ライフサイエンスコーパス: iNKT cell

1 eration of invariant natural killer T cells (iNKT cells).

2 demonstrated markedly less antigenicity for iNKT cells.

3 development and effector differentiation of iNKT cells.

4 senting cells (APCs) modulates activation of iNKT cells.

5 might lead to improved therapeutics based on iNKT cells.

6 re to facilitate broad changes in developing iNKT cells.

7 be responsible for the suppressive effect of iNKT cells.

8 ted protection entails inhibition of NOX2 in iNKT cells.

9 s, overall restraining the iNKT17 program in iNKT cells.

10 rimental settings and in studies focusing on iNKT cells.

11 pression and lineage diversity in developing iNKT cells.

12 be captured by APCs and presented by CD1d to iNKT cells.

13 nts IR injury by blocking NOX2 activation in iNKT cells.

14 paradigm for study of the self-education of iNKT cells.

15 ce reconstituted with WT, but not A2AR(-/-), iNKT cells.

16 KT cells compared with that in the wild type iNKT cells.

17 etic requirements for the differentiation of iNKT cells.

18 cells, as well as the function of peripheral iNKT cells.

19 cell TCR specificity with the generation of iNKT cells.

20 4 induces IL-9 secretion in murine and human iNKT cells.

21 P3 and the induction of suppressive FOXP3(+) iNKT cells.

22 upon activation, as do human CD8alphabeta(+) iNKT cells.

23 (+) dendritic cells and increased numbers of iNKT cells.

24 gh CD1d expression on CLL cells and impaired iNKT cells.

25 otein CD1d, which presents lipid antigens to iNKT cells.

26 lish whether they have potential to activate iNKT cells.

27 ciency in arylsulfatase-A, directly activate iNKT cells.

28 improved detection of cytokines produced by iNKT cells.

29 alphabetaT-cells and innate CD1d-restricted iNKT-cells.

30 re evaluated for their capacity to stimulate iNKT-cells.

31 mature alphabetaT-cells and CD1d-restricted iNKT-cells.

32 agy on the differentiation of invariant NKT (iNKT) cells.

33 ibitory receptors expressed on invariant NK (iNKT) cells.

34 alCer or OCH) to invariant natural killer T (iNKT) cells.

35 he activation of invariant natural killer T (iNKT) cells, a specialized subset of innate T lymphocyte

36 Moreover, increased hepatic iNKT cell abundance in the absence of MTP is associated

37 However, mechanisms for iNKT cell activation after IR and A2AR agonist-mediated

38 xpand our understanding of the mechanisms of iNKT cell activation and suggest that modulation of TPL2

39 yporesponsive state, nor did cytokine-driven iNKT cell activation by LPS or infections.

40 Importantly and consistently with iNKT cell activation during inflammatory conditions, exp

41 ining liposome was associated with a lack of iNKT cell activation in the draining lymph nodes (dLNs)

42 T cells from naive mice do not express IL-9, iNKT cell activation in the presence of TGF-beta and IL-

43 Collectively, these results demonstrate that iNKT cell activation in vivo leads to late PTB by initia

44 These data further our understanding of how iNKT cell activation is regulated and provide insights i

45 Y108 costimulation similarly increased human iNKT cell activation.

46 in cytoskeleton and correlates with enhanced iNKT cell activation.

47 onist R848 increases nanocluster density and iNKT cell activation.

48 may contribute to the endogenous pathway of iNKT cell activation.

49 evented IL-17 production by murine and human iNKT cells after acute hypoxia-reoxygenation by blocking

50 hesis that NOX2 mediates IL-17 production by iNKT cells after IR and that A2AR agonism prevents IR in

51 In this study, we show that Th1-biasing iNKT cell Ags could induce iNKT cell hyporesponsiveness,

52 osinophils, Tregs, and invariant NK T cells (iNKT cells) all help to control adipose tissue inflammat

53 During thymic development, iNKT cells also differentiate into NKT1, NKT2, and NKT17

54 Interestingly, Hdac3-deficient iNKT cells also have lower expression of the nutrient re

55 These iNKT cell alterations were associated with an imbalance

56 model developed a subset of CD8alphabeta(+) iNKT cells among other human-like iNKT subsets.

