ライフサイエンスコーパス: helper cell

1 ssion of Cxcr4 on B6.SJL-CD45.1 T follicular helper cells.

2 ollicular B cells but a loss in follicular T helper cells.

3 hich is necessary for the proliferation of T helper cells.

4 irs the development of Th17 and T follicular helper cells.

5 lls and indirectly by promoting T follicular helper cells.

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

7 interaction between B cells and T follicular helper cells.

8 tment, which correlated with LN T follicular helper cells.

9 argets pre-germinal B cells and depletes Th2 helper cells.

10 dependent on interactions with T follicular helper cells.

11 e paucity of "Th1," "Th17," and T follicular helper cells.

12 ypically associated with CD4(+) T follicular helper cells.

13 ear a phenotypic resemblance to T follicular helper cells.

14 ters and CD4(+) germinal center T follicular helper cells.

15 T cells into different subsets of effector T helper cells.

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

17 led to a profound reduction of T follicular helper cells.

18 also increased the frequency of T follicular helper cells.

19 cterized by proliferation of mature CD4(+) T-helper cells.

20 GCs of lymphoid tissues called follicular T helper cells.

21 exclusively differentiate into T follicular helper cells.

22 xpansion of IFN-gamma-secreting T follicular helper cells.

23 ucosal inflammation driven by Th17 and Th1 T helper cells.

24 features of recently described T peripheral helper cells.

25 o differentiate into CD16(-)/CD25(+)/CD83(+) helper cells.

26 a higher abundance of cytotoxic phenotype T helper cells.

27 ell maturation into CXCR5+PD-1+ T follicular helper cells.

28 levels in part by inhibition of T follicular helper cells.

29 dent cross-activation of myeloid cells and T helper cells.

30 nv (gp120TM) proteins and propagated in Vero helper cells.

31 nes involved in the polarization of CD4(+) T helper cells.

32 ves them unable to regulate CD4 T follicular helper cells.

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

34 pha receptor constant chain and changes in T helper cell 1, T helper cell 2, T helper cell 17, CD8+ e

35 tion, serum IgE level, and T helper cell 2/T helper cell 17 cytokine response.

36 nces of inhibiting components of the IL-23/T-helper cell 17 pathway-the target of next-generation bio

37 anges in T helper cell 1, T helper cell 2, T helper cell 17, CD8+ effector, CD4+ memory, and regulato

38 models, dry eye disease is associated with T helper cell 17-mediated inflammation of the ocular surfa

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

40 tent regulator of immunity through its pro-T helper cell 2 activity.

41 rmatitis-like disease that is dependent on T helper cell 2 cytokines and is associated with high seru

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

43 tant chain and changes in T helper cell 1, T helper cell 2, T helper cell 17, CD8+ effector, CD4+ mem

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

45 ophilic inflammation, serum IgE level, and T helper cell 2/T helper cell 17 cytokine response.

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

47 mune checkpoint therapy induces T follicular helper cell activation of B cells to facilitate the anti

48 ponse are significantly impacted by CD4(+) T helper cell activity.

49 ent displayed increased TH1 and follicular T helper cell and suppressed TH17 cell responses.

50 ion, and failed to control both T follicular helper cell and Th1 effector cell responses.

51 ay be related to development of T follicular helper cells and antiviral inflammatory sequelae derived

52 We enumerated subsets of CD4(+) T helper cells and assessed cytokine production and transc

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

54 ncreased proportions of cytotoxic follicular helper cells and cytotoxic T helper (T(H)) cells (CD4-CT

55 sed DC antigen-presenting cell function to T helper cells and DC calcium mobilization and chemotaxis

56 d with increases in circulating T follicular helper cells and enhanced cytokine production.

57 ifferentiation signals, such as T follicular helper cells and follicular dendritic cells.

58 differentiation and function of T follicular helper cells and germinal center B cells, the two main p

59 D025 had decreased frequency of T follicular helper cells and increased frequency of T follicular reg

60 TT-specific, CD40 ligand-expressing CD4(+) T helper cells and maturation of antigen-presenting cells.

61 omparison of TCRs from conventional memory T helper cells and mTregs isolated from skin revealed litt

62 increase germinal center B and T follicular helper cells and plasma neutralizing antibodies.

