ライフサイエンスコーパス: NKT cell

1 ed by MAIT cells and natural killer T cells (NKT cells).

2 olerance induction through interactions with NKT cells.

3 s of CD28 signals compared to NK1.1- stage 2 NKT cells.

4 the development of a distinct population of NKT cells.

5 e in regulating the inflammatory function of NKT cells.

6 in turn governs the inflammatory function of NKT cells.

7 express diverse TCRs and are termed type II NKT cells.

8 ed to NK-cell depletion, but to CD8(+) T and NKT cells.

9 tive accumulation of adipose-tissue-resident NKT cells.

10 ablation does not result from reductions in NKT cells.

11 rt to the existence of functional subsets of NKT cells.

12 l killer (NK) cells, gammadelta-T cells, and NKT cells.

13 h can be presented by CD1d and recognized by NKT cells.

14 22-producing human and murine gammadelta and NKT cells.

15 onventional NK cells, T cells, and invariant NKT cells.

16 onventional T cells but from CD1d-restricted NKT cells.

17 in driving the activation of thymic resident NKT cells.

18 fector functions of T1D-protective invariant NKT cells.

19 by sulfatide-mediated activation of type II NKT cells.

20 p-regulation in ALD is dependent upon type I NKT cells.

21 ands for TLRs and/or compounds that activate NKT cells.

22 profiles compared with the classical type I NKT cells.

23 cule CD1d to evade the antiviral function of NKT cells.

24 reduced in mice receiving perforin-deficient NKT cells.

25 milar to mammalian CD1d-restricted invariant NKT cells.

26 iant NKT (iNKT) cells and IL-4(+) gammadelta NKT cells.

27 ratio of IFN-gamma:IL-4 production by NK1.1+ NKT cells.

28 ter alcohol feeding is dependent upon type I NKT cells.

29 innate-like functions and characteristics of NKT cells.

30 ve as non-overlapping negative regulators of NKT cells.

31 al details of alphaGSA recognition by murine NKT cells.

32 T cells with that of suppressive Valpha14 DN NKT cells.

33 with expansion of IL-17-producing T, NK, and NKT cells.

34 ncreased removal of senescent hepatocytes by NKT cells.

35 pacity to activate CD1d-restricted invariant NKT cells.

36 nced by engaging help from natural killer T (NKT) cells.

37 ds are potent activator of natural killer T (NKT) cells.

38 d human and murine type II natural killer T (NKT) cells.

39 ctosylceramide to activate natural killer T (NKT) cells.

40 ce expression and suppresses the function of NKT cells, a group of innate T cells with critical immun

41 We found that NKT cells, a population of innate-like T lymphocytes, ar

42 Selective deficiency of either CD8(+) DCs or NKT cells abrogated chimerism and organ graft acceptance

43 Natural killer T (NKT) -cells activated with the glycolipid ligand alpha-g

44 d-peptide conjugate vaccine incorporating an NKT cell-activating glycolipid linked to an MHC class I-

45 T cell responses in vivo by incorporating an NKT cell-activating glycolipid.

46 l bacteria was able to restore ConA-mediated NKT cell activation and liver injury in GF mice.

47 switch within murine (m)CD1d that modulates NKT cell activation by alphaGSAs.

48 nduced by Con A and impinges on hallmarks of NKT cell activation in the liver without affecting NKT c

49 dely used to assess the role of TCR-mediated NKT cell activation in various disease models.

50 role for RIPK3-PGAM5-Drp1/NFAT signalling in NKT cell activation, and further suggest that RIPK3-PGAM

51 ts monovalent form cannot block TCR-mediated NKT cell activation, because 1B1 fails to bind with high

52 To study the role of antigen presentation in NKT cell activation, previous studies have developed sev

53 mical modifications of the antigen on type I NKT cell activation.

54 oss several models of pneumonia, sepsis, and NKT cell activation.

55 alphaGalCer) to induce pneumonia, sepsis, or NKT cell activation.

56 latory function of BTLA in natural killer T (NKT) cell activation has been reported, whether CD160 is

57 works synergistically with Tyr-73 to control NKT cell activity.

58 nal commensal bacteria are important hepatic NKT cell agonist and these antigens are required for the

59 Using an NKT cell agonist that has a modified sphingosine moiety,

60 ted by CD1d, but not the prototypical type I NKT cell agonist, alpha-galactosylceramide.

