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 degrades tryptophan along the kynurenine pathway.

5 IDO derived from endothelial cells promoted apoptosis in

6 IDO expression was primarily limited to the nonlymphocyt

7 IDO has been implicated in diverse processes in health a

8 IDO induction in response to DNP treatment caused dendri

9 IDO inhibitors can enhance the efficacy of common cancer

10 IDO inhibitors re-program inflammatory processes to help

11 IDO is therefore a tumor immunotherapeutic target, and s

12 IDO was defective in murine and human CF.

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

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

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

16 IDO-mediated production of kynurenine and the kynurenine

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

32 an in turn induce Treg differentiation in an IDO-dependent manner.

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

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

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

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

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

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

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

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

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

42 y peroxidase substrates, NO consumption, and IDO nitration was inhibited by l-Trp.

43 ritic cells, the relationship of CTLA4Ig and IDO in in vivo organ transplantation remains unclear.

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

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

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

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

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

49 As IDO enhancement was most notable when cells were continu

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

51 h initiates the same first step of the KP as IDO-1, has likewise recently been shown to be a mechanis

52 acenta, levels of regulatory markers such as IDO and TGF-beta1 were reduced after anti-B7h monoclonal

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

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

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

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

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

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

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

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

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

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

63 d the tolerogenic phenotype was conferred by IDO.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 r inhibition of indoleamine 2,3 dioxygenase (IDO) activity abrogates graft protection by ECDI-SPs inf

79 tes secretion of indolemine 2,3 dioxygenase (IDO) by pDCs resulting in Treg induction.

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

81 e expression of indoleamine 2,3 dioxygenase (IDO), which is essential for the induction of regulatory

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

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

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

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

86 expression of indoleamine 2, 3-dioxygenase (IDO) and its activity upon transplantation while IDO ove

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 Expression of indoleamine-2,3-dioxygenase (IDO) by vascular endothelium is a newly identified vasom

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

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

93 limiting enzyme indoleamine-2,3-dioxygenase (IDO) expressed in tumor cells or antigen-presenting cell

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

110 The heme enzyme indoleamine 2,3-dioxygenase (IDO) was found to catalyze the oxidation of indole by H(

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

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

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

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

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

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

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

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

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

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

121 d by the enzyme indoleamine 2,3-dioxygenase (IDO), is a critical participant in allergic inflammation

122 transcripts for indolamine-2,3-dioxygenase (IDO), kynurenine 3-monooxygenase (KMO), and kynureninase

123 duction of host indoleamine 2,3-dioxygenase (IDO), the first and rate-limiting enzyme of tryptophan c

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

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

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

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

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

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

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

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

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

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

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

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

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

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 Enhanced endothelial IDO ameliorates PH and its associated vascular structura

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

142 Conversely, augmented pulmonary endothelial IDO expression, through a human IDO-encoding Sleeping Be

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

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

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

146 ered activity of the immunomodulatory enzyme IDO.

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

148 es expression of the immunoregulatory enzyme IDO in dendritic cells, the relationship of CTLA4Ig and

149 was mediated by the immune-regulatory enzyme IDO and TGF-beta.

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

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

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

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

154 tudies revealed a counterregulatory role for IDO during leishmaniasis (restraining effector immune re

155 parasite clearance), and no evident role for IDO in herpes simplex virus type 1 (HSV-1) infection.

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

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

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

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

160 lly delivered into mice, shIDO silences host IDO expression and leads to massive intratumoral cell de

161 How IDO deficiency affects immune responses during atherogen

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

163 e discuss recent progress in elucidating how IDO activity promotes local metabolic changes that impac

164 endothelial IDO expression, through a human IDO-encoding Sleeping Beauty (SB)-based nonviral gene-in

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

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

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

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

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

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

171 al subversion of the host defense (IFNgamma, IDO) by an intracellular pathogen for progression of its

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

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

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

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

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

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

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

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

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

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

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

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

184 UPEC induced IDO expression in human uroepithelial cells and polymorp

185 canonical NF-kappaB pathway directly induces IDO and involves the recruitment of TNF receptor-associa

186 d via STING to suppress immunity by inducing IDO.

187 In the bladders of UPEC-infected IDO-deficient mice, we observed augmented expression of

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

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

190 Interestingly, IDO expression was significantly augmented in macrophage

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

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

193 e of catabolizing tryptophan but are largely IDO-negative.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

221 Pharmacologic inhibition of IDO skewed the immune response to apoptotic cells, resul

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

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

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

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

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

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 munomodulation in vivo by CTLA4Ig depends on IDO.

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

241 rite to promote 3-nitrotyrosine formation on IDO.

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

243 feration, primarily via indoleamine oxidase (IDO).

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

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

246 We observed elevated plasma IDO activity in patients with both pain and depression,

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

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

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

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

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

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

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

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

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

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

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

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

259 8, a specific inhibitor of COX-2, suggesting IDO as a mediator.

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

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

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

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

264 n Caucasians further support the notion that IDO has an important role in cytokine-induced behavioral

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

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

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

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

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

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

275 obulin-transgenic mice were treated with the IDO inhibitor 1-methyltryptophan (1-MT) and monitored fo

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

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

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

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

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

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

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

283 Understanding IDO inhibitors as adjuvants to turn immunologically 'col

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

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

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

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

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

289 ression required licensing and proceeded via IDO-mediated tryptophan catabolism.

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

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

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

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

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

295 and its activity upon transplantation while IDO overexpression in islet allografts restored their lo

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