57 Furthermore, both iNKT cells and DCs expressing CD1d and HIV receptors res

58 We confirm that these mice lack iNKT cells and do not respond to lipid antigen stimulati

59 ) mice, we performed an adoptive transfer of iNKT cells and found that only wild-type iNKT cells but

60 ses, is a signaling factor in CD3(+)NK1.1(+) iNKT cells and mediator of hepatic inflammation.

61 3-4 h) and required cell contact between the iNKT cells and monocytes.

62 caused by decreased proliferation of stage 1 iNKT cells and poor development through subsequent stage

63 ulfatide as a self-lipid recognized by human iNKT cells and propose that sulfatide recognition by inn

64 Advances in the study of iNKT cells and the selection of agonists potentiating IL

65 rscores the constitutive memory phenotype of iNKT cells and their activation during inflammatory cond

66 ified as potent microbial lipid antigens for iNKT cells, and their unusual alpha-anomeric linkage has

67 ver, mammals use endogenous lipids to select iNKT cells, and there is compelling evidence for iNKT ce

68 NKT cell numbers as a consequence of altered iNKT cell apoptosis.

69 Despite the fact that iNKT cells are a rare cell population, the almost unlimi

70 iNKT cells are a unique lineage of T cells that recogniz

71 108 interactions between dendritic cells and iNKT cells are critical for robust activation.

72 Both approaches indicate that iNKT cells are pathogenic in TSS.

73 Invariant natural killer T (iNKT) cells are a potent immunoregulatory T-cell subset

74 Invariant NKT (iNKT) cells are a subpopulation of T lymphocytes that re

75 Invariant NKT (iNKT) cells are a unique lineage with characteristics of

76 Invariant Natural Killer T (iNKT) cells are a unique subset of T lymphocytes that ha

77 Invariant NKT (iNKT) cells are critical to the maintenance of tolerance

78 Invariant NKT (iNKT) cells are innate lymphocytes that respond to glyco

79 Invariant NKT (iNKT) cells are innate-like lymphocytes that recognize l

80 Invariant natural killer T (iNKT) cells are innate-like T cells that play a role in

81 Invariant natural killer T (iNKT) cells are innate-like T cells that recognize glyco

82 Invariant NKT (iNKT) cells are innate-like T cells that respond rapidly

83 CD1d-restricted invariant natural killer T (iNKT) cells are innate-like T lymphocytes strongly impli

84 Invariant natural killer T cells (iNKT) cells are T lymphocytes displaying innate effector

85 Invariant NKT (iNKT) cells are unconventional innate-like T cells demon

86 Invariant natural killer T cells (iNKT cells) are innate-like lymphocytes that protect aga

87 Invariant natural killer T cells (iNKT cells) are innate-like T cells that rapidly produce

88 Invariant natural killer T cells (iNKT cells) are lipid-sensing innate T cells that are re

89 Invariant Natural Killer T-cells (iNKT-cells) are an attractive target for immune response

90 ingly asymmetric allospecific alterations in iNKT cells as they develop and mature in an allogeneic e

91 s process, the current report examined naive iNKT cells as they matured in an allogeneic environment.

92 Using natural killer T cells (iNKT cell) as a model of a T cell subset that differenti

93 erentially expressed between WT and Dicer KO iNKT cells at different differentiation stages and predi

94 iously unidentified mechanism that modulates iNKT cell autoreactivity based on the tight control by t

95 iNKT cells, thus opening up a new avenue for iNKT cell-based immunotherapy.

96 by CD1d specifically activate invariant NKT (iNKT) cells bearing an invariant Valpha14-Jalpha18 (mous

97 n the secretion of interleukin-13 (IL-13) by iNKT cells because an antibody blocking this cytokine re

98 e that sulfatide is recognized only by human iNKT cells because of the unique positioning of the 3-O-

99 1beta production was specifically induced by iNKT cells, because similarly activated polyclonal autol

100 rences in the properties and compositions of iNKT cells between the two species, including the presen

101 d our understanding of the role of Bcl11b in iNKT cells beyond their selection and demonstrate that B

102 However, the study of iNKT cell biology and the therapeutic applications of th

103 cient mouse strain will assist in studies of iNKT cell biology.