61 These results indicate that NKT-cell agonists could be used to improve swine vaccine

62 Ags and tetramers for semi-invariant/type I NKT cells allowed this population to be extensively stud

63 e is essential for the effector functions of NKT cells and a high lactate environment is detrimental

64 mor-killing cells such as IFNg+ CD8, NK, and NKT cells and a reversal of the immunosuppressive tumor

65 findings indicate that interactions between NKT cells and CD1d-expressing adipocytes producing endog

66 subset-specific responses by thymic resident NKT cells and contextually shape the milieu in this prim

67 The relationship between NKT cells and intestinal bacterial glycolipids in liver

68 ith a time dependent preponderance of NK and NKT cells and lower proportion of inflammatory monocytes

69 volutionary patterns of the iTRA of MAIT and NKT cells and restricting MH1Like proteins: MR1 appeared

70 t differences in cytokine production by lung NKT cells and that impaired clearance of P. aeruginosa i

71 ctures of natural glycolipids that stimulate NKT cells and to determine how these antigens are recogn

72 or (RARgamma) signaling that inhibits type I NKT cells and, consequently, ALD.

73 h liver tumors, we found that CXCR6 mediated NKT-cell and CD4(+) T-cell removal of senescent hepatocy

74 r (TCR) expressed by natural killer T cells (NKT cells) and the antigen-presenting molecule CD1d is d

75 serum AST and ALT levels, hyperactivation of NKT cells, and enhanced IFN-gamma, TNF, and IL-4 product

76 ed with innate lymphocytes such as NK cells, NKT cells, and gamma-delta T cells.

77 geting CD8alpha, thereby depleting NK cells, NKT cells, and gammadelta T cells, in addition to CD8(+)

78 e cells including natural killer (NK) cells, NKT cells, and memory CD8(+) T cells.

79 eu through the interplay of Tregs, invariant NKT cells, and plasmacytoid dendritic cells, which resul

80 inform the development alphaGSAs as specific NKT cell antagonists to modulate immune responses.

81 NKT cells are a distinct subset that have developmental

82 Semi-invariant/type I NKT cells are a well-characterized CD1d-restricted T cel

83 However, if NKT cells are activated first, then CD8alpha(-) DCs beco

84 male C57BL/6 mice, type I, but not type II, NKT cells are activated, leading to recruitment of infla

85 In this study we show that invariant NKT cells are also recruited to CCL22-expressing islet t

86 on of NKT17 cells, whereas peripheral mature NKT cells are essentially absent.

87 Finally, we find that tumor infiltrating NKT cells are highly enriched for the YY1(lo) subset.

88 NKT cells are less efficient in glucose uptake than CD4

89 mechanism by which IL-4(+)IL-13(+) invariant NKT cells are necessary for IL-4Ralpha signaling that re

90 r T (NKT) cells in Xenopus demonstrated that NKT cells are not restricted to mammals and are likely t

91 During their development, NKT cells are polarized into the NKT1, NKT2, and NKT17 s

92 nteractions between CD8(+) DCs and invariant NKT cells are required for tolerance induction in this s

93 iosis experiments demonstrated that MAIT and NKT cells are resident in the spleen, liver, and lungs,

94 CD4(+) NKT cells are twice as potent as CD4(+) T cells in promo

95 NKT cells are unconventional T cells that respond to sel

96 Surprisingly, Roquin paralog-deficient NKT cells are, in striking contrast to conventional T ce

97 Type I natural killer T (NKT) cells are a population of innate like T lymphocytes

98 Natural killer T (NKT) cells are a subset of T lymphocytes that recognize

99 Natural killer T (NKT) cells are innate lymphocytes that differentiate int

100 Semi-invariant natural killer T (NKT) cells are innate-like lymphocytes with immunoregula

101 Type I and type II natural killer T (NKT) cells are restricted to the lipid antigen-presentin

102 ed in Jalpha18(-/-) mice deficient in type I NKT cells as well as after their inactivation by sulfati

103 ta, Mucosal associated invariant (MAIT), and NKT cells as well as monocytes, macrophages, and epithel

104 The positioning of NKT cells at the interfollicular areas of lymph nodes fa

105 nd granzyme B cytotoxins in promoting CD4(+) NKT cell atherogenicity.