63 lisation assays and circulating follicular T-helper cells and plasmablast cells were measured in seru

64 6 is critical for initiation of T follicular helper cells and production of high-affinity IgG.

65 required for the development of T follicular helper cells and T follicular regulatory (Tfr) cells tha

66 g the reduced expansion of both T follicular helper cells and Th17 cells and a compensatory increase

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

68 e upregulation of type 2 anti-inflammatory T helper cells and the suppression of type 1 T helper cell

69 duced expression of FcgammaRIIIa on CD4(+) T helper cells and their ability to co-stimulate T-cell ac

70 ween the frequency of tonsillar T follicular helper cells and tonsillar Ag-specific Ab-secreting cell

71 a DCs, coupled with reduced CD4 T follicular helper cells and transient B cell help.

72 ior to treatment suggested that T follicular helper cells and various other immune cell subsets may p

73 dendritic cells (which activate T follicular helper cells) and lymphatic sinus-associated SIGNR1(+) m

74 man germinal-centre B cells and T follicular helper cells, and antagonized the induction of phosphory

75 GS did abrogate germinal center T follicular helper cells, and blunted PE-specific germinal center B

76 ce have severely decreased GCs, T follicular helper cells, and high-affinity Abs after immunization w

77 iated by DNA threads released by activated T helper cells, and identify a potential therapeutic targe

78 pitopes that elicit CD8(+) T cells, CD4(+) T helper cells, and IgG2b antibodies, and (ii) adjuvant ac

79 r T cell populations, including T follicular helper cells, and increases germinal center B cells and

80 racterized by infiltration of eosinophils, T helper cells, and mast cells.

81 ion of germinal center B cells, follicular T helper cells, and RABV-specific antibodies.

82 ver time exclusively on cytotoxic T cells, T-helper cells, and regulatory T cells.

83 Th cells (Th1, Th2, and Th17), T follicular helper cells, and regulatory T cells.

84 tion, PI3K in B lymphocytes, iCOS-iCOSL in T helper cells, and the role of NFAT in regulating the imm

85 s comprised both memory Th1 and T follicular helper cells, and were rapidly expanded and activated af

86 tiation and terminal effector functions of T helper cells are biochemically uncoupled.

87 IL-21-stimulated T follicular helper cells are considered a critical element for GC fo

88 IL-4-responsive T helper cells are dispensable for acute OVA-induced airwa

89 es further understanding of how T follicular helper cells are regulated in health and disease.

90 cells, suggesting that the dual costimulated helper cells are themselves helped by a CD134(+) cell(s)

91 which are composed of about 65% T follicular helper cells as defined by the expression of the cell su

92 ponse was predominantly mediated by type-1 T helper cells, as demonstrated by the profiling of the Ig

93 e central memory T cells and of T follicular helper cells associated with specific antibody responses

94 he IL-23R(-/-)MRL.lpr had fewer T follicular helper cells, B cells, and plasma cells, leading to decr

95 novel endotyping approach purely based on T helper cell biomarkers has been developed and has shown

96 d with an increase in proliferating CD4(+) T-helper cells but not with an increase in T-regulatory ce

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

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

99 sed splenic CD3+ T cells, specifically CD4+T helper cells, compared to splenocytes from non-irradiate

100 uced a partial expansion of the T follicular helper cell compartment, essential for B cell memory res

101 T follicular helper cells contribute to the development of long-lasti

102 es abundance was predictive of higher host T-helper cell counts, suggesting an important link between

103 or homologous molecule expressed on type 2 T-helper cells (Crth2).

104 ng in the generation of high levels of CD4 T-helper cell cytokines or increased migration of cytolyti

105 mmunity in fish, through downregulation of T-helper cell cytokines, antigen presentation machinery, a

106 s, which is associated with an increase in T-helper cells, cytotoxic T cells, T-cell functional respo

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

108 at IFN-gamma secreted by pre-existing memory helper cells determines both isotype and specificity of

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

110 cell reconstitution and reduced follicular T helper cell development.

111 +) T cell exhaustion and CD4(+) T follicular helper cell development.