104 of iNKT cells and found that only wild-type iNKT cells but not IFN-gamma(-/-) iNKT cells reversed MZ

105 In vivo stimulation of iNKT cells by alpha-galactosyl-ceramide was effective in

106 Exogenous activation of invariant NKT (iNKT) cells by the superagonist alpha-galactosylceramide

107 In this study, we investigated whether iNKT cells can participate in the innate cell-mediated i

108 e characterize a novel Ag for invariant NKT (iNKT) cells capable of producing an especially robust Th

109 essed at a similar level in mTORC2-deficient iNKT cells compared with that in the wild type iNKT cell

110 Invariant natural killer T (iNKT) cells comprise a small population of alphabeta T l

111 re experiments revealed that the decrease in iNKT cells contributed to the alterations in the B-cell

112 To elucidate the mechanism whereby iNKT cells control MZ B cell accumulation in apoE(-/-) m

113 nd that Tcl1-CLL cells express CD1d and that iNKT cells critically delay disease onset but become fun

114 ther, these protocols allow the detection of iNKT cell cytokines ex vivo and in vitro with increased

115 ew mouse strain will serve as a new model of iNKT cell deficiency to facilitate our understanding of

116 Studies using iNKT cell-deficient mice and chemically induced dextran

117 ng factor, we have generated a new strain of iNKT cell-deficient mice by deleting the Traj18 locus us

118 phox-/-) or NOX2(-/-) mice to Jalpha18(-/-) (iNKT cell-deficient) mice significantly attenuated lung

119 and cell depletion approaches, we generated iNKT cell-deficient, superantigen-sensitive HLA-DR4-tran

120 ans, respectively, induced the activation of iNKT cells, dependent on CD1d.

121 nounced, leading to a selective reduction in iNKT cell-derived IFN-gamma.

122 Invariant NKT (iNKT) cells develop and differentiate in the thymus, seg

123 discrete TCR interaction kinetics influence iNKT cell development and central priming.

124 Thus, we describe a novel role of Runx1 in iNKT cell development and differentiation, particularly

125 Therefore, Hdac3 is required for iNKT cell development and differentiation.

126 Therefore, NKAP regulates multiple steps in iNKT cell development and differentiation.

127 been controversial, and its participation on iNKT cell development and function has not been examined

128 We found that JunB regulated iNKT cell development and that the expression of genes t

129 We found that T cell and iNKT cell development are impaired in germline-deficient

130 t SHIP1 deletion would have major effects on iNKT cell development by altering the thresholds for pos

131 iNKT cell development requires IL-15, and we found that

132 iNKT cell development uniquely depends on interactions b

133 (PLZF), a critical transcription factor for iNKT cell development, is expressed at a similar level i

134 rs were predicted to target Tgfbr2 mRNA upon iNKT cell development.

135 is known about the epigenetic regulation of iNKT cell development.

136 onstrate in this article that invariant NKT (iNKT) cell development is controlled by mTORC2 in a cell

137 elucidate the global impact of miRNAs on the iNKT cell developmental program and uncover the targetin

138 Functionally, iNKT cells devoid of mTORC2 signaling showed reduced num

139 profiles and found that, although monoclonal iNKT cells differentiated into all functional subsets, t

140 r II (TGF-betaRII), critically implicated in iNKT cell differentiation, was found up-regulated in iNK

141 a signaling in the absence of miRNAs rescued iNKT cell differentiation.

142 urprising finding that human, but not mouse, iNKT cells directly recognize myelin-derived sulfatide p

143 Tet2-Tet3 double-knockout (DKO) iNKT cells displayed pronounced skewing toward the NKT17

144 These HSC-engineered iNKT cells displayed the typical iNKT cell phenotype and

145 of SLAM receptors in the differentiation of iNKT cell effector subsets and activation has not been e

146 UTX-deficient iNKT cells exhibited impaired expression of iNKT cell si

147 In mice, iNKT cells express T cell antigen receptors (TCRs) compr

148 Our data indicate that TET proteins regulate iNKT cell fate by ensuring their proper development and

149 of adoptively transferred third-party CD4(+) iNKT cells for protection from lethal GVHD in a murine m

150 determined that both circulating and splenic iNKT cell frequencies were markedly decreased in patient

151 lls to CLL immune surveillance and highlight iNKT cell frequency as a prognostic marker for disease p

152 Multivariable analysis identified iNKT cell frequency as an independent predictor of disea

153 We studied the regulatory capacity of human iNKT cells from control subjects and patients with type

154 hird-party mice were as protective as CD4(+) iNKT cells from donor mice although third-party CD4(+) i

155 In vitro, alphaGalCer-stimulated iNKT cells from H2 R-deficient mice secreted higher leve

156 n this study, we report that although thymic iNKT cells from naive mice do not express IL-9, iNKT cel

157 Adoptive transfer of iNKT cells from p47(phox-/-) or NOX2(-/-) mice to Jalpha

158 Moreover, iNKT cells from patients with HHV-8 MCD displayed a prol

159 We found that low numbers of CD4(+) iNKT cells from third-party mice resulted in a significa

160 Notably, CD4(+) iNKT cells from third-party mice were as protective as C

161 transfer of CD4+ invariant natural killer T (iNKT) cells from third-party mice protects from lethal g

162 role in iNKT cell ontogeny, Ly108 regulates iNKT cell function in mice and humans.

