ライフサイエンスコーパス: IDO

1 IDO activity was 4-fold higher in patients with tubercul

2 IDO activity was also investigated using L. johnsonii cu

3 IDO deficiency in hypercholesterolemic ApoE(-/-) mice ca

4 IDO derived from endothelial cells promoted apoptosis in

5 IDO expression was primarily limited to the nonlymphocyt

6 IDO has been implicated in diverse processes in health a

7 IDO inhibitors can enhance the efficacy of common cancer

8 IDO inhibitors re-program inflammatory processes to help

9 IDO is therefore a tumor immunotherapeutic target, and s

10 IDO was defective in murine and human CF.

11 IDO-1 is induced in response to inflammatory stimuli and

12 IDO-1 mRNA was extracted from diagnostic bone marrow spe

13 IDO-1 protein expression was assessed in 40 cases via im

14 IDO-mediated production of kynurenine and the kynurenine

15 IDO-TM levels were inversely related to RV ejection frac

16 IDO-TMs also identified RV-PV dysfunction in a validatio

17 Indoleamine 2, 3-dioxygenase 1 (IDO) catalyzes 1 rate-limiting step of L-tryptophan meta

18 ction-induced indoleamine 2,3-dioxygenase-1 (IDO) expression in activated monocytes and dendritic cel

19 Indoleamine 2,3 dioxygenase-1 (IDO-1) is an enzyme in the kynurenine pathway which augm

20 immunosuppressive molecules, such as IL-10, IDO, or PD-1.

21 xygenase 1 and tryptophan 2,3-dioxygenase 2 (IDO/TDO) promotes immunosuppression across different can

22 Starting from HTS hit 5, IDO-1 inhibitor 6 (EOS200271/PF-06840003) has been devel

23 H(2)O(2) produced by L. johnsonii abolished IDO activity in vitro, and L. johnsonii feeding resulted

24 Additionally, L. donovani activates IDO/kynurenine/AHR signaling in BMM s to maintain prolon

25 Furthermore, we demonstrated that the AhR-IDO pathway was responsible for the preferential activat

26 allergens and lectins modulate the TLR4-AhR-IDO axis in human monocyte-derived DCs.

27 ole for MR in the modulation of the TLR4-AhR-IDO axis, which has a significant effect on DC behavior

28 press macrophage functions via the TNF-alpha/IDO axis, thereby providing a physiologically relevant c

29 Our results suggest that RT alters IDO-mediated immune status in NSCLC patients and that ch

30 An IDO inhibitor (1-methyl-tryptophan) restored IDO-positiv

31 early in bacterial cystitis by eliciting an IDO-mediated increase in local production of kynurenines

32 linical candidate 6 shows good potency in an IDO-1 human whole blood assay and also shows a very favo

33 ted peripheral blood mononuclear cells in an IDO-dependent manner.

34 We also studied PASMC phenotype in an IDO-high in vivo and in vitro tissue microenvironment.

35 ive capability and stably induced IL-10- and IDO-expressing lymphocytes that maintained their phenoty

36 Both cyclooxygenase-derived PGE(2) and IDO help to induce T(R)1-like cells by MSCs.

37 tory T-cell pathways (i.e. PD-1, CTLA-4, and IDO); and (iv) adoptive cell transfer therapy with T cel

38 pathways downstream of CD80/CD86 in IL-6 and IDO production, identification of a novel cross-talk bet

39 posing roles they play by producing IL-6 and IDO upon their activation, how CD80/CD86 signal remains

40 NG gene ablation abolished IFN-alphabeta and IDO induction by dendritic cells (DCs) after DNA nanopar

41 ciencies in both apolipoprotein e (Apoe) and IDO (Apoe(-/-)/IDO(-/-)) were generated by cross-breedin

42 To evaluate the histological changes and IDO expression, respectively, periodic acid schiff stain

43 significantly increased kynurenine level and IDO activity as compared to healthy controls and mastocy

44 pe 2 molecules (arginase 1, Fizz 1, Mgl, and IDO), number of M2-type macrophages and granulocytic mye

45 chemistry of indole dioxygenation by TDO and IDO, challenging the widely accepted categorization of t

