced Th1-polarized Ab responses, although the Th1 polarization of CD4(+) T cells was more pronounced a

209 . trachomatis, whereas cytokines involved in Th1 polarization, recruitment, and activation were assoc

210 Both Clec9A and Xcr1 targeting induced Th1-polarized Ab responses, although the Th1 polarizatio

211 roperties of this versatile DC population in Th1-polarized infection settings.

212 also enriched Treg and reduced inflammatory Th1 populations in allograft draining lymph nodes.

213 d a Th2-predominant response and the other a Th1-predominant response.

214 The prime-boost also induced a Th1-predominant response.

215 ferase Setdb1 plays a role in inhibiting the Th1 program in committed Th2 cells, and mechanistically,

216 nent inducers of CD8 T cell immunity; elicit Th1-promoting inflammation; and lack interference with i

217 ic functions, which redirect murine neonatal Th1 reactivation to cell death.

218 r, in MHV68-EGFP-infected A(vy)/MIP-TF mice, Th1 reactivity spread from EGFP to other B-cell antigens

219 tivated lymphocytes, switch to a T helper 1 (Th1) regulatory pattern, and Th17 reduction.

220 nscription factor GATA3 and reduction in the Th1-relevant transcription factor Tbet.

221 Overall, we show that modulation of the Th1 response against C. albicans by platelets is depende

222 f OX40L is redundant in a chronic intestinal Th1 response and expression by ILC3s is necessary.

223 control of intracellular pathogens, a strong Th1 response characterized by the production of interfer

224 ng LdCen(-/-) parasites induced an increased Th1 response in naive mice.

225 ), is critical specifically for the effector Th1 response to an acute systemic infection with Listeri

226 bilization to the lungs and blood, decreased Th1 response, and Th2 weighted shift.

227 gamma secreting lymphocytes, both markers of Th1 response, in comparison to antigen loaded NPs delive

228 igen dose-sparing, and induced a T helper 1 (Th1) response.

229 p73-deficient naive CD4(+) T cells increases Th1 responses and augments disease severity.

230 notype of IRF4(DeltaDC) mice to unrestricted Th1 responses and in particular to IFN-gamma- and TNF-al

231 developmental death network weakens neonatal Th1 responses during early life vaccination and increase

232 s, with a specific focus on pro-inflammatory Th1 responses in the development of CHIKV joint inflamma

233 ucted TKO kidneys, suggesting that augmented Th1 responses in the TKO mice may exaggerate renal fibro

234 es to SARS-CoV-2 are robust; however, CD4(+) Th1 responses predominate over CD8(+) T cell responses,

235 in their blood glucose, peri-insulitis, and Th1 responses to EGFP which did not spread to other B-ce

236 by the factors mentioned above, by peak VZV-Th1 responses to ZVL, and by the age of the vaccinee.

237 not correlate with age, but similar to other Th1 responses, VZV-CTL peak and baseline responses were

238 lly drive IL-10 production, and to attenuate Th1 responses.

239 lung metastasis model, leading to decreased Th1 responses.

240 esign of vaccines targeting enhanced CD8 and Th1 responses.

241 their ability to enhance Ag-specific CD8 and Th1 responses.

242 40 in DCs may promote priming of T helper 1 (Th1) responses.

243 a predominantly type 17 helper T-cell (Th17)/Th1 signature, implicating this as its cell of origin.

244 ed inulin was accompanied by a significantly Th1-skewed immune profile characterized by increased T-b

245 rognosis, whereas early innate signaling and Th1-skewed immunity are important for survival.

246 Strong, Th1-skewed T cell responses can drive protective humoral

247 ir production of pro-inflammatory cytokines (Th1 skewers), we generated alpha-galactosylsphingamides

248 )-related genes, largely lacking significant Th1-skewing.

249 (Tbet KO) mice, we showed a partial role for Th1 subset CD4(+) T cells in vaccine protection.

250 and (2) skewed T-lymphoblast cells toward a Th1 subtype, (CD4(+) /CCR5(+) ) that correlated with sig

251 encies of monofunctional and dual functional Th1/T cytotoxic type 1 (Tc1), Th17/Tc17, Th2/Tc2, and Th

252 encies of monofunctional and dual functional Th1/Tc1 and Th17/Tc17 cells and, in contrast, diminishes

253 Vaccination results in the development of Th1, Th17, and antibody responses to FRalpha in the majo

254 ith pro-osteoclastogenic support provided by Th1, Th17, and B cells.