163 t this proinflammatory microbiota influences iNKT cell function upon activation during DSS colitis.

164 Invariant NKT (iNKT) cell functional subsets are defined by key transcr

165 The pivotal role of TPL2 in iNKT cell functions is further endorsed by studies using

166 interfered with IL-15 signaling to suppress iNKT cell generation in the thymus.

167 ns mature T cell production and specifically iNKT cell generation in the thymus.

168 e findings indicate that the localization of iNKT cells governs their cytokine response both at stead

169 n was only apparent when dendritic cells and iNKT cells had a loss of SLAM receptor expression.

170 ens in shaping the phenotype and function of iNKT cells has not been described.

171 Runx1-deficient iNKT cells have altered expression of several genes impo

172 ion factors (TFs) Tbet, Plzf, and Rorgammat, iNKT cells have been classified in effector subsets that

173 The functions of iNKT cells have been investigated in mice lacking the Tr

174 Hdac3-deficient iNKT cells have increased cell death that is not rescued

175 Hdac3-deficient iNKT cells have less Cyto-ID staining and lower LC3A/B e

176 gainst infection with S. pneumoniae in which iNKT cells have previously been found to participate.

177 Three subsets of invariant natural killer T (iNKT) cells have been identified, NKT1, NKT2, and NKT17,

178 Invariant NKT (iNKT) cells have been shown to be effective in preventin

179 Cognate iNKT-cell help drives an early, unsustained germinal cen

180 However, the mechanisms which govern iNKT cell homeostasis after thymic emigration are incomp

181 ransfer of lipids onto CD1d, regulates liver iNKT cell homeostasis in a manner dependent on hepatocyt

182 t alterations in lipid metabolism may affect iNKT cell homeostasis through effects on CD1d-associated

183 that Th1-biasing iNKT cell Ags could induce iNKT cell hyporesponsiveness, as long as a minimum antig

184 some bone marrow-derived cells could induce iNKT cell hyporesponsiveness, selective conditions, depe

185 ic cells nor B cells were required to induce iNKT cell hyporesponsiveness.

186 , and Ly9 expression that is associated with iNKT cell hyporesponsiveness.

187 Thus, iNKT cells in adipose tissue are unique regulators of im

188 Here we found that iNKT cells in adipose tissue had a unique transcriptiona

189 We analyzed iNKT cells in both blood (n = 26) and spleen (n = 9) sam

190 and safety of CM-OIT as well as the role of iNKT cells in CM allergy.

191 expression, indirectly suggesting a role for iNKT cells in control of HIV-1 infection.

192 Removal of iNKT cells in H2 R-deficient (CD1d(-/-) H2 R(-/-) ) anim

193 mportance of CD1d-dependent control of liver iNKT cells in maintaining immunological homeostasis in t

194 vivo development and functionality of clonal iNKT cells in mice.

195 This study further extends the importance of iNKT cells in regulating MZ B cell compartment.

196 We investigated the impact of iNKT cells in the natural history of the disease in the

197 hymocytes has been shown to cause absence of iNKT cells in the thymus and periphery due to defective

198 f autophagy, there is reduced progression of iNKT cells in the thymus through the cell cycle, as well

199 e an alternative approach for stimulation of iNKT cells in vitro that allows a significantly improved

200 on the ability of this lipid Ag to stimulate iNKT cells in vivo, with increased IFN-gamma production

201 Invariant NKT (iNKT) cells in healthy people express iNKT-TCRs with wid

202 ritical role for invariant natural killer T (iNKT) cells in switching inflammation to tissue repair i

203 of activated CD1d-restricted invariant NKT (iNKT) cells in the third trimester by administration of

204 iNKT cells indeed hinder CLL survival in vitro by restra

205 se results suggest that IL-2-activated human iNKT cells induce monocytes to produce IL-1beta through

206 Invariant NKT (iNKT) cells influence immune responses in numerous disea

207 iNKT cell interleukin 4 production and GC migration were

208 Transfer of purified Tet2-Tet3 DKO iNKT cells into immunocompetent recipient mice resulted

209 , following identification of IL-9-producing iNKT cells involved in mucosal inflammation, their devel

210 Decline of iNKT cells is associated with age or HIV infection, both

211 d-mediated presentation of lipid antigens to iNKT cells is contributing to the pathology.

