ライフサイエンスコーパス: T-helper cell

1 mucosal inflammation driven by Th17 and Th1 T helper cells.

2 1 as crucial to induce IL-10 in inflammatory T helper cells.

3 ptimal expression of CCR9 and alpha4beta7 by T helper cells.

4 on CD40-mediated interaction of B cells with T helper cells.

5 but also requires IL-13 production by CD4(+) T helper cells.

6 ry behaviors of different lineages of CD4(+) T helper cells.

7 f environmental antigens for presentation to T helper cells.

8 , it is desirable to elicit activated type 1 T helper cells.

9 ) T cells into different subsets of effector T helper cells.

10 ic development that parallel those of CD4(+) T helper cells.

11 T helper cells and the suppression of type 1 T helper cells.

12 in GCs of lymphoid tissues called follicular T helper cells.

13 ral immunity in mice with preexisting memory T-helper cells.

14 in normal immune responses, largely require T-helper cells.

15 molecules in membranes and trigger specific T-helper cells.

16 racterized by proliferation of mature CD4(+) T-helper cells.

17 adaptive immune system and involve waves of T helper cell 1 (Th1), Th17, and CD8 cells that infiltra

18 ated genes whereas it inhibits expression of T-helper cell 1 (TH1) and TH17 signature genes.

19 hexon-specific T cells, predominantly of the T-helper cell 1 (Th1) phenotype, in 30 patients with AdV

20 ory tumor-infiltrating CD8(+) T cells with a T-helper cell 1 (TH1) profile.

21 However, the response is dependent on CD4+ T-helper cell 1 (Th1) recruitment and activation.

22 ecause of its role in suppressing protective T-helper cell 1 (Th1) responses.

23 us-specific T-cell clones mainly exhibited a T-helper cell 1 phenotype and recognized a broad variety

24 he P2X7R pathway was also shown to stimulate T-helper cell 1/T-helper cell 17 cell generation.

25 s associated with reduced T-cell activation, T-helper cell 1/T-helper cell 17 differentiation, and in

26 mation, serum IgE level, and T helper cell 2/T helper cell 17 cytokine response.

27 16L1, IRGM), and genes in the interleukin-23-T helper cell 17 pathway indicate the important roles of

28 a (IFNgamma) responses and led to developing T helper cell 17/22 (Th17/Th22) responses after SHIV/mal

29 ic production of serum factors that promoted T-helper cell 17 (Th17) differentiation from anti-CD3/CD

30 was also shown to stimulate T-helper cell 1/T-helper cell 17 cell generation.

31 h reduced T-cell activation, T-helper cell 1/T-helper cell 17 differentiation, and inhibition of STAT

32 uences of inhibiting components of the IL-23/T-helper cell 17 pathway-the target of next-generation b

33 ediated by collagen type V (col(V)) specific T-helper-cell 17 (Th17) cells.

34 ration of Bryo-1 triggered a TLR-4-dependent T helper cell 2 (Th2) cytokine response and expanded a s

35 skew allergic inflammation from eosinophilic T helper cell 2 (TH2) to neutrophilic TH17 polarity.

36 Asthma is characterized by T helper cell 2 (Th2) type inflammation, leading to airw

37 potent regulator of immunity through its pro-T helper cell 2 activity.

38 dermatitis-like disease that is dependent on T helper cell 2 cytokines and is associated with high se

39 (0/0) mice, which was because of an impaired T helper cell 2 polarization.

40 ve T cells was diminished while displaying a T helper cell 2-biased phenotype.

41 inophilic inflammation, serum IgE level, and T helper cell 2/T helper cell 17 cytokine response.

42 However, conversely, the T-helper cell 2 bias that characterizes immune responses

43 ed antigen for the intrarenal stimulation of T helper cells, a function important for glomerulonephri

44 s undergo rapid reprogramming into activated T helper cells after vaccination with antigen plus Toll-

45 tient displayed increased TH1 and follicular T helper cell and suppressed TH17 cell responses.