46 ght to be the active oxidant in both TDO and IDO, which, following O-O bond cleavage, presumably gene

47 ctions of 3-HAA into Apoe(-/-) and Apoe(-/-)/IDO(-/-) mice for 6 weeks increased the expression and a

48 h apolipoprotein e (Apoe) and IDO (Apoe(-/-)/IDO(-/-)) were generated by cross-breeding IDO(-/-) mice

49 AAA in Apoe(-/-) mice, but not in Apoe(-/-)/IDO(-/-) mice, which presented decreased elastic lamina

50 As IDO enhancement was most notable when cells were continu

51 avoximod, that were first to be evaluated as IDO inhibitors in clinical trials.

52 have important clinical implications because IDO inhibitors are used to treat cancer in clinical tria

53 itory mediators, including IL-10, TGF-beta1, IDO, and programmed death ligand 2, T. cruzi infection i

54 In 2-year biopsies, IDO expression was mainly found in infiltrating inflamma

55 Both IDO and kynureninase controlled the production of 3-HAA

56 In contrast, both IDO enzymatic activity and IFN-gamma-induced AhR express

57 We have demonstrated that LPS induces both IDO isoforms (IDO1 and IDO2) in DCs, with partial involv

58 PS-primed DCs, induced higher levels of both IDO isoforms together with the transcription factor aryl

59 IDO inhibitors to mediate rejection of both IDO-expressing and nonexpressing poorly immunogenic tumo

60 cytokine expression in the liver and brain, IDO activation, and brain-derived neurotrophic factor (B

61 )/IDO(-/-)) were generated by cross-breeding IDO(-/-) mice with Apoe(-/-) mice.

62 d the tolerogenic phenotype was conferred by IDO.

63 Zn triggered tryptophan degradation by IDO and kynurenine production by DCs and strongly suppre

64 ases, we found that in patients with cancer, IDO is preferentially upregulated compared with KYNU, wh

65 to the poor prognosis of tumors coexpressing IDO and SLC1A5.

66 In conclusion, 'composite IDO-1 score' is a prognostic tool that can help identify

67 her IDO-1 mRNA (p = 0.005), higher composite IDO-1 score (p < 0.0001) and not undergoing allogeneic s

68 e aforementioned variables, higher composite IDO-1 score (p = 0.007) and not undergoing allogeneic SC

69 ts who failed induction had higher composite IDO-1 score (p = 0.01).

70 emistry and quantified by a novel 'composite IDO-1 score'.

71 d AhR expression were required for continued IDO transcription in vitro and in vivo.

72 h a receiver operating characteristic curve, IDO activity had a sensitivity of 97%, a specificity of

73 ibitory role of both tumor- and host-derived IDO.

74 Six months before tuberculosis diagnosis, IDO activity was significantly higher in all patients wh

75 At the time of tuberculosis diagnosis, IDO activity was significantly higher in patients with t

76 icle, we examine the effect of two different IDO enzymes, IDO1 and IDO2, on the development of autoim

77 e expression of indoleamine-2,3-dioxegenase (IDO) 1, an immune regulator known for driving maternal-f

78 Indoleamine 2,3 dioxygenase (IDO) and arginase 1 (ARG1), which catabolize Trp and Arg

79 sing the enzyme indoleamine 2,3 dioxygenase (IDO) can mediate potent local effects on innate and adap

80 mma (IFNgamma), indoleamine 2,3 dioxygenase (IDO), and human leukocyte antigen G (HLA-G) was determin

81 hanisms such as indoleamine 2,3 dioxygenase (IDO).

82 CD274/PD-L1 and indoleamine 2,3 dioxygenase (IDO).

83 nzymes [i.e. the indolamine-2,3 dioxygenase (IDO)1 and IDO2) in the placenta.

84 g, can regulate indoleamine 2,3-dioxygenase (IDO) activity, favoring TH2 responses.

85 their increased indoleamine 2,3-dioxygenase (IDO) activity.