212 Importantly, the reduction in Th1-biased iNKT cells is most pronounced, leading to a selective re

213 environmental lipid antigens encountered by iNKT cells is not well defined.

214 The number of Th2-type effector iNKT cells is variable in different strains of mice, and

215 iNKT cells lacking all three miR-17 approximately 92 fam

216 ceramide, strongly activates human and mouse iNKT cells, leading to the assumption that iNKT cell phy

217 However, the iNKT cell ligands have had limited efficacy in human ant

218 or the block in positive selection into the iNKT cell lineage in CD4-cre NKAP conditional knockout m

219 mice with a specific deletion of NKAP in the iNKT cell lineage, leading to severe reductions in thymi

220 ty was a key mechanism for commitment to the iNKT cell lineage.

221 ial cell-intrinsic factor that controlled an iNKT-cell lineage-specific gene-expression program and e

222 genes that were targets of both JunB and the iNKT cell master transcription factor PLZF was UTX depen

223 Therefore, agonism of A2ARs on iNKT cells may be a novel therapeutic strategy to preven

224 Therefore, iNKT cells may constitute an attractive therapeutic targ

225 is associated with susceptibility to severe iNKT cell-mediated hepatitis, thus demonstrating the imp

226 NOX2 plays a key role in inducing iNKT cell-mediated IL-17 production and subsequent lung

227 hereas IL-10 can enhance FOXP3 expression in iNKT cells, mTOR inhibition is solely required for promo

228 r data reveal LEF1 as a central regulator of iNKT cell number and Th2-type effector differentiation.

229 function of CD1d and show increased hepatic iNKT cell numbers as a consequence of altered iNKT cell

230 Loss of Runx1 leads to a severe decrease in iNKT cell numbers in the thymus, spleen and liver.

231 kemia zinc finger transgene does not restore iNKT cell numbers or the block in positive selection int

232 the conditional deletion of the Rictor gene, iNKT cell numbers were reduced in the thymus and periphe

233 o severe reductions in thymic and peripheral iNKT cell numbers.

234 Importantly, however, FOXP3(+) iNKT cells only acquired suppressive abilities when cult

235 including the presence of a CD8(+) subset of iNKT cells only in humans.

236 Thus, in addition to its established role in iNKT cell ontogeny, Ly108 regulates iNKT cell function i

237 sed by unchecked expansion of invariant NKT (iNKT) cells or a unique subset of innate-like CD1d-indep

238 sults in a severe reduction in the number of iNKT cells, particularly of NKT1 cells.

239 neration of iNKT cells, resulting in reduced iNKT cell percentages and numbers in the thymus.

240 -engineered iNKT cells displayed the typical iNKT cell phenotype and functionality.

241 e iNKT cells, leading to the assumption that iNKT cell physiology in human and mouse is similar.

242 iNKT cells play important roles in immune regulation by

243 ly, adoptive transfer of an enriched IL-9(+) iNKT cell population leads to exacerbated allergic infla

244 hway, we observed a profound decrease in the iNKT cell population.

245 H3K27me3 leads to a drastic reduction of the iNKT cell population.

246 ing intestinal inflammation, it appears that iNKT cells protect from Th1-mediated inflammation but ex

247 Invariant Natural killer T (iNKT) cells rapidly produce copious amounts of multiple

248 gests that SHIP1 calibrates the threshold of iNKT cell reactivity.

249 the affinity of human CD1d-sulfatide for the iNKT cell receptor is relatively low compared with CD1d-

250 Invariant natural killer T (iNKT) cells recognize endogenous and exogenous lipid ant

251 Invariant natural killer T (iNKT) cells recognize lipid antigens presented by CD1d a

252 with a TH2-polarizing glycolipid agonist of iNKT cells reduced SEB-inflicted morbidity/mortality.

253 anisms regulating such "tonic" activation of iNKT cells remain unclear.