112 During infection, naive CD4(+) T helper cells differentiate into specialized effector sub

113 und that activation of glycolysis supports T helper cell differentiation by controlling acetyl-coA an

114 the mechanisms by which cytokines regulate T helper cell differentiation decisions is increasingly im

115 ICOS stimulates T follicular helper cell differentiation in lymphoid tissue, suggesti

116 factor-dependent T follicular regulatory and helper cell differentiation in the Peyer's patches.

117 T helper cell differentiation requires lineage-defining tr

118 The effect of glucosamine on T helper cell differentiation was similar to that induced

119 mily transcription factors regulate CD4(+) T helper cell differentiation.

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

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

122 ) T cells and influences IL-2 response and T helper cell differentiation.

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

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

125 od (R848) is a potential inhibitor of type 2 helper cell-driven inflammatory responses.

126 cell epitopes, impedes the presentation of T helper cell epitopes, and attracts mannose binding prote

127 germinal center formation, and T follicular helper cells, especially when the load of the antigen is

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

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

130 of the core regulatory network governing Th2 helper cell fates.

131 promoted the differentiation of T follicular helper cells followed by an enhanced germinal center res

132 increase in T cell activation and follicular helper cells for the following months; and a progressive

133 d that the preservation of CXCR5(+) CD4(+) T helper cell frequencies and activation status of B cells

134 e of significantly increased LN T follicular helper cell frequencies and LN follicles.

135 enic germinal center B-cell and T-follicular helper cell frequencies that collaborate to produce anti

136 Type 1 T helper cells from hosts with accepted and rejected graft

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

138 has been associated with a loss of CD4(+) T helper cell function and with the accumulation of anergi

139 all these factors come together to influence helper cell function.

140 at lack CD4 expression despite maintaining T helper cell functionalities.

141 Germinal center T follicular helper cells (GCTfh) in lymphatic tissue are critical fo

142 ling-selective variants reduced T follicular helper cells, germinal center formation, immunoglobulin,

143 on concerning the analysis of an augmented T-helper cell GRN is provided.

144 Additionally, gp130-deficient T follicular helper cells had lower expression of Maf, IL-21, and ICO

145 oduced mainly by Th17 cells and T follicular helper cells, has been intensively investigated in B cel

146 CD4 T cell responses while maintaining CD4 T helper cell identity.

147 uction, and nomenclature parallel those of T helper cells, ILCs do not require adaptive immune progra

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

149 ed signaling to the promotion of effective T helper cell immune responses, during both anti-fungal ho

150 As such, T follicular helper cells impact immunodeficiencies, autoimmunity, an

151 T helper cells import the amino acid methionine to synthes

152 o A. muciniphila are limited to T follicular helper cells in a gnotobiotic setting, without appreciab

153 ly expand alloreactive IL-18R1+ T peripheral helper cells in allograft tissues to promote donor-speci

154 olific innate killers, NK cells are also key helper cells in antiviral defense, influencing adaptive

155 T-helper cells in GC have been shown to have a central rol

156 vidence concerning the roles of T follicular helper cells in regulating pathogenic GC and autoreactiv

157 lular immune response of type-1 and type-2 T helper cells in rhesus macaques.

158 creased numbers of T-lymphocytic cells and T-helper cells in the junctional epithelium of SPF mice co

159 accumulation of CXCR3(+)CD4(+) T follicular helper cells in the spleen and enhanced Ab responses to

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

161 fferences between TPH cells and T follicular helper cells, including altered expression of BCL6 and B

162 nscriptional characteristics of follicular T helper cells increasingly shaped the circulating HCV-spe

163 center (GC) reaction, in which T follicular helper cells interact with GC B cells to produce antibod

164 ated that reduction of Pparg expression in T-helper cells is critical for spontaneous SLE-like autoim

165 urred in CD4 T cells expressing T follicular helper cell markers and inhibitory co-receptors.

166 analysis showed upregulation of T follicular helper cell markers, most notably CXCR5 and its ligand C

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

168 d memory B cells and induced by T follicular helper cell-mediated signals.

169 T follicular helper cells (odds ratio [OR] = 1.34, 95% CI 1.14-1.57;

170 trend toward reduced lymph node T follicular helper cells (P=0.06).

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

172 lper type 1 differentiation and T-follicular-helper cell polarization and increased the abundance of

173 the effect of increased STAT1 activity on T helper cell polarization and to investigate the therapeu

174 late IL-12p70 production by DCs, affecting T helper cell polarization.