86 cules including indoleamine 2,3-dioxygenase (IDO) and programmed cell death ligand 1 (PD-L1), and res

87 ough the enzyme indoleamine 2,3-dioxygenase (IDO) and subsequent production of kynurenine.

88 ges can express indoleamine 2,3-dioxygenase (IDO) and thus actively deplete their own tryptophan supp

89 y expression of indoleamine 2,3-dioxygenase (IDO) and tryptophan 2,3-dioxygenase (TDO) resulted in AT

90 The enzyme indoleamine-2,3-dioxygenase (IDO) catalyses degradation of the essential amino acid t

91 urine biomarker indoleamine 2,3-dioxygenase (IDO) enzyme activity and peripheral blood CD4-ATP levels

92 Additionally, indoleamine 2,3-dioxygenase (IDO) expression was only modestly increased in a brain r

93 abolism through indoleamine 2.3-dioxygenase (IDO) has been previously proposed to predict acute rejec

94 Indoleamine 2,3-dioxygenase (IDO) has immunoregulatory roles associated with tryptoph

95 ulatory enzyme, indoleamine 2,3-dioxygenase (IDO) in dermal fibroblasts generates a tryptophan-defici

96 gulatory enzyme indoleamine 2,3-dioxygenase (IDO) in plasmacytoid DCs and the CCL22 chemokine in myel

97 with NLG919, an indoleamine 2,3-dioxygenase (IDO) inhibitor currently used for reversing tumour immun

98 ics, radiation, indoleamine 2,3-dioxygenase (IDO) inhibitors, inhibitors of T cell checkpoints, agoni

99 The heme enzyme indoleamine 2,3-dioxygenase (IDO) is a key regulator of immune responses through cata

100 Indoleamine 2, 3-dioxygenase (IDO) is an immunoregulatory enzyme that breaks down tryp

101 Indoleamine 2,3-dioxygenase (IDO) is the enzyme that catalyzes the degradation of try

102 Indoleamine 2,3-dioxygenase (IDO) is the first and rate-limiting enzyme in the kynure

103 ibitory role of indoleamine 2,3-dioxygenase (IDO) on the antitumor efficacy of CTLA-4 blockade.

104 munosuppressive indoleamine 2,3-dioxygenase (IDO) pathway.

105 enase (TDO) and indoleamine 2,3-dioxygenase (IDO) play a central role in tryptophan metabolism and ar

106 atabolic enzyme indoleamine 2,3-dioxygenase (IDO) represent a vanguard of new immunometabolic adjuvan

107 relationship of indoleamine 2,3-dioxygenase (IDO) systemic activity on clinical outcomes in RT-treate

108 egrading enzyme indoleamine 2,3-dioxygenase (IDO) were analyzed using flow cytometry and quantitative

109 ation activates indoleamine 2,3-dioxygenase (IDO) which metabolizes tryptophan into kynurenine.

110 e expression of indoleamine 2,3-dioxygenase (IDO), a known immunosuppressor, was significantly higher

111 and activity of indoleamine-2,3-dioxygenase (IDO), a primary mediator of MSC immunomodulatory functio

112 al induction of indoleamine 2,3-dioxygenase (IDO), a tryptophan catabolic enzyme previously shown to

113 igher levels of indoleamine 2,3-dioxygenase (IDO), an enzyme associated with tolerance induction.

114 e expression of indoleamine 2,3-dioxygenase (IDO), an enzyme involved in tryptophan catabolism, in ma

115 Expression of indoleamine-2,3-dioxygenase (IDO), an immunosuppressive enzyme in human tumors, leads

116 the activity of indoleamine 2,3-dioxygenase (IDO), an intracellular enzyme that converts tryptophan i

117 itor of indoleamine-pyrrole 2,3-dioxygenase (IDO), but not by NSC-398, a specific inhibitor of COX-2,

118 enase (TDO) and indoleamine 2,3-dioxygenase (IDO), during its conversion to N-formylkynurenine in the

119 t that inhibits indoleamine 2,3-dioxygenase (IDO), encapsulated in the nMOF channels to induce system

120 ncentrations of indoleamine 2,3-dioxygenase (IDO), KYN, kynurenic acid (KynA), and quinolinic acid (Q