46 We enumerated subsets of CD4(+) T helper cells and assessed cytokine production and tran

47 ory cytokine that is produced by specialized T helper cells and contributes to the development of sev

48 essed DC antigen-presenting cell function to T helper cells and DC calcium mobilization and chemotaxi

49 comparison of TCRs from conventional memory T helper cells and mTregs isolated from skin revealed li

50 ells including plasmacytoid dendritic cells, T helper cells and plasma cells, and also autoantibody p

51 few years examining the epigenetic states in T helper cells and the mechanisms by which they are esta

52 the upregulation of type 2 anti-inflammatory T helper cells and the suppression of type 1 T helper ce

53 induced expression of FcgammaRIIIa on CD4(+) T helper cells and their ability to co-stimulate T-cell

54 acrophages, and efficiently activated CD4(+) T-helper cells and CD8(+) cytotoxic T lymphocyte cells.

55 ally, antibiotic pretreatment reduced CD4(+) T-helper cells and Ifngamma transcript levels in gastric

56 ralisation assays and circulating follicular T-helper cells and plasmablast cells were measured in se

57 uire interactions between B cells and CD4(+) T helper cells, and it is now well recognized that T fol

58 yl transferase PRMT-1 is highly expressed in T helper cells, and ligation of the T cell antigen and c

59 haracterized by infiltration of eosinophils, T helper cells, and mast cells.

60 ation of germinal center B cells, follicular T helper cells, and RABV-specific antibodies.

61 imulated DCs were cocultured with autologous T-helper cells, and concentrations of T-helper (Th) 1-,

62 over time exclusively on cytotoxic T cells, T-helper cells, and regulatory T cells.

63 IL-4-responsive T helper cells are dispensable for acute OVA-induced air

64 Thus, CD4(+) T helper cells are not required for robust CD8(+) T cell

65 production and improved proliferation of CD4 T helper cells are restricted to viremic individuals.

66 CD4(+) T helper cells are well known for their role in providin

67 The most recently defined subset of T-helper cells are termed Th9 and are identified by the

68 levance of directing antigen-specific CD4(+) T helper cells as part of effective anticancer immunothe

69 T-helper cell-associated transcripts at the terminal rec

70 tigated the expression profiles of T-reg and T-helper-cell-associated genes and their response to glu

71 As with T helper cells, B cells can be classified into subsets a

72 As such, dendritic cells, T helper cells, B cells, and plasma cells all contribute

73 a novel endotyping approach purely based on T helper cell biomarkers has been developed and has show

74 that regulates the differentiation of naive T helper cells but also possesses anti-inflammatory prop

75 Previous studies have shown that T helper cells but not cytotoxic T cells are critical fo

76 AT3 was required for RORgammat expression in T helper cells, but not in ILC3s.

77 e we show that these CD4(+)CD44(hi)CD62L(lo) T helper cells by gene expression are a distinct T-cell

78 Activation of T helper cells by MHC-II on Schwann cells thus promotes

79 Foxp3(+) CD4(+) T helper cells called regulatory T (T reg) cells play a

80 IRF4 function in T helper cells can be modulated by its interaction with

81 cytokine, increasing evidence suggests that T helper cells can produce IL-22 even without IL-17 expr

82 Frequency of CD4+T helper cells (CD4+Th) secreting interferon (IFN)-gamma

83 dependent signaling pathways, initiating CD4 T helper cell clonal expansion and differentiation.

84 CD4(+) T helper cells control the migration of CTL indirectly t

85 ales abundance was predictive of higher host T-helper cell counts, suggesting an important link betwe

86 t3a, but not Dnmt3b, regulated expression of T helper cell cytokine genes, with the Il13 gene most pr

87 ting in the generation of high levels of CD4 T-helper cell cytokines or increased migration of cytoly

88 immunity in fish, through downregulation of T-helper cell cytokines, antigen presentation machinery,

89 is, three distinct T-cell populations-CD4(+) T helper cells, cytotoxic CD8(+) T cells, and gammadelta

90 lls, which is associated with an increase in T-helper cells, cytotoxic T cells, T-cell functional res

91 r with CD4(+) T cells, which also eliminated T helper cell-dependent Ab responses, restored vv-VCPko

92 with a specific emphasis on the promotion of T helper cell-dependent inflammation through direct TLR

93 and lineage-specific gene expression during T helper cell development is well documented.

94 A novel role for BCL6 in follicular T helper cell development was recently uncovered.

95 of these loci at two distinct stages in CD4+ T helper cell development.

96 he resolution of some longstanding issues in T helper cell development.