175 IL-1 induced IL-22 production from a mixed T helper cell population comprised of Th1, Th17, and Th22

176 ell functions and influence the T follicular helper-cell population; this active role of B cells coul

177 pecific transcription factors for distinct T-helper cell populations, we focus on signal transducer a

178 ing degrees of plasticity between effector T helper cell populations.

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

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

181 ) mouse leads to a shift of the follicular T helper cell program from follicular T helper (Tfh)-IL-17

182 d DCs, coupled with greater CD4 T follicular helper cells, prolonged B cell activation, autoantibody

183 e analyzed the B and T peripheral follicular helper cell (pTfh) responses.

184 l subsets designated peripheral T follicular helper cells (pTfh cells) and non-pTfh cells to assess H

185 te acquisition of the virus because CD4(+) T helper cells, required for an effective immune response,

186 The activation of T helper cells requires antigens to be exposed on the surf

187 e demonstrate that the CoV-2-specific CD4+ T helper cell response is directed against all 3 proteins

188 ge malaria and interfere with conventional T helper cell responses and follicular T helper (TFH)-B ce

189 ide a baseline for optimizing HIV-1-specific helper cell responses by vaccination.

190 Magnitude and functionality of T helper cell responses differ substantially in season vs.

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

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

193 S. Typhi porins programs type I T follicular helper cell responses that contribute to the diversifica

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

195 synergistically reduced spontaneous type 1 T-helper cell responses to autoantigens, ABT-induced IL-4

196 a murine skin infection model, we compared T helper cell responses to yeast and filamentous C. albica

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

198 interferons, normalized TH1 and follicular T helper cell responses, improved TH17 differentiation, cu

199 lymph node germinal center and T follicular helper cell responses.

200 F mutations are the result of dysregulated T helper cell responses.

201 associated with decreased antigen-specific T helper cell responses.

202 that Env engagement of the CD4 receptor on T-helper cells results in anergic effects on T-cell recrui

203 tial B-cell clonal composition, T-follicular helper cell signaling, increased rounds of productive so

204 Increased expression of the type 2 T helper cell signature correlated with poorer survival in

205 CV-specific CD4+ T cells with a follicular T helper cell signature that is maintained after therapy-i

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

207 In CD4+ T helper cells, sodium lactate also induces a switch towar

208 Ps distinctly enriched in the enhancers of T helper cell subpopulations, and demonstrated relevant ce

209 ning algorithms, we identified an expanded T helper cell subset in patients with MS, characterized by

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

211 omoting disease) and a specific T follicular helper cell subset that contributes to IgG4 isotype swit

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

213 ifferent types of immune cell and for five T helper cell subsets.

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

215 T-helper cell subtype specific cytokines and transcription

216 of this effector program become T follicular helper cells, supporting development of B cells expressi

217 T follicular helper cells (T(FH) ) are crucial in T-dependent B-cell

218 d at high levels as a result of T follicular helper cell (TFH) and B cell interactions in germinal ce

219 exhibiting significantly higher follicular T helper cell (Tfh) and germinal center B cell frequencies

220 In the GC, TFR control T follicular helper cell (TFH) expansion and modulate the development

221 Germinal centres (GCs) are T follicular helper cell (Tfh)-dependent structures that form in resp

222 eady state interactions between T follicular helper cells (TfH) and B cells to limit mucosal IgA resp

223 T follicular helper cells (TFH) are critical for the development and

224 T follicular helper cells (Tfh) are critical for the longevity and qu

225 T follicular helper cells (Tfh) are crucial for the initiation and ma

226 lls to give rise to specialized T follicular helper cells (TFH) critical to initiating appropriate Ab

227 CD4(+) T follicular helper cells (TFH) in germinal centers are required for

228 T follicular helper cells (TFH) play an important role in the regulat

229 nd other lymphomas derived from follicular T-helper cells (TFH) represent a large proportion of perip

230 inin (HA) by promoting a potent T follicular helper cells (TFH) response, which directly controls the

231 ve follicles, B-cells encounter T-follicular helper cells (Tfh) that produce interleukin (IL)-21, IL-

232 d data suggest that a subset of T follicular helper cells (TFH) within germinal centers (GC) is highl

233 T follicular helper cells (Tfh), a subset of CD4+ T cells, provide re

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

235 lication is concentrated within T follicular helper cells (TFH).