121 e expression of indoleamine 2,3-dioxygenase (IDO), the first enzyme in the kynurenine pathway of tryp

122 Indoleamine 2,3-dioxygenase (IDO), the rate-limiting enzyme in the tryptophan-kynuren

123 Indoleamine 2,3-dioxygenase (IDO), which degrades tryptophan (Trp) to kynurenine (Kyn

124 pressive enzyme indoleamine 2,3-dioxygenase (IDO), which depletes local pools of the essential amino

125 ith circulating indoleamine 2,3-dioxygenase (IDO)-dependent tryptophan metabolites (TMs), tricarboxyl

126 oduced from the indoleamine 2,3-dioxygenase (IDO)-mediated kynurenine pathway and are present in the

127 n of the enzyme indoleamine-2,3-dioxygenase (IDO).

128 bolizing enzyme indoleamine-2,3-dioxygenase (IDO).

129 gulatory enzyme indoleamine-2,3-dioxygenase (IDO).

130 e production of indoleamine 2,3-dioxygenase (IDO).

131 bolizing enzyme indoleamine 2,3-dioxygenase (IDO).

132 han catabolism, indoleamine 2,3-dioxygenase (IDO).

133 bolizing enzyme indoleamine 2,3-dioxygenase (IDO).

134 PD-L1; Tim-3; indoleamine 2, 3-dioxygenase (IDO); and interleukin 10.

135 enzymes such as indoleamine 2,3-dioxygenase (IDO-1) to induce an immunosuppressive environment.

136 2,3-dioxygenase/tryptophan 2,3-dioxygenase (IDO/TDO) inhibitors.

137 ed before CART administration, downregulated IDO expression in lymphoma cells and improved the antitu

138 tory mechanisms contributed to dysfunctional IDO activity that, in turn, correlated with imbalanced T

139 othelium was the primary site for endogenous IDO production within mouse lung, and the mice lacking t

140 ermine the therapeutic effect of endothelial IDO in hypoxia-induced PH in mice and monocrotaline-indu

141 coids, budesonide or dexamethasone, enhanced IDO expression following IFN-gamma stimulation in multip

142 microparticles and exhibited 4-fold enhanced IDO activity compared to budesonide preconditioned and n

143 Treatments enhancing IDO function or preventing pathogenic Th17-cell activati

144 ered activity of the immunomodulatory enzyme IDO.

145 Conversely, the immunoregulatory enzyme IDO blocked loss of Eos and prevented the Eos-labile Tre

146 F-beta1, and IL-2) and a tolerogenic enzyme (IDO) in bone marrow-derived dendritic cells as well as s

147 PD-L2, and the tryptophan degrading enzyme, IDO.

148 e used a xenograft lymphoma model expressing IDO as a transgene.

149 schiff staining and immunohistochemistry for IDO were performed on biopsies taken at 6 months and 2 y

150 the reconstitution of bone marrow cells from IDO(+/+) mice.

151 staining with the antibodies against 3-HAA, IDO, and kynureninase than those in adjacent nonaneurysm

152 tolerance process, and we presume that high IDO activity is associated with nonresponsiveness to foo

153 , high risk cytogenetics (p = 0.002), higher IDO-1 mRNA (p = 0.005), higher composite IDO-1 score (p

154 How IDO deficiency affects immune responses during atherogen

155 rs characterized by low antigenicity and how IDO inhibition can overcome this state by attenuating tu

156 observed in UVA-irradiated lenses from human IDO/human sodium-dependent vitamin C transporter-2 mice,

157 of IDO-expressing cells or recombinant human IDO (rIDO) to H(2)O(2) inhibited dioxygenase activity in

158 X-ray crystal structure of 6 bound to human IDO-1, which shows that 6, differently from most of the

159 e known to promote Treg expansion identified IDO-positive dendritic cells as the primary mediator of

160 This study identifies IDO as a heme peroxidase that, in the absence of substra

161 teins also inhibited PIV3, including IFITM1, IDO (indoleamine 2,3-dioxygenase), PKR (protein kinase,

162 ed the expression and secretion of IFNgamma, IDO, and HLA-G.

