ライフサイエンスコーパス: NKT cell

1 e blood cell known as natural killer T cell (NKT cell).

2 ffector functions of natural killer T cells (NKT cells).

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

4 22-producing human and murine gammadelta and NKT cells.

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

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

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

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

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

10 profiles compared with the classical type I NKT cells.

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

12 reduced in mice receiving perforin-deficient NKT cells.

13 milar to mammalian CD1d-restricted invariant NKT cells.

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

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

16 with both the gammadelta T and the invariant NKT cells.

17 ility to present alpha-galactosylceramide to NKT cells.

18 cyte CD1d expression and very low numbers of NKT cells.

19 development but not either Ag-experienced or NKT cells.

20 phospholipids are also recognized by type II NKT cells.

21 es able to bind to CD1d and activate type II NKT cells.

22 icians to exploit the antitumor potential of NKT cells.

23 ivity score and frequency of CD107a positive NKT cells.

24 the development of a distinct population of NKT cells.

25 an regulate CD1d-mediated Ag presentation to NKT cells.

26 endent on both T-bet and IL-15, similarly to NKT cells.

27 the CAR.GD2 enhanced in vivo persistence of NKT cells.

28 f Bcl-xL led to increased Ag presentation to NKT cells.

29 a-glucosylceramide, was distinct from type I NKT cells.

30 e in regulating the inflammatory function of NKT cells.

31 in turn governs the inflammatory function of NKT cells.

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

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

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

35 ablation does not result from reductions in NKT cells.

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

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

38 olerance induction through interactions with NKT cells.

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

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

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

42 unction and development of natural killer T (NKT) cells.

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

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

45 onstrating that CD1d-independent (CD1d(ind)) NKT cells, a population of CD1d-unrestricted NKT cells,

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

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

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

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

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

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

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

53 IL-12 is required for NKT cell activation in vitro but is not sufficient, wher

54 In vivo, NKT cell activation was abolished in IL-12(-/-) mice inf

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

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

57 tion or knockdown of Bcl-xL led to decreased NKT cell activation.

58 e benefit from the vaccine, despite inducing NKT-cell activation.

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

60 emia cells loaded with the natural killer T (NKT)-cell agonist alpha-galactosylceramide (alpha-GalCer

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 Like NK cells, NKT cells also produce high levels of IFN-gamma rapidly

64 KT cells leads to anergy induction in type I NKT cells and affords protection from Con A-induced hepa

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

66 In addition, type I NKT cells and dendritic cells (DCs) in the periphery, as

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

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

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

70 al the characteristics of polyclonal type II NKT cells and their potential role in antitumor immunoth

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

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

75 nition by innate cell populations (NK cells, NKT cells, and gammadelta T cells) and also by dendritic

76 duced activated intrahepatic CD8(+) T cells, NKT cells, and inflammatory cytokines, similar to NASH p

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

78 T helper (Th) 17 cells, gammadelta T cells, NKT cells, and newly described innate lymphoid cells (IL

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

80 inistration of alpha-GalCer causes long-term NKT cell anergy, but the molecular mechanism is unclear.

81 d death 1 and cbl-b in NKT cells, leading to NKT cell anergy.

82 NKT cells are a distinct subset that have developmental

83 NKT cells are a unique subset of T cells that recognize

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

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

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

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

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

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

90 administration, and mice deficient in type I NKT cells are not protected from disease.

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

92 Type I NKT cells are often referred to as invariant owing to th

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

94 Type II NKT cells are potently activated by beta-D-glucopyranosy

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

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

97 NKT cells are unconventional T cells that respond to sel

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

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 CD1d-restricted natural killer T (NKT) cells are innate-like T cells with potent immunomod

102 NKT cells, a population of CD1d-unrestricted NKT cells, are endowed with a hybrid function far superi

103 , we identified a critical role for the CD1d-NKT cell arm of innate immunity in promoting the develop

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

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

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

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

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

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

110 CD8(+) T cells and NKT cells but not myeloid cells promote NASH and HCC thr

111 4-1BB is expressed on invariant (i)NKT cells, but its role is unclear.

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

113 d a striking T helper 1-like polarization of NKT cells by 4-1BB-containing CARs.

114 d-mediated Ag processing and presentation to NKT cells by altering the late endosomal compartment and

115 t CCR7 controls the development of invariant NKT cells by enabling their access to IL-15 trans-presen

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

117 hat activation of sulfatide-reactive type II NKT cells by sulfatide prevents induction of EAE.

118 Furthermore, type II NKT cells can be activated by CpG oligodeoxynucletides t

119 CD1d-restricted NKT cells can be divided into two groups: type I NKT cel

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

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

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

123 sion in Valpha24-invariant natural killer T (NKT) cells can build on the natural antitumor properties

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

125 In the absence of NKT cells, CD1d-deficient keratinocytes, dendritic cells

126 Similar to type I natural killer T (NKT) cells, CD1d-lipid Ag-reactive delta/alphabeta T cel

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

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

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

130 NKT cells constitute a small population of T cells devel

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

132 eatosis via secreted LIGHT, while CD8(+) and NKT cells cooperatively induce liver damage.

