ライフサイエンスコーパス: helper cell

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

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

3 also increased the frequency of T follicular helper cells.

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

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

6 GCs of lymphoid tissues called follicular T helper cells.

7 exclusively differentiate into T follicular helper cells.

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

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

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

11 imal expression of CCR9 and alpha4beta7 by T helper cells.

12 l immunity in mice with preexisting memory T-helper cells.

13 rapid conversion into biologically important helper cells.

14 nd functional similarities with T follicular helper cells.

15 interaction between B cells and T follicular helper cells.

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

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

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

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

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

21 ear a phenotypic resemblance to T follicular helper cells.

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

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

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

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

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

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

28 -specific T-cell clones mainly exhibited a T-helper cell 1 phenotype and recognized a broad variety o

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

30 associated with reduced T-cell activation, T-helper cell 1/T-helper cell 17 differentiation, and inhi

31 as also shown to stimulate T-helper cell 1/T-helper cell 17 cell generation.

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

33 reduced T-cell activation, T-helper cell 1/T-helper cell 17 differentiation, and inhibition of STAT3

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

35 (IFNgamma) responses and led to developing T helper cell 17/22 (Th17/Th22) responses after SHIV/malar

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

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

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

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

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

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

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

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

44 turn activated NKT cells, as well as natural helper cells, a newly described non-T, non-B, innate lym

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

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

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

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

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

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

51 , T(H)2, T(H)9, T(H)17, T(H)22, T follicular helper cells and different subsets of regulatory T cells

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

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

54 ly, antibiotic pretreatment reduced CD4(+) T-helper cells and Ifngamma transcript levels in gastric t

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

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

57 ls including plasmacytoid dendritic cells, T helper cells and plasma cells, and also autoantibody pro

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

59 6 is critical for initiation of T follicular helper cells and production of high-affinity IgG.

60 This effect was independent of T follicular helper cells and resulted in a loss of plasma cells gene

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

62 ay of helper subtypes including T follicular helper cells and Th17 cells.

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

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

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

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

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

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

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

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

71 atural helper cells, nuocytes, innate type 2 helper cells, and multipotent progenitor type 2 (MPP(typ

72 IL-2 and IL-21 were produced by T follicular helper cells, and neutralizing both cytokines abolished

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

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

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

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

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

78 ntly, we demonstrated that T extrafollicular helper cells are dependent on IL-21R for their generatio

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

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

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

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

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

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

85 vance of directing antigen-specific CD4(+) T helper cells as part of effective anticancer immunothera

86 phytic generation." Different populations of helper cells assist in this transgenerational journey, w

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

88 T-helper cell-associated transcripts at the terminal rectu

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

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

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

92 Previous studies have shown that T helper cells but not cytotoxic T cells are critical for

93 3 was required for RORgammat expression in T helper cells, but not in ILC3s.

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

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

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

97 From this perspective, helper cells can be viewed as pluripotent precursors tha

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

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

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

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

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

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

104 th a specific emphasis on the promotion of T helper cell-dependent inflammation through direct TLR si

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

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

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

108 demonstrate increased Th17 and T follicular helper cell development, early onset experimental autoim

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

110 Naive T helper cells differentiate into functionally distinct ef

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

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

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

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

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

116 display decreased cytokine production and T helper cell differentiation in vitro, which we confirmed

117 okine expression during the early phase of T helper cell differentiation is significantly larger than

118 tilizes to negatively regulate alternative T helper cell differentiation pathways such as the Th2 and

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

120 Although there are aspects of helper cell differentiation that can be modeled as a cla

121 cific B cell subclasses, and deviates CD4+ T helper cell differentiation toward IL-17-producing T hel

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

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

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

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

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

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

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

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

130 ferentiation and maintenance of T follicular helper cells during viral infection.

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

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

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

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

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

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

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

138 th their wild type equivalents, T follicular helper cells from PTPN22 KO mice proliferate and accumul

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

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

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

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

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

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

145 mild AD, particularly if they have memory T-helper cells generated after immunizations with conventi

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

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

148 In lymph nodes and tonsils, T-follicular helper cells have been identified as the T cells subset

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

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

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

152 d for the pathogenicity of IL-17 producing T helper cells in autoimmunity.

153 loser examination of the role of NK cells as helper cells in enhancing antitumor responses will revea

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

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

156 XCR5, markers characteristic of T follicular helper cells in the lymph nodes.

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

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

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

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

161 information about how the co-expression of T helper cell lineage-defining transcription factors impac

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

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

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

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

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

167 mmasome played a critical role in inducing T-helper cell migration into the CNS.