97 Long noncoding RNAs play a pivotal role in T-helper cell development but little is known about thei

98 Naive T helper cells differentiate into functionally distinct

99 During infection, naive CD4(+) T helper cells differentiate into specialized effector s

100 T helper cell differentiation and activation require spe

101 found that activation of glycolysis supports T helper cell differentiation by controlling acetyl-coA

102 f the mechanisms by which cytokines regulate T helper cell differentiation decisions is increasingly

103 3 transcription factor signaling in specific T helper cell differentiation has been well described, a

104 ce display decreased cytokine production and T helper cell differentiation in vitro, which we confirm

105 In the periphery, T helper cell differentiation is a key event orchestrati

106 T helper cell differentiation is controlled by a network

107 ytokine expression during the early phase of T helper cell differentiation is significantly larger th

108 T helper cell differentiation occurs in the context of t

109 utilizes to negatively regulate alternative T helper cell differentiation pathways such as the Th2 a

110 However, its role in regulating T helper cell differentiation remains unknown.

111 pecific B cell subclasses, and deviates CD4+ T helper cell differentiation toward IL-17-producing T h

112 The effect of glucosamine on T helper cell differentiation was similar to that induce

113 hypertension by favorably modulating CD4(+) T helper cell differentiation.

114 rved decreased expression of p38alpha during T helper cell differentiation.

115 es of IL-2 in broadly modulating T cells for T helper cell differentiation.

116 ework for understanding complexity of CD4(+) T helper cell differentiation.

117 cell receptor (TCR) signaling and modulates T helper cell differentiation.

118 and AhR in IDO regulation and its effect on T helper cell differentiation.

119 (+) T cells and influences IL-2 response and T helper cell differentiation.

120 family transcription factors regulate CD4(+) T helper cell differentiation.

121 ine-secreting potential, in a process termed T-helper cell differentiation, is a response to multiple

122 c changes in the expression of ERK1/2 during T-helper cell differentiation.

123 ncluding T-cell activation and tolerance and T-helper cell differentiation.

124 NIP45-deficient T helper cells displayed profound defects in the express

125 late their p27 protein levels, and propose a T helper cell exhaustion model resembling that of stem c

126 an increase in T regulatory (Treg) cells and T helper cells expressing PD-1 and CTLA4.

127 antagonize the gene programs for alternative T helper cell fates.

128 ved that the preservation of CXCR5(+) CD4(+) T helper cell frequencies and activation status of B cel

129 Type 1 T helper cells from hosts with accepted and rejected gra

130 Activated T-helper cells from the HHV-8-negative variant carriers

131 on has been associated with a loss of CD4(+) T helper cell function and with the accumulation of aner

132 that lack CD4 expression despite maintaining T helper cell functionalities.

133 IL-10 is needed for T-helper cell functions, T-cell immune surveillance, and

134 in lipid rafts affects antigen-specific CD4 T-helper cell functions.

135 th mild AD, particularly if they have memory T-helper cells generated after immunizations with conven

136 s to our understanding of the flexibility of T helper cell genetic programs.

137 tion concerning the analysis of an augmented T-helper cell GRN is provided.

138 role of adaptive immunity, especially CD4(+) T-helper cells, has not yet been systematically investig

139 s CD4 T cell responses while maintaining CD4 T helper cell identity.

140 fection on the development of their adaptive T helper cell immune response has not been addressed.

141 activated by IL-4 plays an important role in T helper cell immunity and B cell responses.

142 and for the pathogenicity of IL-17 producing T helper cells in autoimmunity.

143 interleukin (IL)-17+CD4(+)alpha/beta+ (Th17) T helper cells in lungs.

144 lleled by an increased number of resting CD4 T helper cells in periphery.

145 nd undergo clonal expansion is controlled by T helper cells in the GC LZ, which discern between LZ B

146 -4 receptor alpha (IL-4Ralpha) expression on T helper cells in these responses.

147 T-helper cells in GC have been shown to have a central r

148 Increased numbers of T-lymphocytic cells and T-helper cells in the junctional epithelium of SPF mice

149 Two years ago, T helper cells, including Th1, Th2 and Th17 cells, were

150 ese results demonstrate that differentiating T helper cells integrate multiple STAT protein signals d

151 une responses rely on differentiation of CD4 T helper cells into subsets with distinct effector funct

152 In CD4(+) T helper cells, IRF4 plays an essential role in the regu

153 trated that reduction of Pparg expression in T-helper cells is critical for spontaneous SLE-like auto

154 Here, we report that type 1 T helper cell-like effector cells that arose in tumor-be

155 d information about how the co-expression of T helper cell lineage-defining transcription factors imp

156 proteases, and cytokines capable of driving T-helper cell lineage polarization without evidence of c

157 Wei et al. each investigate the stability of T helper cell lineages and find that commitment to these

158 This review discusses the T helper cell lineages pertinent to transplantation and

159 Simulations showed that a T helper cell mediated antibody and neutrophil response

160 Regulatory T cells (Tregs) control type 2 T helper cell-mediated (Th2-mediated) lung inflammation,

161 lammasome played a critical role in inducing T-helper cell migration into the CNS.