236 inal centers, all attributes of T follicular helper cells (Tfh17).

237 During the past decade, T follicular helper cells (TFHs) have been characterized as the main

238 of less T-central-memory cells, T-follicular-helper cells, TGF-beta response, and CD4( +) T memory re

239 pression with cyclosporin after SCT limits T-helper cell (Th) 1 differentiation and interferon-gamma

240 regulatory cells (Treg cells) and effector T helper cells (Th cells), and recently identified innate

241 ers have described miR-155 upregulation in T helper cells (Th) during the development of experimental

242 SIDS increased CNS antigen-specific Type1 T helper cell (Th1) responses in the brains of 2D2 mice 14

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

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

245 ant mediator for the development of type 2 T-helper cell (Th2)-driven inflammatory disorders and has

246 Classical IL-22-producing T helper cells (Th22 cells) mediate inflammatory responses

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

248 they affect adaptive immune cells such as T helper cells that express IL-17a (T(H)17 cells) or regul

249 ignature associated with CD4(+) T follicular helper cells that is associated with longer progression-

250 differentiation of T cells into Th1 and Th2 helper cells that mediate cell-based and humoral immune

251 helper (Tfh) cells are a subset of CD4(+) T helper cells that migrate into germinal centers and prom

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

253 tor function of CXCR5(+)PD-1(+) T follicular helper cells, thereby controlling germinal center format

254 fects tumor surveillance by depleting CD4+ T helper cells through lipotoxic mechanisms associated wit

255 cific mechanisms are activated in tolerant T helper cells to directly repress expression of effector

256 he abilities of peripheral CXCR5(+) CD4(+) T helper cells to induce antibody secretion by autologous

257 Like PD-1(hi)CXCR5(+) T follicular helper cells, TPH cells induce plasma cell differentiati

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

259 -gamma transcripts and the number of CD4 + T-helper cells transcribing this gene were elevated (P < 0

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

261 upon heterologous challenge, particularly T helper cell type 1 polarizing and typically monocyte-der

262 n and mucin domain 3, which down-regulates T-helper cell type 1 proinflammatory responses and is asso

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

264 were hyperkeratosis, hypergranulosis, mild T helper cell type 1-dominant lymphocytic inflammation, pl

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

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

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

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

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

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

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

272 strain failed to induce the nonprotective T helper cell type 2 (Th2) responses characteristic of wil

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

274 he ability to suppress lymphadenopathy and T helper cell type 2 activation.

275 F [hepatocyte growth factor]) coupled with T-helper cell type 2 and natural killer cell signaling in

276 We document that T helper cell type 2 cytokine-conditioned murine macrophag

277 ubtypes associated with high expression of T-helper cell type 2 cytokines and lack of corticosteroid

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

279 to host defense as components of adaptive T helper cell type 2 immune responses to helminths, ticks,

280 ignificantly increased induction of airway T-helper cell type 2 responses.

281 the most from specific agents that target T-helper cell type 2-mediated inflammation and/or corticos

282 ith a high dose of T. muris that induces a T helper cell type 2-polarized immune response did not aff

283 pment of anaphylaxis or heightened recall, T-helper cell type 2-skewed responses to postnatal encount

284 gramming driving their conversion from one T helper cell type to another, a process known as transdif

285 a leads to increased colonic expression of T helper cell type-2 cytokines and IL-17, associated with

286 nt to herpes SK with marked suppression of T helper cells type 1 and 17 responses both in the ocular

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

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

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

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

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

292 iated with germinal centers and T follicular helper cells were examined using immunohistochemistry an

293 Signals delivered by T follicular helper cells were not required to initiate differentiati

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

295 T follicular helper cells, which also underwent expansion in infected

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

297 mory B cells and a reduction in T follicular helper cells with a phenotype suggesting recent GC activ

298 Thus, T helper cells with specificity for an antigen in cardiomy

299 This study suggests that CD4 T helper cells with Th1/17 polarization have a preferentia

300 cence confirmed the presence of T follicular helper cells within tertiary lymphoid organs.