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 ear transfer, have increased tissue resident iNKT cells.

3 new biologically relevant lipid self-Ags for iNKT cells.

4 tive burst, differentiation and functions of iNKT cells.

5 sue resident and CD69(-) S1P1(+) nonresident iNKT cells.

6 ant expansion of effector cytokine-producing iNKT cells.

7 induction of the purinergic receptor P2X7 on iNKT cells.

8 oside GD3-as endogenous activators for mouse iNKT cells.

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

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

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

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

13 ion and effector differentiation programs of iNKT cells.

14 lish whether they have potential to activate iNKT cells.

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

16 improved detection of cytokines produced by iNKT cells.

17 demonstrated markedly less antigenicity for iNKT cells.

18 development and effector differentiation of iNKT cells.

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

20 ment of biomarkers or therapeutics targeting iNKT cells.

21 geneity and its influence on CD1d-restricted iNKT cells.

22 ells (HSCs) to provide a continual source of iNKT cells.

23 -Jalpha18 rearrangements of human and murine iNKT cells.

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

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

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

27 g lipid-reactive invariant natural killer T (iNKT) cells.

28 ttributed to a deficiency in invariant NK T (iNKT) cells.

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

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

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

32 Invariant natural killer T (iNKT) cells acquire effector functions during developmen

33 In summary, in vivo iNKT cells activated mTORC1 in NK cells to produce IFN-g

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

35 ous lipid species, which results in enhanced iNKT cell activation both in vitro and in vivo.

36 viously unidentified mechanism that controls iNKT cell activation during sterile inflammation.

37 ogen-derived lipid antigens that can trigger iNKT cell activation under sterile and nonsterile condit

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

39 Y108 costimulation similarly increased human iNKT cell activation.

40 in cytoskeleton and correlates with enhanced iNKT cell activation.

41 cell surface, which contributes to enhanced iNKT cell activation.

42 1,3,4-nonanetriol] (OCH), a T(H)2-polarizing iNKT cell agonist, before they received alpha-galactosyl

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

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

45 These iNKT cell alterations were associated with an imbalance

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

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

48 cells as well as invariant natural killer T (iNKT) cells and mucosal-associated invariant T (MAIT) ce

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

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

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

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

53 Defective antigen presentation and decreased iNKT cells are also observed in ASM-deficient humans wit

54 cificity differences between mouse and human iNKT cells are conserved between pigs and humans, indica

55 108 interactions between dendritic cells and iNKT cells are critical for robust activation.

56 We found that iNKT cells are divided into CD69(+) sphingosine-1-phosph

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

58 The numbers of CD1d-restricted iNKT cells are tightly controlled in mucosal tissues, bu

59 Human invariant natural killer T (iNKT) cells are a rare innate-like lymphocyte population

60 Invariant natural killer T (iNKT) cells are a specialized subset of T cells contribu

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

62 Invariant natural killer (iNKT) cells are among the first innate immune cells to e

63 Invariant NKT (iNKT) cells are an innate-like population characterized

64 Invariant NKT (iNKT) cells are attractive therapeutic targets in sepsis

65 Invariant NKT (iNKT) cells are innate lipid-reactive T cells that devel

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

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

68 Invariant natural killer T (iNKT) cells are innate-like lymphocytes with unique sign

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

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

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

72 Invariant NKT (iNKT) cells are innate-like T lymphocytes that recognize

73 Invariant natural killer T (iNKT) cells are potent immune cells for targeting cancer

74 Semi-invariant natural killer T (iNKT) cells are self-reactive lymphocytes, yet how this

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

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

77 our results have identified double-negative iNKT cells as promising cellular targets to prevent AD p

78 rter platform which, compared to traditional iNKT cell assays, is characterized by a shorter turnarou

79 This positions iNKT cells at an apex to support or inhibit B cell respo

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

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

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

83 c requirement for IL-18 signaling by splenic iNKT cells but not liver iNKT cells, suggesting that the

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

85 We stimulated iNKT cells by cognate glycolipid antigen alpha-galactosy

86 The regulation of iNKT cells by vitamin A by the P2X7 pathway is important

87 ntional T cells, which require TCR ligation, iNKT cells can also be stimulated independently of their

88 n this study, we exploited the fact that pig iNKT cells can be purified using a mouse CD1d tetramer r

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

90 We propose a new concept in which iNKT cells can rapidly respond to pre-existing self-mole

91 iNKT cells can serve both as helpers for effector B cell

92 livestock with an established invariant NKT (iNKT) cell-CD1d system.