162 eas NIP45 deficiency does not interfere with T helper cell NFAT activation or lineage-specific transc

163 on on B cells coincided with an autoreactive T helper cell phenotype in MS patients.

164 type cytokine produced by the Th17 subset of T-helper cells, plays a role in inflammatory responses,

165 ne the effect of increased STAT1 activity on T helper cell polarization and to investigate the therap

166 ts an anti-inflammatory potency by directing T helper cell polarization via targeting the IL-6 pathwa

167 gulate IL-12p70 production by DCs, affecting T helper cell polarization.

168 , IL-1 induced IL-22 production from a mixed T helper cell population comprised of Th1, Th17, and Th2

169 tudy of HIV progression and for defining the T helper cell population in immunological applications.

170 A recently described T-helper cell population, known as Th-17, has been impli

171 rying degrees of plasticity between effector T helper cell populations.

172 -specific transcription factors for distinct T-helper cell populations, we focus on signal transducer

173 Pip4k2c(-/-) mice had an increase in T-helper-cell populations and a decrease in regulatory T

174 mice with disrupted DC ITAMs show defective T helper cell priming in vivo and are protected from exp

175 We propose a novel mechanism for control of T helper cell priming.

176 o induce the expansion of Th17 cells (CD4(+) T helper cells producing IL-17).

177 of myeloid cells, required for induction of T-helper cells producing interleukin-17 (Th17 cells) and

178 ts the germinal-centre B cell and follicular T-helper cell programs.

179 etransplant limiting dilution assay revealed T helper cells recognizing both donor and third-party pe

180 T cells, but B cell-deficient muMT mice and T helper cell-reconstituted Rag-1-deficient mice were co

181 CD4(+) T-helper cells regulate immunity and inflammation throug

182 nd had increased circulating IL-17 producing T helper cells-related cytokines.

183 mote acquisition of the virus because CD4(+) T helper cells, required for an effective immune respons

184 The activation of T helper cells requires antigens to be exposed on the su

185 T helper cell rerouting in EAE was dependent on IL-4, wh

186 ated with C. parapsilosis displayed a skewed T-helper cell response, producing more interleukin 10 an

187 tage malaria and interfere with conventional T helper cell responses and follicular T helper (TFH)-B

188 ng of HC/C2 mixture substantially suppressed T helper cell responses and inhibitor formation against

189 hat modified Foxp3 mRNA rebalanced pulmonary T helper cell responses and protected from allergen-indu

190 ogressive fungal infectious burdens and that T helper cell responses are protective against lethal fu

191 Magnitude and functionality of T helper cell responses differ substantially in season v

192 Antigen-specific CD4(+) T helper cell responses have long been recognized to be

193 urine vaccine models have shown that induced T helper cell responses including Th17 responses have sh

194 Thus, C. albicans morphology drives distinct T helper cell responses that provide tissue-specific pro

195 g a murine skin infection model, we compared T helper cell responses to yeast and filamentous C. albi

196 I interferons, normalized TH1 and follicular T helper cell responses, improved TH17 differentiation,

197 ), a vitamin A metabolite, modulates mucosal T helper cell responses.

198 GOF mutations are the result of dysregulated T helper cell responses.

199 regulatory cytokines that are implicated in T helper cell responses.

200 t synergistically reduced spontaneous type 1 T-helper cell responses to autoantigens, ABT-induced IL-

201 d that Env engagement of the CD4 receptor on T-helper cells results in anergic effects on T-cell recr

202 T cells and their target Qa-1(+) follicular T-helper cells results in the development of a lethal sy

203 a peripheral T cell lymphopenia and unusual T helper cell skewing.

204 In CD4+ T helper cells, sodium lactate also induces a switch tow

205 TAT4 and STAT6 play wide regulatory roles in T helper cell specification.

206 SNPs distinctly enriched in the enhancers of T helper cell subpopulations, and demonstrated relevant

207 ly identified interleukin-9 (IL-9) secreting T helper cell subset are still poorly defined.

