ライフサイエンスコーパス: T-helper cell

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

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

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

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

5 1 as crucial to induce IL-10 in inflammatory T helper cells.

6 ng a higher abundance of cytotoxic phenotype T helper cells.

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

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

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

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

11 endent cross-activation of myeloid cells and T helper cells.

12 kines involved in the polarization of CD4(+) T helper cells.

13 follicular B cells but a loss in follicular T helper cells.

14 which is necessary for the proliferation of T helper cells.

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

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

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

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

19 alpha receptor constant chain and changes in T helper cell 1, T helper cell 2, T helper cell 17, CD8+

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

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

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

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

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

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

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

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

28 16L1, IRGM), and genes in the interleukin-23-T helper cell 17 pathway indicate the important roles of

29 changes in T helper cell 1, T helper cell 2, T helper cell 17, CD8+ effector, CD4+ memory, and regula

30 l models, dry eye disease is associated with T helper cell 17-mediated inflammation of the ocular sur

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

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

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

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

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

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

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

38 (0/0) mice, which was because of an impaired T helper cell 2 polarization.

39 nstant chain and changes in T helper cell 1, T helper cell 2, T helper cell 17, CD8+ effector, CD4+ m

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 mpanies atherosclerosis, autoreactive CD4(+) T-helper cells accumulate in the atherosclerotic plaque.

45 esponse are significantly impacted by CD4(+) T helper cell activity.

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

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

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

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

50 d TT-specific, CD40 ligand-expressing CD4(+) T helper cells and maturation of antigen-presenting cell

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

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

53 Interactions between T helper cells and the complement system promote loss of

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

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

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

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

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

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

60 ediated by DNA threads released by activated T helper cells, and identify a potential therapeutic tar

61 epitopes that elicit CD8(+) T cells, CD4(+) T helper cells, and IgG2b antibodies, and (ii) adjuvant

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

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

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

65 nction, PI3K in B lymphocytes, iCOS-iCOSL in T helper cells, and the role of NFAT in regulating the i

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

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

68 entiation and terminal effector functions of T helper cells are biochemically uncoupled.

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

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

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

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

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

74 esponse was predominantly mediated by type-1 T helper cells, as demonstrated by the profiling of the

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

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

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

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

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

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

81 ted with an increase in proliferating CD4(+) T-helper cells but not with an increase in T-regulatory

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

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

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

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

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

87 eased splenic CD3+ T cells, specifically CD4+T helper cells, compared to splenocytes from non-irradia

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

89 ptor homologous molecule expressed on type 2 T-helper cells (Crth2).

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

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

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

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

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

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

96 upon subsequent stimulation with the CD4(+) T helper cell-derived factor CD40L.

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

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

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

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

101 B-cell reconstitution and reduced follicular T helper cell development.

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

103 Naive T helper cells differentiate into functionally distinct

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

105 T helper cell differentiation and activation require spe

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

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

108 3 transcription factor signaling in specific T helper cell differentiation has been well described, a

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

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

111 T helper cell differentiation occurs in the context of t

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

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

114 T helper cell differentiation requires lineage-defining

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

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

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 eacetylates NFkappaB-p65 at K310 to modulate T helper cell differentiation.

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

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

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

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

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

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

127 B cell epitopes, impedes the presentation of T helper cell epitopes, and attracts mannose binding pro

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

143 oduction, and nomenclature parallel those of T helper cells, ILCs do not require adaptive immune prog

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

145 uced signaling to the promotion of effective T helper cell immune responses, during both anti-fungal

146 T helper cells import the amino acid methionine to synth

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

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

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

150 ellular immune response of type-1 and type-2 T helper cells in rhesus macaques.

151 -4 receptor alpha (IL-4Ralpha) expression on T helper cells in these responses.

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

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

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

155 ranscriptional characteristics of follicular T helper cells increasingly shaped the circulating HCV-s

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

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

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

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

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

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

162 We analyzed expression levels of T helper cell-mediated (TH2) chemokines CCL18, CCL17, an

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

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

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

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

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

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

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

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

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

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

176 ) ) mouse leads to a shift of the follicular T helper cell program from follicular T helper (Tfh)-IL-

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

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

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

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

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

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

183 We demonstrate that the CoV-2-specific CD4+ T helper cell response is directed against all 3 protein

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

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

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

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

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

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

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

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

192 Analysis of CD4(+) T helper cell responses revealed that co-administration

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

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

195 T(H)2 cell and, especially, IL-17-producing T helper cell responses, and promoting memory T cell dif

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

197 s associated with decreased antigen-specific T helper cell responses.

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

199 GOF mutations are the result of dysregulated 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 Increased expression of the type 2 T helper cell signature correlated with poorer survival

203 HCV-specific CD4+ T cells with a follicular T helper cell signature that is maintained after therapy

204 n of select signatures, including the type 2 T helper cell signature, was increased in CIMP RCC.

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

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

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

208 arning algorithms, we identified an expanded T helper cell subset in patients with MS, characterized

209 ow that a new interleukin (IL)-13-expressing T helper cell subset specifically promotes high-affinity

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

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

212 est discriminate among immune cell types and T helper cell subsets using RNA-seq datasets.

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

214 different types of immune cell and for five T helper cell subsets.

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

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

217 T-helper cell subtype specific cytokines and transcripti

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

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

220 s exhibiting significantly higher follicular T helper cell (Tfh) and germinal center B cell frequenci

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

236 spond to tissue wounding by producing type 2 T helper cell (Th2) cytokines in mice.

237 rtant mediator for the development of type 2 T-helper cell (Th2)-driven inflammatory disorders and ha

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

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

240 er they affect adaptive immune cells such as T helper cells that express IL-17a (T(H)17 cells) or reg

241 7 cells are recognized as a unique subset of T helper cells that have critical roles in the pathogene

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

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

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

245 ng CD4(+) (Th9) cells are a subset of CD4(+) T-helper cells that are endowed with powerful antitumor

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

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

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

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

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

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

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

253 FN-gamma transcripts and the number of CD4 + T-helper cells transcribing this gene were elevated (P <

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

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

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

257 s that leads to the development of a chronic T helper cell type 1-polarized systemic immune response

258 of T(H)1, T helper cell type 2 (T(H)2), and T helper cell type 17 (T(H)17), and of follicular-helper

259 We test our methods in the context of T Helper Cell Type 17 (Th17) differentiation, generating

260 and anti-inflammatory transcripts of T(H)1, T helper cell type 2 (T(H)2), and T helper cell type 17

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

262 is strain failed to induce the nonprotective T helper cell type 2 (Th2) responses characteristic of w

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

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

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

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

267 with a high dose of T. muris that induces a T helper cell type 2-polarized immune response did not a

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 T cells in vivo, limits the accumulation of T helper cells type 1, and reduces the development of at

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 es enriched for TLR (Toll-like receptor) and T-helper cell type 17 (Th17) signaling and endoplasmic r

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

278 There was no reciprocal increase of T-helper cell type 2 (Th2) cytokine genes or the Th2 che

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

280 er IFN-gamma-type response than RV-A without T-helper cell type 2 (Th2) upregulation.

281 HGF [hepatocyte growth factor]) coupled with T-helper cell type 2 and natural killer cell signaling i

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

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

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

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

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

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

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

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

290 e expression, and HIF promoted glycolysis in T helper cells via TCR or cytokine stimulation, as well

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

292 creased, and conversion of T(reg) cells into T helper cells was increased by AMD3100 treatment.

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

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

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

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

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

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

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

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