106 CD4(+) natural killer T (NKT) cells augment atherosclerosis in apolipoprotein E-d

107 Type I, but not type II, NKT cells become activated after alcohol feeding.

108 In contrast to type I NKT cells, betaGL1-22- and LGL1-specific NKT cells const

109 We found that NKT cells, but not CD4 or CD8 T cells, have dramatically

110 Inhibition of type I NKT cells by retinoids or by sulfatide prevents ALD.

111 These initial results suggest that CAR-NKT cells can be expanded to clinical scale and safely a

112 In fact, the initial activation of NKT cells can condition multiple DC subsets to respond m

113 These data indicate that CD4(+) NKT cells can exert proatherogenic effects independent o

114 Human betaGL1-22- and LGL1-specific NKT cells can provide efficient cognate help to B cells

115 dies have shown that human natural killer T (NKT) cells can promote immunity to pathogens, but their

116 Invariant NKT cell (CD3(+)Valpha24(+)) proportions were higher in

117 l profiling reveals a unique signature of PP-NKT cells, characterized by tissue residency.

118 CD1d-restricted NKT cells comprise an unusual innate-like T cell subset

119 ha-GalCer resulted in a systemic increase in NKT-cell concentrations, including in the respiratory tr

120 NKT cells constitute a small population of T cells devel

121 e I NKT cells, betaGL1-22- and LGL1-specific NKT cells constitutively express T-follicular helper (TF

122 alpha24-Jalpha18 Ab, human primary invariant NKT cells could be divided into Valpha24 low- and high-i

123 trength as well as reduced natural killer T (NKT) cell counts.

124 In good agreement, CD28 blockade suppressed NKT cell cytokine secretion, lowering the ratio of IFN-g

125 alling node-only partially recapitulated the NKT cell deficiency observed in IkappaBDeltaN (tg) mouse

126 CD4(+) NKT cells deficient in IL-4, interferon-gamma, or IL-21

127 Transfer of CD4(+) NKT cells deficient in perforin or granzyme B failed to

128 ent in these molecules were transferred into NKT cell-deficient ApoE(-/-)Jalpha18(-/-) mice.

129 avage, activates human dendritic cells in an NKT-cell dependent manner, and generates a pool of activ

130 To investigate the role of NKT cell-derived interferon-gamma, IL-4, and IL-21 cytok

131 d the roles of bystander T, B, and NK cells; NKT cell-derived interferon-gamma, interleukin (IL)-4, a

132 interleukin (IL)-4, and IL-21 cytokines; and NKT cell-derived perforin and granzyme B cytotoxins in p

133 cient IkappaBDeltaN transgenic mouse rescues NKT cell development and differentiation in this mouse m

134 caused by absence of ABCA7 negatively affect NKT cell development and function.

135 These data suggest that Pak2 controls thymic NKT cell development by providing a signal that links Eg

136 iciency, but not the Fas-deficiency, rescued NKT cell development in IkappaBDeltaN (tg) mice.

137 ll activation in the liver without affecting NKT cell development in the thymus.

138 A20 is differentially expressed during NKT cell development, regulates NKT cell maturation, and

139 e recognition of CD1d, significantly altered NKT cell development, which resulted in the selective ac

140 rough cell-intrinsic mechanisms early during NKT cell development.

141 e into PKC-theta null mouse failed to rescue NKT cell development.

142 n, a TCR costimulatory receptor required for NKT cell development.

143 activated kinase 2 (Pak2), was essential for NKT cell development.

144 ras, we show that CD160 is not essential for NKT cell development.

145 We found that NKT cells did indeed play a critical role in the clearan

146 Invariant NKT cells differentiate into three predominant effector

147 ymphocytes during endotoxemia suggested that NKT cells drove IFN-gamma production by NK cells via mTO

148 antigens are required for the activation of NKT cells during ConA-induced liver injury.

149 primarily reported in T cells, NK cells, and NKT cells, during acute pneumonic infection with Klebsie

150 ession of CREMalpha did not influence NK and NKT-cell effector functions either.

151 or the development of natural killer T cell (NKT cell) effector functions.