208 Sle1b.Slamf6-H1 or B6 mice, contain a memory T-helper cell subset identified by ]mt]2-fold increase i

209 dendritic cells as well as newly identified T helper cell subsets such as Th17 and Th22 cells.

210 ctor cytokines that in variety match that of T helper cell subsets.

211 Interleukin-22 is produced by certain T helper cells subsets (Th17, Th22) and at lower levels

212 We characterized T-helper cell subsets in the peripheral blood of childre

213 T-helper cell subtype specific cytokines and transcripti

214 ntially induce differentiation of follicular T helper cells (T(FH) cells) in vitro.

215 Follicular T helper cells (T(FH)) are key regulators of humoral imm

216 cing CD4 T cells (T(H)17) and follicular CD4 T helper cells (T(FH)), has been implicated in autoimmun

217 Interleukin (IL)-17-producing T helper cells (T(H)17) are a recently identified CD4(+)

218 Interleukin (IL)-17-producing T helper cells (T(H)17) are a recently identified subset

219 nctional potential of FL-infiltrating CD4(+) T-helper cells (T(H)) compared with reactive and normal

220 antigen-stimulated activation of follicular T helper cells (TFH cells), coupled with heightened form

221 on the function of CD4(+)CXCR5(+) follicular T helper cells (Tfh).

222 and other lymphomas derived from follicular T-helper cells (TFH) represent a large proportion of per

223 T cells expressing T helper cell (Th) 2 cytokines are critical for experime

224 TSLPR(-/-) mice also lost T helper cell (Th) 2-mediated inflammation in the jejunu

225 atarrhalis and H. influenzae induced a mixed T helper cell (Th) type 1/Th2/Th17 response with high le

226 ch is shedding new light on the role of both T helper cell (Th)1 and Th17 responses in the pathogenes

227 tant for the differentiation of naive CD4(+) T helper cells (Th cells) into the Th1 phenotype.

228 Memory T helper cells (Th cells) play an important role in host

229 T regulatory cells (Treg cells) and effector T helper cells (Th cells), and recently identified innat

230 thers have described miR-155 upregulation in T helper cells (Th) during the development of experiment

231 hn's disease, the major cytokines arise from T-helper cell (Th) 1 and Th17 CD4(+) T-cell differentiat

232 uppression with cyclosporin after SCT limits T-helper cell (Th) 1 differentiation and interferon-gamm

233 , monocyte-derived dendritic cells (DCs) and T-helper cell (Th) subsets, but its role in liver diseas

234 CD69-expressing T cells, and the release of T-helper cell (TH)-1 cytokines.

235 of SIDS increased CNS antigen-specific Type1 T helper cell (Th1) responses in the brains of 2D2 mice

236 /-) dendritic cells to T cells in vitro were T helper cell (Th1)-polarized relative to presentation b

237 mportant regulator of IL-17-producing CD4(+) T helper cells (Th17) cell proliferation.

238 l cytokines to induce IL-17-producing CD4(+) T helper cells (TH17); yet their signalling network rema

239 trated that PKC lambda/iota is necessary for T-helper cell (Th2) cytokine production and optimal T-ce

240 Classical IL-22-producing T helper cells (Th22 cells) mediate inflammatory respons

241 These results suggest that CD4(+) T helper cells that are important in maintaining mucosal

242 7 cells are recognized as a unique subset of T helper cells that have critical roles in the pathogene

243 ar helper (Tfh) cells are a subset of CD4(+) T helper cells that migrate into germinal centers and pr

244 ufficient to induce the appearance of CD4(+) T helper cells that produce IL-17 and IL-22 (Th17 cells)

245 Th17 cells are a distinct lineage of T helper cells that protect the body from bacterial and

246 lper T (Tfh) cells are the class of effector T helper cells that regulates the step-wise development

247 Th17 cells represent a subset of CD4+ T helper cells that secrete the proinflammatory cytokine

248 expressed CD103 (alphaE integrin), and CD4+ T helper cells that were predominately type 1.