93 Reduced iNKT cell CD4+ subsets as a result of HIV-1 infection ma

94 These HSC-iNKT cells closely resembled endogenous human iNKT cells

95 iNKT cells constitutively express high levels of Nr4a1-e

96 hypothesis that invariant natural killer T (iNKT) cells contribute to innate immune dysfunction asso

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

98 NKT cells closely resembled endogenous human iNKT cells, could deploy multiple mechanisms to attack t

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

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

101 y long-lasting contacts (12 to 24 h) between iNKT cells, DCs, and CD8(+) T cells occurring in a 3-way

102 , the symptomatic corneas CD1d KO mice, with iNKT cell deficiency, had increased levels of the inflam

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

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

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

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

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

108 mitochondrial homeostasis and quiescence in iNKT cell development and effector lineage differentiati

109 tablishment of quiescence programs underlies iNKT cell development and effector maturation.

110 y not only confirmed the role of miR-183C in iNKT cell development and function but also demonstrated

111 istic CD1d-associated lipids is critical for iNKT cell development and function in vivo and represent

112 but the role played by individual miRNAs in iNKT cell development and function is still not clear.

113 on, mTEC specialization controls intrathymic iNKT cell development and function, and determines iNKT

114 ritical involvement of microRNAs (miRNAs) in iNKT cell development and function, but the role played

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

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

117 iNKT cell development uniquely depends on interactions b

118 7(tg) (Nur77(tg);Valpha14(tg)) mouse rescued iNKT cell development up to the early precursor stage, s

119 of Mst1 alone or together with Mst2 impedes iNKT cell development, associated with defective IL-15-d

120 ce with miR-183C deletion showed a defective iNKT cell development, sublineage differentiation, and c

121 RNA 183 cluster (miR-183C) expression during iNKT cell development.

122 how this transcription factor controls early iNKT cell development.

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

124 bolism that are dynamically regulated during iNKT cell development.

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

126 on (Nur77(tg)) in mouse thymocytes abrogates iNKT cell development.

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

128 nd found that both monoclonal and polyclonal iNKT cells differentiated into functional subsets that f

129 However, iNKT cell differentiation was biased toward the iNKT2/17

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

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

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

133 Specifically, iNKT cells drive B cell proliferation, class switch, and

134 We found iNKT cell-driven expansion of pre-mNK cells to be depend

135 Our findings suggest that Shp1 controls iNKT cell effector differentiation independently of posi

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

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

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

139 In vitamin A deficiency, iNKT cells fail to express P2X7 and are, therefore, resi

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

141 e potential to provide therapeutic levels of iNKT cells for a patient's lifetime.

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

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

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

145 Relatively increased iNKT cell frequency in patients with HIV-1 infection and

146 Consistent with this, iNKT cells from different organs show distinct basal act

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

148 By analysing iNKT cells from lymphoid tissues of mice and humans we d

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

150 We detected iNKT cells from tissues in which they are rare, includin

151 Adoptive transfer experiments confirmed that iNKT cells from Valpha14(Tg) mice but not from Vbeta8(Cg

152 Double-negative iNKT cells from Valpha14(Tg) NC mice showed a T helper t

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

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

155 sets as a result of HIV-1 infection may skew iNKT cell functionality toward cytotoxicity.

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

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

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

159 BCL-6-deficient iNKT cells had reduced expression of genes that were ass

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

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

162 TCR-dependent and -independent activation of iNKT cells have been relatively well established, the ex

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

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

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

166 Invariant natural killer T (iNKT) cells have been tested for their potential use in

167 Invariant NKT (iNKT) cells have the unique ability to shape immunity du

168 The CD69(+) S1P1(-) tissue-resident iNKT cells highly express P2X7 and are effectively contr

169 ularly high on intestinal iNKT cells, making iNKT cells highly susceptible to P2X7-mediated cell deat

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

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

172 tify a novel role of vitamin A in regulating iNKT cell homeostasis in many tissues throughout the bod

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

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

175 24:1 ceramide backbone were able to activate iNKT cells in a CD1d-dependent manner.