255 ays a role in regulating the polarization of Th1, Th17, and possibly T regulatory cells in PDAC tumor

256 ficantly increased gastric mucosal levels of Th1, Th17, and Th2 cytokines compared with Nod1 wild-typ

257 nd was associated with the downregulation of Th1/Th17 and upregulation of Foxp3(+)Treg.The study show

258 y CCL2 was associated with downregulation of Th1/Th17 cells and upregulation of TGF-beta and inductio

259 riatic HSC (pHSC) by incorporating polarized Th1/Th17 cells or CCR6+CLA+ T cells derived from psorias

260 oimmune disease sustained by proinflammatory Th1/Th17 cells.

261 helper T (TH) cells in functional assays of TH1/TH17 differentiation and measured the concentration

262 m infected children were attenuated in their TH1/TH17 differentiation capacity and expressed less int

263 Our data are consistent with a model wherein TH1/TH17 differentiation is attenuated in NTM-infected c

264 terfere with the development of a protective Th1/Th17 immune response to C. immitis at the site of in

265 ies have been previously shown in innate and Th1/Th17 predominant inflammatory models.

266 ) functionally analogous to T helper type 1 (Th1), Th2, and Th17 cells are well characterized, an ILC

267 ell effector program [e.g., T helper type 1 (Th1), Th2, Th17].

268 ncer drug known to modulate T-helper type 1 (Th1)/Th2 responses and has the potential to regulate imm

269 cells showed significant cytokine responses (Th1, Th2, and granulocyte-macrophage colony-stimulating

270 turn, is associated with elevated levels of TH1, TH2, and proinflammatory cytokines, indicating an a

271 erences in cytokine production were found in Th1, Th2, and Th17 immunity in response to both unspecif

272 e intestine associated with helper T cells' (Th1, Th2, and Th17) specific pathways.

273 TCC secreted Th1, Th2, and Th22 cytokines and effector molecules and

274 rofile of cytokine responses, by stimulating Th1, Th2, Th17, and Tfh cytokines.

275 ) IgG(+) , IgE(+) and IgA(+) memory B cells, Th1, Th2, Th17, and Treg-memory cells from venous blood.

276 uman and mouse CD4 T cells were activated in Th1, Th2, Th17, or regulatory T cell (Treg) environments

277 The expression levels of Th1, Th2, Th17, or T regulatory-associated cytokines and

278 ngs demonstrate deficiencies in mediators of Th1-Th2 immunity, which have paradoxical or no impact.

279 observations expand our understanding of the Th1-Th2 paradigm during infection.

280 We found that low Th1/Th2 activity ratios were associated with a significa

281 naffected by deliberate changes in the early Th1/Th2 balance.

282 or the ratio of CXCR5IFN-gammaCD8 T cells to Th1/Th2 CD4 T cells) may identify recipients at risk for

283 of CXCR5IFN-gammaCD8 T cell to combined CD4 Th1/Th2 cell subsets (IFN-gammaCD4 and IL-4CD4 cells; P

284 Supported by a mixed Th1/Th2 cell-mediated immunity, P27A induced a marked sp

285 tion, lung histology, and elevated pulmonary Th1/Th2 cytokine levels.

286 Nasal symptoms, Th1/Th2 cytokines in nasal secretion and serum were eval

287 ating a potential mixed and antigen-specific Th1/Th2 immune response, which is different from the Th2

288 report that prior to influencing activation, Th1/Th2 immunity first controls the size of the permissi

289 , known for its ability to induce a balanced Th1/Th2 immunity.

290 ter transcription factors and framing of the Th1/Th2 paradigm ignited the CD4(+) T cell field.

291 Gal-3 has been shown to regulate Th1/Th2 polarization of CD4(+) T cells; however, the ext

292 airway molecular phenotype that has elevated Th1/Th2 ratios.

293 reast cancer patients, whereas an unbalanced Th1/Th2 response was correlated with poorer survival of

294 gh titers of antibodies and elicited a mixed Th1/Th2 response.

295 ys, with upstream drivers including hallmark Th1/Th2- and inflammation-associated genes.

296 functional FOXP3(+) Treg cells and promotes Th1/Th2/Th17 responses.

297 Th2-, Th1-, Th9- and Tr1-type cytokines decreased over the cou

298 BB-Cl-amidine treatment induced a shift from Th1 to Th2 cytokines in the serum and an increase in the

299 Protection was associated with a Th1/Treg-dominated cytokine response, increased Foxp3(+)

300 comorbidity and impairment of CoV-2-specific Th1-type cellular immunity, thereby supporting a concept

301 CONCLUSIONThe breadth of the antibodies, the Th1-type cellular response, and killing mechanisms elici