168 type 2 innate lymphoid cells (ILCs) (natural helper cells, nuocytes), T-helper (Th)2 lymphocytes, mas

169 roup-2 innate lymphoid cells (ILC2s, natural helper cells, nuocytes), the major producers of IL-5 and

170 four innate cell populations, named natural helper cells, nuocytes, innate type 2 helper cells, and

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

172 d cells (ILC2s; also called nuocytes, innate helper cells, or natural helper cells) provide protectiv

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

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

175 an anti-inflammatory potency by directing T helper cell polarization via targeting the IL-6 pathway.

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

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

178 dy of HIV progression and for defining the T helper cell population in immunological applications.

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

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

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

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

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

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

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

186 Circulating T-follicular helper cells promote plasma cell differentiation and hav

187 ed nuocytes, innate helper cells, or natural helper cells) provide protective immunity during helmint

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

189 CD4(+) T-helper cells regulate immunity and inflammation through

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

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

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

193 T helper cell rerouting in EAE was dependent on IL-4, whic

194 ed with C. parapsilosis displayed a skewed T-helper cell response, producing more interleukin 10 and

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

196 of HC/C2 mixture substantially suppressed T helper cell responses and inhibitor formation against FV

197 t modified Foxp3 mRNA rebalanced pulmonary T helper cell responses and protected from allergen-induce

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

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

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

201 ine vaccine models have shown that induced T helper cell responses including Th17 responses have show

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

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

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

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

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

207 d germinal center reaction, and T follicular helper cell responses.

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

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

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

211 d to effectively regulate these T follicular helper cells, resulting in an increase in B cell numbers

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

213 peripheral T cell lymphopenia and unusual T helper cell skewing.

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

215 nd metabolic alterations, that contribute to helper cell specificity and plasticity.

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

217 at contribute to the differentiation of this helper cell subset are incompletely understood, although

218 e1b.Slamf6-H1 or B6 mice, contain a memory T-helper cell subset identified by ]mt]2-fold increase in

219 We characterized T-helper cell subsets in the peripheral blood of children

220 To what extent different helper cell subsets maintain their characteristic gene e

221 endritic cells as well as newly identified T helper cell subsets such as Th17 and Th22 cells.

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

223 T-helper cell subtype specific cytokines and transcription

224 redominated over CD4-positive T lymphocytes (helper cells) surrounding the necrobiotic foci and were

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

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

227 The T follicular helper cell (Tfh) subset of CD4 T cells provides B cell

228 T follicular helper cells (Tfh cells) play a pivotal role in germinal

229 ntigen-stimulated activation of follicular T helper cells (TFH cells), coupled with heightened format

230 how here that the proportion of T follicular helper cells (Tfh) and production of high-affinity antib

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

232 CD4(+) T follicular helper cells (TFH) are critical for the formation and fu

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

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

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

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

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

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

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

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

241 CD4 T cell differentiation into T follicular helper cells (Tfh).

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

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

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

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

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

247 arrhalis and H. influenzae induced a mixed T helper cell (Th) type 1/Th2/Th17 response with high leve

248 D69-expressing T cells, and the release of T-helper cell (TH)-1 cytokines.

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

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

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

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

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

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

255 ackbone (RV-WN/TBE) grew more efficiently in helper cells than candidates based on Langat E5, TBE, an

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

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

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

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

260 CD4(+) T-helper cells (THs) dominate the classical Hodgkin lympho

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

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

263 ation by DC, suggesting that NK cells act as helper cells to prime or reactivate tumor-specific T cel

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

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

266 factors are considered as they relate to the helper cell transcriptome and epigenome.

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

268 t role in mediating interleukin-12-induced T-helper cell type 1 lineage differentiation.

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

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

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

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

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

274 P, a cytokine known to promote and amplify T helper cell type 2 (Th2) immune responses, was also incr

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

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

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

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

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

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

287 larization of the immune response into the T helper cell types 2 and 17 and can be a clue to develop

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

289 everely diminished, and the development of T helper cells was impaired.

290 of germinal center B cells and follicular T helper cells were also readily detectable in the drainin

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

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

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

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

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

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

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

298 ccumulation of nonproliferating T follicular helper cells within GCs, but with an abundance of cells

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

300 orphology in the absence of additional islet-helper cells would improve transplantation outcome in di