176 To elucidate the precise role of iNKT cells in AD development of NC mice, we employed two

177 igen presentation and restores the levels of iNKT cells in ASM-deficient mice.

178 iNKT cells in bone marrow chimeras that reconstituted th

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

180 Deletion of iNKT cells in Cd1d-/- mice or inhibition of mTOR by rapa

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

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

183 expression of intestinal immune markers and iNKT cells in CS mice but was not sufficient to restore

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

185 enic structures that drive the activation of iNKT cells in health and disease.

186 iNKT cells in HIV-associated TB had increased surface CD

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

188 that controls the population size of mucosal iNKT cells in mice.

189 derpins the distinct antigen specificity for iNKT cells in peripheral tissues.

190 active TB commencing antiretroviral therapy, iNKT cells in TB-IRIS patients and non-IRIS controls wer

191 iNKT cells in TB-IRIS were CD4+CD8- subset depleted and

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

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

194 he efficient and long-term generation of HSC-iNKT cells in vivo.

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

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

197 Moreover, glycolipid-activated iNKT cells increased the serum concentration of autoanti

198 iNKT cells indeed hinder CLL survival in vitro by restra

199 iNKT cell interleukin 4 production and GC migration were

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

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

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

203 Interestingly, their ability to activate iNKT cells is highly dependent on the ceramide backbone

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

205 The function of Nur77 in iNKT cells is unknown.

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

207 ection in the thymus, resulting in decreased iNKT cell levels and resistance to iNKT cell-mediated in

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

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

210 Tissue-resident iNKT cells maintain tissue homeostasis and peripheral su

211 n of P2X7 is particularly high on intestinal iNKT cells, making iNKT cells highly susceptible to P2X7

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

213 Therefore, iNKT cells may constitute an attractive therapeutic targ

214 Increased CD4- cytotoxic iNKT cells may contribute to immunopathology in TB-IRIS.

215 ur knowledge, our findings shed new light on iNKT cells' mechanism of action and glycolipid-based imm

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

217 decreased iNKT cell levels and resistance to iNKT cell-mediated inflammatory conditions.

218 (ITC), including invariant natural killer T (iNKT) cells, mucosal-associated invariant T (MAIT) cells

219 unique subset of invariant natural killer T (iNKT) cells (NKT2) in the thymus in the steady state, wh

220 T cell-specific deletion of Shp1 had normal iNKT cell numbers and peripheral distribution.

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

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

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

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

225 e, we employed two distinct murine models of iNKT cell over-representation: Vbeta8 TCR congenic and V

226 tant to P2X7-mediated cell death, leading to iNKT cell overpopulation.

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

228 M activity in healthy humans correlates with iNKT cell phenotype.

229 Our study identifies human iNKT cell phenotypes associated with human disease that

230 data revealed novel and previously described iNKT cell phenotypes with distinct functions.

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

232 iNKT cells play important roles in immune regulation by

233 Rather, Shp1 dampened iNKT cell proliferation in response to IL-2, IL-7, and I

234 Invariant NKT (iNKT) cells provide rapid innate T cell responses to gly

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

236 Within peripheral tissues iNKT cell recent thymic emigrants exhibit a different TC

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

238 11 and Vbeta8.2 segments of human and murine iNKT cell receptors.

239 Invariant natural killer T (iNKT) cells recognize activating self and microbial lipi

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

241 n CD8(+) T cells, dendritic cells (DCs), and iNKT cells recruited outside the white pulp; 2) followed

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

243 ss is known about how heterogeneity in human iNKT cells relates to disease.

244 The factors driving the central priming of iNKT cells remain obscure, although strong/prolonged TCR

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

246 nvironment shapes the antigen specificity of iNKT cells remains unknown.