163 regulatory and effector pathways illuminate IDO as an inflammatory modifier.

164 In IDO knockout mice treated with anti-CTLA-4 antibody, we

165 hat the AHR pathway is selectively active in IDO/TDO-overexpressing tumors and is associated with res

166 s, we investigated the role of MR and AhR in IDO regulation and its effect on T helper cell different

167 eamine 2,3-dioxygenase, and was confirmed in IDO-KO mouse model.

168 in immune modulation, has been implicated in IDO activation in response to TLR stimulation.

169 sma and aortas of Apoe(-/-) mice, but not in IDO(-/-) mice.

170 ngs suggest that blocking the AHR pathway in IDO/TDO expressing tumors would overcome the limitation

171 Selective AHR blockade delays progression in IDO/TDO-overexpressing tumors, and its efficacy is impro

172 In vivo kynurenine supplementation in IDO-deficient mice abrogates the protective effects of I

173 daptive immune regulatory factors, including IDO-1, arginase-1, Foxp3, TGF-beta, IL-10, and decreased

174 neoantigen-expressing LLC, nor did it induce IDO in TDLN.

175 promote growth of B16 melanoma or to induce IDO activity in TDLN in this setting.

176 Although STING also induced IDO in tumor-draining lymph nodes (TDLN) during EL4 thym

177 lysosome fusion, inhibited poly I:C-induced IDO and HLA-G expression, whereas cycloheximide and a TL

178 o IL-6, we have found that CD80/CD86-induced IDO production by DC at late time points is also depende

179 CLL cells induced IDO(hi) MDSCs from healthy donor monocytes suggesting bi

180 from Tfh cell differentiation system induced IDO expression on MSCs.

181 d via STING to suppress immunity by inducing IDO.

182 blocking glutamine metabolism also inhibited IDO expression of both the tumor and myeloid-derived cel

183 CD19-CARTs inhibited IDO-negative tumor growth but had no effect on IDO-posit

184 stant human ovarian cancer cells, inhibiting IDO by transcriptional deregulation of the autocrine-sig

185 Interestingly, IDO expression was significantly augmented in macrophage

186 d by an IFN-gamma-induced pathway, involving IDO, and that regulatory T cell activities may also regu

187 This IFN-gamma-licensed veto property is IDO-dependent.

188 ex, and body mass index (BMI), post-ketamine IDO levels were significantly lower than baseline at all

189 enhance T cell activation, followed by later IDO production to self-limit this activation.

190 The in vivo experiments revealed that local IDO expression delivered by lentiviral vector prolonged

191 deregulation of the autocrine-signaling loop IDO-AHR-IL6, which blocks kynurenine production and prom

192 of the kynurenine-AhR pathway in maintaining IDO expression in tolerogenic DC.

193 induction of the anti-inflammatory mediators IDO, IL-10, and PGE2 in a COX-2-dependent manner.

194 gulate their IDO activity, we found that MSC IDO catalytic function is dispensable with regard to MSC

195 itate the structure-based drug design of new IDO inhibitors.

196 creased expression of KATII and KMO, but not IDO, in vitro in BDV-infected C6 astroglioma cells.

197 ation may modulate the biological actions of IDO expressed in inflammatory tissues where the levels o

198 eral blood, spleen and lymph node B cells of IDO-deficient compared with IDO-competent ApoE(-/-) mice

199 of the immune system with the combination of IDO inhibition by the small-molecule immunotherapy agent

200 However, the precise contributions of IDO function to autoimmunity remain unclear.

201 a (AML) have shown a negative correlation of IDO-1 mRNA expression with outcomes.

202 cardiomyocyte or myeloid cell deficiency of IDO and challenged with acute myocardial infarction.

203 boring endothelial cell-specific deletion of IDO show an improvement of cardiac function as well as c

204 r tryptophan metabolism enzyme downstream of IDO, L-kynureninase (KYNU), is heavily upregulated.

205 The antiviral effect of IDO, the enzyme that catalyzes the first step of tryptop

206 ent mice abrogates the protective effects of IDO deletion.