254 Invariant NKT (iNKT) cells represent a subset of innate-like T lymphocy

255 Importantly, iNKT cells responded specifically to rare DCs productive

256 ed animals, while dimaprit dampened the lung iNKT cell response to alphaGalCer.

257 cells, and there is compelling evidence for iNKT cell responses in various types of sterile inflamma

258 c overexpression also impaired generation of iNKT cells, resulting in reduced iNKT cell percentages a

259 CD1d-restricted activation of invariant NKT (iNKT) cells results in the abundant production of variou

260 aken together, our data show that peripheral iNKT cells retain the capacity of shaping their function

261 wild-type iNKT cells but not IFN-gamma(-/-) iNKT cells reversed MZ B cell accumulation in apoE(-/-)

262 together, these findings suggest that innate iNKT cell sensing of HIV-1 infection in DCs is an early

263 iNKT cells, whereas nonsuppressive FOXP3(+) iNKT cells showed a predominance of cytoplasmically loca

264 on of Teff suppression; however, T1D-derived iNKT cells showed impaired regulation that could be attr

265 iNKT cells exhibited impaired expression of iNKT cell signature genes due to a decrease in activatio

266 n stages and predicted to be targeted by the iNKT cell-specific miRNAs.

267 how that IL-2-activated human invariant NKT (iNKT) cells stimulate the secretion of IL-1beta protein

268 cells have been reported to be essential for iNKT cell stimulation, neither dendritic cells nor B cel

269 low CD1d expression on CLL cells and normal iNKT cells, suggesting indirect leukemia control.

270 We identified iNKT cell super-enhancers and demonstrated that UTX-medi

271 We demonstrate that control iNKT cells suppress the proliferation of effector T cell

272 (Dicer KO) in thymocytes selectively impairs iNKT cell survival and functional differentiation.

273 Notch selectively regulates hepatic iNKT cell survival via tissue-restricted control of B ce

274 ine 27 trimethylation (H3K27me3) in coupling iNKT cell TCR specificity with the generation of iNKT ce

275 omoting the development of Th2-like effector iNKT cells that produce IL-4, including those that also

276 ificantly modified program in these neonatal iNKT cells that ultimately led to their malignant transf

277 r 1 (LEF1) in the postselection expansion of iNKT cells through a direct induction of the CD127 compo

278 reveal how UTX regulates the development of iNKT cells through multiple epigenetic mechanisms.

279 to generate a long-term supply of engineered iNKT cells, thus opening up a new avenue for iNKT cell-b

280 Invariant NKT (iNKT) cell thymic development can lead to distinct commi

281 r, these results support the contribution of iNKT cells to CLL immune surveillance and highlight iNKT

282 mediated postselection deletion of Bcl11b in iNKT cells to determine its intrinsic role in these cell

283 te, confirming the ability of IL-9-producing iNKT cells to mediate proinflammatory effects in vivo, a

284 hese mice to investigate the contribution of iNKT cells to metabolic disease and found a pathogenic r

285 The ability of iNKT cells to recognize endogenous antigens represents a

286 Neutrophils can thus license iNKT cells to regulate potentially harmful autoreactive

287 with the reduced capacity of invariant NKT (iNKT) cells to produce IFN-gamma and IL-4 after activati

288 nnate-type invariant natural killer T cells (iNKT cells) to regulate B cell responses.

289 Newly selected iNKT cells undergo a burst of proliferation, which is de

290 luated the consequences of SHIP1 deletion on iNKT cells using germline-deficient mice, chimeric mice,

291 ipulated TCRs in vivo to generate clonotypic iNKT cells using TCR retrogenic chimeras.

292 ression of the death-receptor ligand FasL by iNKT cells was needed to restrict autoantibody productio

293 d reliable in vivo models for studying human iNKT cells, we recently developed the first humanized mo

294 The adipose iNKT cells were a tissue-resident population that induce

295 The total numbers of iNKT cells were reduced in the absence of Bcl11b both in

296 from donor mice although third-party CD4(+) iNKT cells were rejected early after allogeneic HCT.

297 ocalization of FOXP3 in suppressive FOXP3(+) iNKT cells, whereas nonsuppressive FOXP3(+) iNKT cells s

298 may lead to the expansion of IL-10-producing iNKT cells, which could counteract the benefits of incre

299 functional subset of Valpha14 invariant NKT (iNKT) cells with important effector functions in infecti

300 ther innate-like invariant natural killer T (iNKT) cells, with remarkable immunomodulatory properties