247 CD1d-restricted invariant natural killer T (iNKT) cells represent a heterogeneous population of lipi

248 fferentiation and function of invariant NKT (iNKT) cells require a well-defined set of transcription

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

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

251 While investigating mouse iNKT cell responses to alpha-GalCer in vivo, we found a

252 eramide, the prototypic glycolipid ligand of iNKT cells, result in anergy.

253 hed CD1d-restricted antigen presentation and iNKT cell selection in the thymus, resulting in decrease

254 Invariant natural killer T (iNKT) cells serve as early rapid responders in the innat

255 ptomatic corneas of CD1d KO mice, which lack iNKT cells, showed (i) decreases in the levels of IFN-ga

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

257 or gT) iNKT1 cell subset was the predominant iNKT cell subset in infected asymptomatic corneas.

258 Rgammat(lo) iNKT1 cells were the predominant iNKT cell subset in infected corneas of asymptomatic B6

259 mice born by CS, whereas the invariant NKT (iNKT) cell subset was increased compared with vaginal de

260 ng diverse functions, and the composition of iNKT cell subsets can alter disease outcomes.

261 TANCE We investigated the protective role of iNKT cell subsets in asymptomatic ocular herpesvirus inf

262 The role of the iNKT cell subsets iNKT1, iNKT2, and iNKT17 in herpesviru

263 mined the protective role of cornea-resident iNKT cell subsets using the mouse model of ocular herpes

264 he frequency and function of the three major iNKT cell subsets were analyzed and correlated with symp

265 both quantitative and qualitative changes in iNKT cells such as a biased expansion of the double-nega

266 ceramide shows enhanced fecal IgG1 titers in iNKT cell-sufficient mice.

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

268 ignaling by splenic iNKT cells but not liver iNKT cells, suggesting that there might be diversity, ev

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

270 ta demonstrate that glycolipids which engage iNKT cells support antigen-specific B cell help during i

271 Moreover, the iNKT cell TCR repertoire changes following immunisation

272 Nonetheless, the developing thymic iNKT cells that emerged in these chimeras expressed the

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

274 ch, may be useful for developing human-based iNKT cell therapies for cancer, infectious diseases, and

275 cancer therapy potential of the proposed HSC-iNKT cell therapy and laid a foundation for future clini

276 wed no toxicity or tumorigenicity of the HSC-iNKT cell therapy.

277 hematopoietic stem cell-engineered iNKT (HSC-iNKT) cell therapy with the potential to provide therape

278 ted that miR-183C achieved the regulation of iNKT cells through integrated targeting of multiple sign

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

280 ating that the response of porcine and human iNKT cells to CD1d-restricted Ags may be similar.

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

282 designed a double-hit treatment that allows iNKT cells to escape anergy and exert beneficial effects

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

284 s accumulation of neutrophils, which license iNKT cells to negatively regulate autoreactive B cells v

285 This feature allows iNKT cells to respond even in the absence of glycolipid

286 9 was used for beta2M knock out in JE6-1(REP-iNKT) cells to abrogate CD1d expression and thus excludi

287 als emanating from the TCR to control thymic iNKT cell tolerance induction, terminal differentiation,

288 on factor BCL-6 was transiently expressed in iNKT cells upon exit from positive selection and was req

289 entiating thymic invariant natural killer T (iNKT) cells using single-cell RNA sequencing to produce

290 The proposed approach effectively exploits iNKT cells' versatility in biphasic sepsis and may have

291 Further, activation of iNKT cells via cognate glycolipid during IL-18-mediated

292 Reporter induction in JE6-1(REP-iNKT) cells was assessed by flow cytometry.

293 ffect the direct and indirect stimulation of iNKT cells, we used mice deficient for either MyD88 or t

294 Shp1-deficient iNKT cells were also functionally biased toward the prod

295 frican patients with active TB and controls, iNKT cells were enumerated using alpha-galactosylceramid

296 Circulating iNKT cells were reduced in HIV-1 infection, most signifi

297 Activation of invariant NKT (iNKT) cells with glycolipid antigen drove immunosuppress

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

299 ass of T lymphocytes (MAIT, gammadeltaT, and iNKT cells) with potent antimicrobial and regulatory fun

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