207 Exposure of IDO-expressing cells or recombinant human IDO (rIDO) to

208 feron-gamma, which induced the expression of IDO and kynureninase and increased 3-hydroxyanthranilic

209 omotes their ability to induce expression of IDO by dendritic cells.

210 Expression of IDO gene was measured by real-time PCR.

211 The expression of IDO suppressed the proliferation of alloantigen-stimulat

212 Distinct loss of function of IDO in smooth muscle cells, inflammatory cells, or cardi

213 2)O(2)) activates the peroxidase function of IDO to induce protein oxidation and inhibit dioxygenase

214 nter-regulatory and tolerogenic functions of IDO can be targeted for cancer immunotherapy and present

215 ation, in human and murine CF, the impact of IDO on lung inflammation and immunity in murine CF, and

216 esponse to apoptotic cells and the impact of IDO on Treg cell function.

217 bits T cell effector function independent of IDO but through the ligands for PD1.

218 ith C4BP(beta(-)) prevented the induction of IDO and BIC-1, whereas TGF-beta1 expression was maintain

219 In agreement, inhibition of IDO activity or depletion of Tregs restored disease susc

220 ic deletion or pharmacological inhibition of IDO limits cardiac injury and cardiac dysfunction after

221 ults imply the probability of involvement of IDO in development of tolerance process, and we presume

222 erapies using IDO inhibitors irrespective of IDO expression by the tumor cells.

223 ells, which correlates with higher levels of IDO in CCL22-expressing islet grafts.

224 Long-term maintenance of IDO expression was found to be independent of exogenous

225 viously shown to be an essential mediator of IDO-dependent, long-term tolerance.

226 C-type lectin receptor-induced modulation of IDO activity in DCs.

227 Extended monitoring of IDO(+) DC in the tumor-draining lymph nodes of IL-12 plu

228 The frequency of genetic polymorphisms of IDO did not reveal a significant association with Trp, K

229 Here, we investigate the potential of IDO/trp degradation along the kynurenine (kyn) pathway t

230 pling demonstrated transpulmonary release of IDO-TMs.

231 However, the role of IDO in food allergy has not yet been elucidated.

232 mor microenvironment, we examine the role of IDO in response to apoptotic cells and the impact of IDO

233 Here we investigated the role of IDO in shaping DCs phenotype and function under endotoxi

234 ta demonstrate the immunosuppressive role of IDO in the context of immunotherapies targeting immune c

235 caque model of inhalation TB, suppression of IDO activity reduced bacterial burden, pathology, and cl

236 Furthermore, we could show upregulation of IDO mediated by AhR engagement.

237 atory neutrophils and the concomitant use of IDO to modulate inflammation.

238 nd PD-L2 - which were partially dependent on IDO.

239 O-negative tumor growth but had no effect on IDO-positive tumors.

240 ould explain the regulatory effects of MR on IDO expression.

241 feration, primarily via indoleamine oxidase (IDO).

242 to dissect the molecular basis of persistent IDO expression in post-IL-12 DC.

243 Plasma IDO activity is suitable as a biomarker of active tuberc

244 ree supernatant (CFS) with affinity-purified IDO and HT-29 intestinal epithelial cells.

245 ve immunohistochemical technique to quantify IDO-1 expression on diagnostic bone marrow biopsies of A

246 L. johnsonii CFS significantly reduced IDO activity in HT-29 intestinal epithelial cells (47% r

247 n in multiple donors and was able to restore IDO expression in over-passaged MSCs.

248 IDO inhibitor (1-methyl-tryptophan) restored IDO-positive tumor control.

249 We found the impact of RT on these serum IDO markers to be heterogeneous in patients.

250 tumor immunotherapeutic target, and several IDO inhibitors are currently undergoing clinical trials.

251 mors would overcome the limitation of single IDO or TDO targeting agents and constitutes a personaliz

252 tients can potentially benefit from specific IDO-1 inhibitor therapy, currently in clinical trials.

253 let grafts were prepared by embedding stable IDO-expressing fibroblasts and allogeneic islets into a

254 ional composite scaffold within which stable IDO-expressing fibroblasts serve as source of local immu

255 ur novel matrix that is equipped with stable IDO-expressing fibroblasts prolongs allograft survival.