249 T-helper cells that produce interleukin-17 (T(H)17 cells

250 CD4(+) T-helper cells that selectively produce interleukin (IL)

251 SLAT expression regulates the development of T helper cells through Cdc42- and Rac1-mediated activati

252 affects tumor surveillance by depleting CD4+ T helper cells through lipotoxic mechanisms associated w

253 V-1, but facilitate infection of co-cultured T-helper cells through a process of trans-enhancement.

254 CD4(+) T-helper cells (THs) dominate the classical Hodgkin lymp

255 ficiency virus is its ability to infect CD4+ T helper cells, thus impairing helper cell responses and

256 pecific mechanisms are activated in tolerant T helper cells to directly repress expression of effecto

257 the abilities of peripheral CXCR5(+) CD4(+) T helper cells to induce antibody secretion by autologou

258 in Th17 cytokines or RORgammat, but diverted T helper cell trafficking to the gut, which improved EAE

259 ckout mice and was associated with augmented T helper cell type 1 (Th1) but not Th17 immunity.

260 es upon heterologous challenge, particularly T helper cell type 1 polarizing and typically monocyte-d

261 P were hyperkeratosis, hypergranulosis, mild T helper cell type 1-dominant lymphocytic inflammation,

262 SLP, a cytokine known to promote and amplify T helper cell type 2 (Th2) immune responses, was also in

263 of antibodies (Abs) in orchestrating crucial T helper cell type 2 (Th2) protective immune responses t

264 the ability to suppress lymphadenopathy and T helper cell type 2 activation.

265 We document that T helper cell type 2 cytokine-conditioned murine macroph

266 Here, we demonstrate that T helper cell type 2 cytokines and, in particular, IL-4

267 te to host defense as components of adaptive T helper cell type 2 immune responses to helminths, tick

268 rogramming driving their conversion from one T helper cell type to another, a process known as transd

269 eta leads to increased colonic expression of T helper cell type-2 cytokines and IL-17, associated wit

270 tant to herpes SK with marked suppression of T helper cells type 1 and 17 responses both in the ocula

271 nabled the direct test of Treg regulation of T-helper cell type 1 (Th1) differentiation.

272 ent role in mediating interleukin-12-induced T-helper cell type 1 lineage differentiation.

273 lin and mucin domain 3, which down-regulates T-helper cell type 1 proinflammatory responses and is as

274 ; increased neutrophil counts; and decreased T-helper cell type 1 responses.

275 mentous bacteria (SFB), in inducing a robust T-helper cell type 17 (Th17) population in the small-int

276 IL-25 (IL-17E) is a T-helper cell type 2 (Th2) cytokine best described as a

277 T-helper cell type 2 (Th2) cytokines were measured in ce

278 subtypes associated with high expression of T-helper cell type 2 cytokines and lack of corticosteroi

279 significantly increased induction of airway T-helper cell type 2 responses.

280 it the most from specific agents that target T-helper cell type 2-mediated inflammation and/or cortic

281 lopment of anaphylaxis or heightened recall, T-helper cell type 2-skewed responses to postnatal encou

282 valence, which results from an inappropriate T helper cell, type 2 (Th2) response to pollen.

283 rthermore, Che(-) mutant infections lack the T-helper cell, type 17 (Th17) component of the immune re

284 n accordance with previous observations that T-helper cell, type 17 responses in Citrobacter rodentiu

285 polarization of the immune response into the T helper cell types 2 and 17 and can be a clue to develo

286 s differentiate into phenotypically distinct T helper cells upon antigenic stimulation.

287 severely diminished, and the development of T helper cells was impaired.

288 es of germinal center B cells and follicular T helper cells were also readily detectable in the drain

289 y 10-fold fewer coronary artery-infiltrating T helper cells were IL-17 producers than IFN-gamma produ

290 The total T-lymphocytes and T-helper cells were significantly reduced, while T-cytot

291 Intermediate PD-1(+) cells, such as T helper cells, were dispensable for suppression.

292 IgG4-RD lesions are infiltrated by T helper cells, which likely cause progressive fibrosis

293 cells, the most recently described subset of T helper cells, which play crucial roles in host immunit

294 trates unique outcomes in naive and effector T-helper cells, which may affect the proliferation, diff

295 feron, gave rise to activated polyfunctional T helper cells with high interleukin-7 receptor, rapid c

296 Thus, T helper cells with specificity for an antigen in cardio

297 This study suggests that CD4 T helper cells with Th1/17 polarization have a preferent

298 conclusion, coactivating TAA-specific CD4(+) T-helper cells with DCs pulsed with both MHC class I and

299 family members direct the differentiation of T helper cells, with specific STAT proteins promoting di

300 Ns can be actively reprogrammed in situ into T-helper cells, without the need for physical depletion,