152 phase 1 dose-escalation trial of autologous NKT cells engineered to co-express a GD2-specific chimer

153 f using 1B1 to assess antigen recognition by NKT cells, especially when investigating antigens that d

154 ion and glycolipid-reactive, CD1d-restricted NKT cells exacerbate the development of obesity and insu

155 Accordingly, ROS-high NKT cells exhibited increased susceptibility and apoptot

156 CAR-NKT cells expanded in vivo, localized to tumors and, in

157 a mature phenotype and, distinct from other NKT cells, expressed almost no ThPOK or Tbet.

158 l, we observed an increase in splenic NK and NKT cells expressing TLR3 in infected B6 mice, suggestin

159 Mouse NKT cells expressing wild-type levels of PLZF, but defic

160 -2 proteins as central regulators of murine NKT cell fate decisions.

161 key transcription factors for acquiring the NKT cell fate, were markedly diminished in the absence o

162 Although most initial studies on NKT cells focused on a subset with semi-invariant TCR te

163 e induces CD1d-dependent activation of human NKT cells following enzymatic cleavage, activates human

164 NKT cells from adipose tissues that do not express PLZF

165 -kappaB activation was protecting developing NKT cells from death signals emanating either from high

166 integration by NF-kappaB protects developing NKT cells from death signals emanating from TNFR1, but n

167 d perforin and granzyme B cytotoxins, CD4(+) NKT cells from mice deficient in these molecules were tr

168 strate that RIPK3 plays an essential role in NKT cell function via activation of the mitochondrial ph

169 nt study, we investigated the role of ROS in NKT cell function.

170 g the significance of glucose metabolism for NKT cell function.

171 Crucial to Natural Killer T (NKT) cell function is the interaction between their T-ce

172 operties, such as natural killer (NK) cells, NKT cells, gammadelta T cells, and macrophages, are prom

173 c finger seemed to play a role in regulating NKT cells' glucose metabolism.

174 Gene-expression data revealed that, in NKT cells, glucose is preferentially metabolized by the

175 scertain the therapeutic potential of type I NKT cell GSL activators.

176 how that CD1d-deficient mice, which lack all NKT cells, harbor an altered intestinal microbiota that

177 ) to activate type I natural killer T cells (NKT cells) has been known for 2 decades.

178 Valpha24-invariant natural killer T (NKT) cells have shown potent anti-tumor properties in mu

179 Natural killer T cells (NKT cells) have stimulatory or inhibitory effects on the

180 In the absence of NKT cells hepatic proliferating cell nuclear antigen and

181 rate that ABCA7 regulates the development of NKT cells in a cell-extrinsic manner.

182 d in their conclusions regarding the role of NKT cells in clearance of P. aeruginosa from the lung.

183 failed to trigger the activation of hepatic NKT cells in GF mice.

184 f type I NKT cells, our knowledge of type II NKT cells in health and disease remains unclear.

185 th high affinity, only a few activate type I NKT cells in in vivo or in vitro experiments.

186 s are bound by the T cell receptor of type I NKT cells in real time binding assays with high affinity

187 Loss of Pak2 in T cells reduced stage III NKT cells in the thymus and periphery.

188 ncrease in respective lipid-specific type II NKT cells in vivo and downstream induction of germinal c

189 e unambiguous discovery of natural killer T (NKT) cells in Xenopus demonstrated that NKT cells are no

190 nearly all of the unique characteristics of NKT cells including their rapid and potent response to a

191 wn to express glycolipid antigens activating NKT cells, increased the incidence of these PTCLs, where

192 Type I NKT cell-induced inflammation and neutrophil recruitment

193 adverse events, as they occurred before CAR-NKT cell infusion, and no dose-limiting toxicities were

194 Peripheral invariant NKT cells (iNKT) and CD8(+) tissue-resident memory T cel

195 Invariant NKT cells (iNKT) are potent immunoregulatory T cells tha

196 s of innate-like T cells including invariant NKT cells (iNKT), CD8alphaalphaTCRalphabeta small intest

197 In contrast, the loss of peripheral NKT cells is due to cell-extrinsic factors.

198 d glucose uptake and IFN-gamma expression in NKT cells is inversely correlated with bacterial loads i

199 nal T cells, regulatory T cells, and type Ib NKT cells is normal.

200 activation of T cells, but how ROS influence NKT cells is unknown.