256 As such, IDO-1 is a nexus for the induction of a key immunosuppre

257 8, a specific inhibitor of COX-2, suggesting IDO as a mediator.

258 : Radiotherapy appears to influence systemic IDO activity and to exert a significant impact on metast

259 We measured systemic IDO activity (calculated as the ratio of plasma levels o

260 In vitro, sCD83 induced long-term IDO expression in both conventional and plasmacytoid den

261 IDO activity was blocked restored long-term IDO expression in wild-type DC but not in AhR-deficient

262 We demonstrate that IDO-Kyn-AHR-mediated immunosuppression depends on an int

263 We hypothesized that IDO could play a key role to locally regulate cardiac ho

264 Recent findings reveal that IDO can be triggered by innate responses during tumorige

265 series of in vitro experiments revealed that IDO-expressing fibroblasts do not compromise islet funct

266 Here, we show that IDO activity induced by STING activity in the tumor micr

267 These data suggest that IDO could constitute a new therapeutic target during acu

268 cells in vivo and in vitro, suggesting that IDO may induce immunoregulatory functions of B cells in

269 Culture of PBMC experiments yielded that IDO mRNA expression was not different between tolerant a

270 This is accomplished by conjugating the IDO inhibitor, indoximod (IND), to a phospholipid that a

271 Instead, metabolites in the IDO pathway, particularly L-kynurenine, directly suppres

272 ergistic with Indoximod (IND) inhibiting the IDO pathway to activate immune response for immunotherap

273 h shows that 6, differently from most of the IDO-1 inhibitors described so far, does not bind to the

274 We show that the IDO pathway induces production of IL-10 in B cells in vi

275 ese findings support the hypothesis that the IDO-GCN2 pathway in glomerular stromal cells is a critic

276 ugh IFN-gamma-licensed MSCs upregulate their IDO activity, we found that MSC IDO catalytic function i

277 We show that kynurenine generation through IDO is markedly induced after MI in mice.

278 Tissue IDO was investigated using quantitative RT-PCR and Weste

279 t whereas IFN-gamma induction was transient, IDO expression in DC was maintained long-term.

280 After 6 months of tuberculosis treatment, IDO activity in patients with tuberculosis declined to l

281 Kyn/Trp (IDO activity) was significantly lower in subjects with f

282 Because tumor IDO inhibits CD19-CARTs, antagonizing this enzyme may be

283 To investigate the effects of tumor IDO on CD19-CART therapy, we used a xenograft lymphoma m

284 Understanding IDO inhibitors as adjuvants to turn immunologically 'col

285 by FICZ reduces FcepsilonRI and upregulates IDO expression in LC.

286 gest that there exists a potential for using IDO inhibition as an effective and clinically relevant h

287 ype, cytokine profile, immunogenicity (using IDO activity as a surrogate), and downstream T cell pola

288 inically explore combination therapies using IDO inhibitors irrespective of IDO expression by the tum

289 t that targeting pathogenic inflammation via IDO-mimetic drugs may benefit patients with CF.

290 ous production of tryptophan metabolites via IDO is an essential feedback loop that controls atheroge

291 We investigated whether IDO activity, as measured by the ratio of Kyn to Trp, co

292 Here, we investigated the mechanism by which IDO induction attenuates PMN migration.

293 Local tryptophan limitation, by which IDO is known to influence T cell longevity and prolifera

294 current understanding of mechanisms by which IDO participates in the control of inflammation and in p

295 atabolite kynurenine to DC cultures in which IDO activity was blocked restored long-term IDO expressi

296 olic adjuvants to widen therapeutic windows, IDO inhibitors may leverage not only immuno-oncology mod

297 node B cells of IDO-deficient compared with IDO-competent ApoE(-/-) mice.

298 is preferentially upregulated compared with IDO.

299 Dioxygenase inhibition correlated with IDO-catalyzed H(2)O(2) consumption, compound I-mediated

300 hat CTLA-4 blockade strongly synergizes with IDO inhibitors to mediate rejection of both IDO-expressi