ライフサイエンスコーパス: IDO

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

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

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

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

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

6 feration, primarily via indoleamine oxidase (IDO).

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

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

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

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

11 is preferentially upregulated compared with IDO.

12 ered activity of the immunomodulatory enzyme IDO.

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

14 d via STING to suppress immunity by inducing IDO.

15 rite to promote 3-nitrotyrosine formation on IDO.

16 munomodulation in vivo by CTLA4Ig depends on IDO.

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

18 d the tolerogenic phenotype was conferred by IDO.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

61 IDO activity was also investigated using L. johnsonii cu

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

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

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

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

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

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

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

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

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

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

72 Enhanced endothelial IDO ameliorates PH and its associated vascular structura

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

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

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

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

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

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

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

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

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

82 gher levels of downstream effector molecules ido and nos2.

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

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

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

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

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

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

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

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

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

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

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

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

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

96 8, a specific inhibitor of COX-2, suggesting IDO as a mediator.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

117 successful conversion to the desired beta-d-ido-configuration found in the target heptopyranoside (2

118 nto one molecule, which include (1) the rare ido-configuration, (2) the unusual 7-carbon backbone, an

119 Biphenyl-substituted L-ido-configured deoxynojirimycin derivatives are selectiv

120 rk, we synthesized a series of D-gluco and L-ido-configured iminosugars N-modified with a variety of

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

122 How IDO deficiency affects immune responses during atherogen

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

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

125 IDO degrades tryptophan along the kynurenine pathway.

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

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

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

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

130 IDO derived from endothelial cells promoted apoptosis in

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

132 n elimination-addition sequence leading to l-ido disaccharide (GH unit) with a total yield of 24% (36

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

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

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

136 As IDO enhancement was most notable when cells were continu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

163 IDO expression was primarily limited to the nonlymphocyt

164 were elevated in tumor-bearing rats, whereas Ido expression was reduced.

165 Interestingly, IDO expression was significantly augmented in macrophage

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

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

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

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

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

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

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

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

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

175 IDO has been implicated in diverse processes in health a

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

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

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

179 The 6-deoxy-beta-d-ido-heptopyranoside related to the capsular polysacchari

180 t successful synthesis of the 6-deoxy-beta-d-ido-heptopyranoside, which could possess interesting imm

181 ino}-3-phenylpropanamido]-7-[6-(4-iodobenzam ido)hexanamido]-2-oxoheptyl 2,4,6-trimethylbenzoate, was

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

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

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

185 o describe the symptoms included Hawan jinin ido ("hypertension of the eye").

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

204 IDO induction in response to DNP treatment caused dendri

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

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

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

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

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

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

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

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

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

214 Understanding IDO inhibitors as adjuvants to turn immunologically 'col

215 IDO inhibitors can enhance the efficacy of common cancer

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

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

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

219 IDO inhibitors re-program inflammatory processes to help

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

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

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

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

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

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

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

227 IDO is therefore a tumor immunotherapeutic target, and s

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

244 IDO-mediated production of kynurenine and the kynurenine

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

269 d the correlation between the yield of the l-ido product and the size of protecting groups used.

270 anoside resulted in exclusive formation of l-ido product with high yield.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

285 pling demonstrated transpulmonary release of IDO-TMs.

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

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

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

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

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

291 IDO was defective in murine and human CF.

292 IkappaBalpha was greater in hippocampus, and Ido was greater in hypothalamus.

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

294 b, IkappaBalpha, indolamine 2,3-deoxygenase [Ido]) was quantified by qPCR in the hippocampus, hypotha

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

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

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

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

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

300 sugars of both configurations (D-gluco and L-ido) with the aim to introduce structural features known