201 al and synthetic, can alter the responses of NKT cells, leading to dramatic changes in the global imm

202 adipocytes can present endogenous ligands to NKT cells, leading to IFN-gamma production, which in tur

203 d-expressing adipocytes producing endogenous NKT cell ligands play a critical role in the induction o

204 of their semi-invariant TCR, which triggers NKT cell lineage commitment and maturation.

205 Within NKT subsets, however, stage 3 NKT cells, marked by higher NK1.1 expression, were signi

206 essed during NKT cell development, regulates NKT cell maturation, and specifically controls the diffe

207 Thus, targeting mucosal NKT-cells may provide a novel and potent platform for im

208 We ex vivo expanded highly pure NKT cells (mean +/- s.d., 94.7 +/- 3.8%) and treated pat

209 ficient vaccines in the future to boost host NKT cell-mediated immune responses against herpesviruses

210 e is known about the involvement of RIPK3 in NKT cell-mediated immune responses.

211 ogical inhibition of Drp1 protects mice from NKT cell-mediated induction of acute liver damage.

212 These results implicated an NKT cell/mTOR/IFN-gamma axis in immunosuppression follow

213 NKT cells, mucosa-associated invariant T cells, and germ

214 Because NKT cells normally depend on signals from CD8(+) dendrit

215 h the unusually high level of variability in NKT cell number and function among different genetic bac

216 is significant strain-dependent variation in NKT cell number and function among different inbred stra

217 production correlated with reduced invariant NKT cell numbers as well as lower IL-23 levels.

218 relationship of these changes, especially in NKT cell numbers, to patient outcomes such as MODS warra

219 Cer, which effectively increased DN CD38(hi) NKT cell numbers.

220 sociation between absolute natural killer T (NKT) cell numbers and the subsequent development of MODS

221 pressing cells that influence the effects of NKT cells on the progression of obesity remain incomplet

222 We found that NKT cells operate distinct metabolic programming from CD

223 he antigen reactivity and function of type I NKT cells, our knowledge of type II NKT cells in health

224 .8%) and treated patients with 3 x 10(6) CAR-NKT cells per square meter of body surface area after ly

225 GF-beta and IL-4, adopting an IL-9-producing NKT cell phenotype able to mediate proinflammatory effec

226 CD4(+) NKT cells potently promote atherosclerosis by perforin a

227 PP-NKT cells produce the majority of the IL-4 in Peyer's pa

228 When activated, YY1(lo) NKT cells produced little IL-4 or IFN-gamma.

229 sults in liver tissue damage whereas type II NKT cells protect from injury in ALD.

230 Natural killer T (NKT) cells rapidly respond to antigenic stimulation with

231 NKT cells recognize lipid Ags presented by a class I MHC

232 NKT cells recognize lipid-based Ags presented by CD1d.

233 A subset of mature NKT cells remain thymic resident, but their activation a

234 nal(s) integrated by NF-kappaB in developing NKT cells remains incompletely defined.

235 However, the diversity of the NKT cell repertoire and the ensuing interactions with CD

236 rototypical TRAV10-TRAJ18-TRBV25-1(+) type I NKT cell repertoire.

237 NKT cells represent a small subset of glycolipid-recogni

238 ted invariant T (MAIT) and natural killer T (NKT) cells, respectively, may result from a coevolution

239 Ripk3(-/-) mice show reduced NKT cell responses to metastatic tumour cells, and both

240 Natural killer T cells (NKT cells) restricted by the antigen-presenting molecule

241 s with vascular access, but not LN or thymic NKT cells, resulting in systemic interferon-gamma and IL

242 Indeed, NKT cells secrete an early wave of IL-4 and constitute u

243 In the periphery, these NKT cells showed a strong Th1-biased cytokine response a

244 We characterized this specific NKT cell subpopulation that developed during influenza i

245 D8(-) double-negative (DN) natural killer T (NKT) cell subpopulation that protects the mice as adults

246 However, this NKT cell subset has not been characterized, and the unde

247 therefore, defines a previously unrecognized NKT cell subset that is committed to producing IL-10.

248 The marker-enriched NKT cell subset was then analyzed for its cytokine profi

249 have analyzed purified populations of thymic NKT cell subsets at both the transcriptomic level and ep

250 ogs regulate the development and function of NKT cell subsets in the thymus and periphery.

251 ely ignored how the differentiation into the NKT cell subsets is regulated.