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

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

135 teractions leading to inactivation of type I NKT cells, DCs, and microglial cells in suppression of a

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

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

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

139 ariant NKT cell-knockout (Jalpha18(-/-)) and NKT cell-deficient (TCRalpha(-/-)) mice, which express C

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

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

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

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

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

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

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

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

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

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

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

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

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

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

154 development and the completion of invariant NKT cell development.

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

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

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

158 Invariant NKT cells differentiate into three predominant effector

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

160 These CAR.GD2 NKT cells effectively localized to the tumor site had po

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

162 Natural killer T (NKT) cells, enriched in the liver and comprised of at le

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

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

165 ess CD1d but are deficient in CD1d-dependent NKT cells, exhibited as much cutaneous tissue injury and

166 Also, some splenic NKT cells expressed GFP, whereas naive NK cells and B2 c

167 -2 proteins as central regulators of murine NKT cell fate decisions.

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

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

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

171 o cell types, as well as the significance of NKT cells for host resistance, remain unknown.

172 NKT cells from adipose tissues that do not express PLZF

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

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

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

176 were preferentially recognized by Vbeta7(+) NKT cells from mice, whereas the alpha-galactosylceramid

177 , was preferentially recognized by Vbeta8(+) NKT cells from mice.

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

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

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

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

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

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

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

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

186 CAR.GD2 expression rendered NKT cells highly cytotoxic against NB cells without affe

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

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

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

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

191 not only understanding activation of type II NKT cells in physiological settings, but also for the de

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

193 Furthermore, adoptive transfer of liver NKT cells in T-cell-deficient mice showed reduction of f

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

195 y, we report a striking deficiency of type I NKT cells in the wild-derived inbred strains PWD/PhJ, SP

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

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

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

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

200 Type I NKT cell-induced inflammation and neutrophil recruitment

201 Invariant NKT cells (iNKT cells) are innate lymphocytes that recog

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

203 CD1d-reactive invariant NKT cells (iNKT) play a vital role in determining the ch

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

205 Transfer of CD4(+) NKT cells into T- and B-cell-deficient ApoE(-/-)Rag2(-/-

206 Transfer of CD4(+) NKT cells into T-, B-cell-deficient, and NK cell-deficie

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

208 The frequency of NKT cells is highly variable in humans and in mice, but

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

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

211 trast, the skins of UVB-irradiated invariant NKT cell-knockout (Jalpha18(-/-)) and NKT cell-deficient

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

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

214 hich induced programmed death 1 and cbl-b in NKT cells, leading to NKT cell anergy.

215 the activation of sulfatide-reactive type II NKT cells leads to a significant reduction in the freque

216 thermore, LPC-mediated activation of type II NKT cells leads to anergy induction in type I NKT cells

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

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

219 a14-Jalpha18 TCR instructs commitment to the NKT cell lineage, but the precise signaling mechanisms t

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

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

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

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

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

225 NKT cells mount strong antitumor responses and are a maj

226 PLZF(+)CD4(+) T cells are not CD1d-dependent NKT cells, MR1-dependent MAIT cells, or gammadelta T cel

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

228 s such as gammadelta TCR(+) cells, invariant NKT cells, mucosal-associated invariant T cells, and H2-

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

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

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

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

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

234 Here we characterized type II NKT cells on a polyclonal level by using a Jalpha18-defi

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

236 e a subset of alphabeta or gammadelta TCR(+) NKT cells or mucosal-associated invariant T (MAIT) cells

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

238 We further show that NK and NKT cells play an important role in mediating control of

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

240 NKT cells primarily cause steatosis via secreted LIGHT,

241 Compared with type I NKT cells, type II NKT cells produce lower levels of IFN-gamma but comparab

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

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

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

245 A major subset of type II NKT cells recognizes myelin-derived sulfatides and is se

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

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

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

249 NKT cells represent a small subset of glycolipid-recogni

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

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

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

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

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

255 Highly target-specific liver NKT cells selectively remove activated HSCs through an N

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

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

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

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

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

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

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

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

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

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

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

267 NKT cell survival during development requires signal pro

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

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

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

271 Among these T lymphocytes, NKT cells that express an invariant TCRalpha-chain and r

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

273 cells identify a hybrid feature in CD1d(ind)NKT cells that truly fulfills the dual function of an NK

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

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

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

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

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

279 d that IL-30 recruits natural-killer-like T (NKT) cells to the liver to remove activated hepatic stel

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

281 expression of PLZF, the signature invariant NKT cell transcription factor, in these innate CD4(+) T

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

283 Compared with type I NKT cells, type II NKT cells produce lower levels of IFN

284 ted neutralization studies showed that liver NKT cells up-regulate the natural killer group 2, member

285 ore, alpha-GalCer-induced egr-2/3 in hepatic NKT cells upregulated their TRAIL in addition to Fas lig

286 cells can be divided into two groups: type I NKT cells use a semi-invariant TCR, whereas type II expr

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

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

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

290 Transferred NKT cells were identified in the liver and atherosclerot

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

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

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

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

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

296 icrobial lipid antigens to natural killer T (NKT) cells, which are involved in the pathogenesis of co

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

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

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