252 is highly conserved between mice and humans, NKT cell subsets might be targeted for potential therape

253 estigated whether differential activation of NKT cell subsets orchestrates inflammatory events leadin

254 similar antigen specificity, the functional NKT cell subsets were highly divergent populations with

255 ion of YY1 and PLZF, therefore, might define NKT cell subsets with distinct effector functions.

256 Among different NKT cell subsets, Pak2 was necessary for the generation

257 some Ags can preferentially activate type I NKT cell subsets.

258 TCLs showed phenotypic features of activated NKT cells, such as PD-1 up-regulation and loss of NK1.1

259 efficacy of the invariant natural killer T (NKT) cell superagonist, alpha-galactosylceramide (alpha-

260 f cells in the lung and that some subsets of NKT cells suppress AHR.

261 high lactate environment is detrimental for NKT cell survival and proliferation.

262 NKT cell survival during development requires signal pro

263 ole of cell metabolism for natural killer T (NKT) cell survival, proliferation, and function.

264 his patch ablated recognition of CD1d by the NKT cell TCR but not interactions of the TCR with MHC.

265 role in maintaining the conformation of the NKT cell TCR.

266 ctosylceramide (alpha-GalCer)-reactive human NKT cells that differ markedly from the prototypical TRA

267 inct gene programs on subsets of innate-like NKT cells that probably impart differences in proliferat

268 Here we describe a population of type II NKT cells that recognise and respond to the microbial an

269 set with semi-invariant TCR termed invariant NKT cells, the majority of CD1d-restricted lipid-reactiv

270 In contrast to studies with peripheral NKT cells, the proliferation of thymic NKT cells was sig

271 s has been suggested for mammalian invariant NKT cells, they may serve as immune regulators polarizin

272 r that delivers antigen-dependent signals in NKT cells to dampen cytokine production during early inn

273 thereby maximising the potential for type II NKT cells to detect different lipid antigens.

274 s within CD4(+) and CD8(+) T lymphocytes and NKT cells to negatively regulate IFN-gamma responses in

275 downstream NF-kappaB activation- sensitized NKT cells to TNF-alpha-induced cell death in vitro.

276 mouse model required host natural killer T (NKT) cells to induce tolerance.

277 to lymphocytes (T, natural killer [NK], and NKT cells), to acute and chronic liver injury models.

278 TfH wave of IL-4 secreted by interfollicular NKT cells triggers the seeding of germinal center cells

279 Overall, our study reveals that NKT cells use distinct arms of glucose metabolism for th

280 We found that the strain-dependent role of NKT cells was associated with significant strain-depende

281 of mice, we investigated whether the role of NKT cells was dependent on the host genetic background.

282 A subset of NKT cells was identified that expressed low levels of YY

283 heral NKT cells, the proliferation of thymic NKT cells was significantly impaired when CD28 engagemen

284 We observed that sorted ROS-high NKT cells were enriched in NKT1 and NKT17 cells, whereas

285 YY1(lo) NKT cells were found in all tissues, had a mature phenot

286 YY1(lo) NKT cells were found to constitutively transcribe IL-10

287 Transferred NKT cells were identified in the liver and atherosclerot

288 CD4(+) T cells or NKT cells were isolated from the spleen and liver of CD4

289 Accordingly, NKT cells were less activated, IFN-gamma production was

290 High ROS in the peripheral NKT cells were primarily produced by NADPH oxidases and

291 virus persistence was largely prevented when NKT-cells were targeted via the respiratory route.

292 Similar observations were made with human NKT cells where different CDR3beta-encoded residues dete

293 monocytes, B1 cells, gammadelta T cells and NKT cells, whereas dendritic cells, B2 cells, CD4(+) T a

294 ction, SSMs activate B and natural killer T (NKT) cells while secreting inflammatory mediators.

295 ) DCs induced the development of tolerogenic NKT cells with a marked T helper 2 cell bias that, in tu

296 Furthermore, treatment of NKT cells with antioxidants led to reduced frequencies o

297 We showed that DN NKT cells with high CD38 expression produced IFN-gamma,

298 mRNA expression profile of wild-type CD4(+) NKT cells with that of suppressive Valpha14 DN NKT cells

299 Activation of invariant (i)NKT cells with the model Ag alpha-galactosylceramide ind

300 new population of type II natural killer T (NKT) cells with follicular helper phenotype (TFH), which