ライフサイエンスコーパス: CIA

1 CIA and EIA stenoses predominantly involved the distal a

2 CIA decreased the Hill coefficient of steady-state force

3 CIA is often considered to be a consequence of the antim

4 CIA was determined in dialysates obtained from wheat (2.

5 CIA was induced in DBA mice by immunization with collage

6 CIA was induced in DBA/1 mice by immunization with type

7 CIA was induced in DBA/1 mice by injection of collagen t

8 CIA was induced in DBA/1J mice by immunization with type

9 CIA(+)/RPR(-)/TP-PA(+) (n = 38) women were more likely t

10 CIA(+)/RPR(-)/TP-PA(-) serology in pregnancy is likely t

11 CIA, EIA, and femoral lesions were not randomly associat

12 CIA-DCs differentially expressed genes associated with i

13 CIA-DCs required programming by CP- and ILF-resident CCR

14 CIA-positive, RPR-negative, TP-PA-negative serology may

15 Upon hip flexion, 23 CIA and 116 EIA stenoses showed kinking (mean amplitude,

16 After repeat testing, 7/31 (23%) CIA-positive, RPR-negative, TP-PA--negative patients ser

17 Among the 77 (49%) CIA(+)/RPR(-)/TP-PA(-) women who were retested, 53% beca

18 Whether this Ca2+-independent activation (CIA) occurs under physiological conditions remains uncle

19 olvation using collision induced activation (CIA), time-resolved hydrogen/deuterium back exchange (HD

20 ed, soluble CFA/I fimbriae protected against CIA as effectively as did Salmonella-CFA/I and found tha

21 -1(-/-)) mice were equally protected against CIA as were wild-type mice, suggesting a limited role fo

22 of IL-17 may explain the protection against CIA afforded by ES-62.

23 published by the Central Information Agency (CIA), including the per capita gross domestic product, t

24 A Compound Identification Algorithm (CIA) was previously developed for automated elemental fo

25 Chemotherapy-induced hair loss (alopecia) (CIA) remains a major unsolved problem in clinical oncolo

26 igh-resolution chemical index of alteration (CIA) records in the sediments of South China prior to th

27 Zr/Al, and the Chemical Index of Alteration (CIA) upon time sequence, suggest enhanced continental we

28 However, the KO mice presented ameliorated CIA in terms of clinical scores, disease incidence, and

29 Co-inertia analysis (CIA) is a multivariate statistical analysis method that

30 ap was also seen between CHIKV arthritis and CIA.

31 hat a regulatory circuit involving FBXL5 and CIA acts through both IRPs to control iron metabolism an

32 hylogenetic analyses reveal that the ISC and CIA pathways are predominantly bacterial, but their cyto

33 licly available microarray studies of RA and CIA.

34 on, baking and in vitro digestion on TIA and CIA were studied.

35 Also, we propose another CIA method that incorporates structure/network informati

36 RA mouse models, collagen-induced arthritis (CIA) and collagen antibody-induced arthritis (CAIA), via

37 e development of collagen-induced arthritis (CIA) and discover cellular and molecular mechanisms of I

38 as determined in collagen-induced arthritis (CIA) and local joint TLR5 ligation models.

39 the rat model of collagen-induced arthritis (CIA) and to evaluate the contribution of neuroimmune int

40 protects against collagen-induced arthritis (CIA) by eliciting two regulatory T cell (Treg) subsets:

41 KLH) study and a collagen-induced arthritis (CIA) disease model of rheumatoid arthritis.

42 Collagen induced arthritis (CIA) is an animal model of RA.

43 tion (MSCT) into collagen-induced arthritis (CIA) mice prevented arthritis progression by inhibiting

44 The collagen-induced arthritis (CIA) model and DR-1 transgenic mice were used to study t

45 cy in the murine collagen-induced arthritis (CIA) model for rheumatoid arthritis (RA) supported 14l a

46 op in the murine collagen-induced arthritis (CIA) model of inflammatory arthritis.

47 oss in the mouse collagen-induced arthritis (CIA) model of RA.

48 h collagen II, a collagen-induced arthritis (CIA) model, resulted in an accelerated onset of arthriti

49 In the collagen-induced arthritis (CIA) model, while ectopic expression of FGF2 in vivo exa

50 nd damage in the collagen-induced arthritis (CIA) model.

51 model of RA, the collagen-induced arthritis (CIA) model.

52 neered MSCs in a collagen-induced arthritis (CIA) model.

53 ogression in the collagen-induced arthritis (CIA) mouse model to an extent just shy of disease abroga

54 e erosion in the collagen-induced arthritis (CIA) mouse.

55 g(-/-) mice with collagen-induced arthritis (CIA) or K/BxN serum transfer-induced arthritis (STIA).

56 e destruction in collagen-induced arthritis (CIA) rat models.

57 ovial cells from collagen-induced arthritis (CIA) rats and RA patients.

58 Collagen-induced arthritis (CIA) was induced in male DBA/1J mice.

59 anism of action, collagen-induced arthritis (CIA) was therapeutically treated with anti-IL-7 Ab or Ig

60 with established collagen-induced arthritis (CIA) was undertaken to determine whether substitution of

61 ical features of collagen-induced arthritis (CIA) were significantly reduced in fXIII-deficient mice.

62 otective against collagen-induced arthritis (CIA), a model of rheumatoid arthritis (RA).

63 the progress of collagen-induced arthritis (CIA), a mouse model for RA.

64 inflammation in collagen-induced arthritis (CIA), a mouse model for RA.

65 sess its role in collagen-induced arthritis (CIA), a mouse model of human rheumatoid arthritis.

66 ities with RA or collagen-induced arthritis (CIA), a mouse model of RA.

67 C57BL/6 mice to collagen-induced arthritis (CIA), a well-established mouse model of RA.

68 pon induction of collagen-induced arthritis (CIA), tau-tg mice displayed an increased incidence and a

69 d into mice with collagen-induced arthritis (CIA), this T cell line specifically enhanced the severit

70 thritis, namely, collagen-induced arthritis (CIA).

71 ion in mice with collagen-induced arthritis (CIA).

72 of inflammation, collagen-induced arthritis (CIA).

73 murine model of collagen-induced arthritis (CIA).

74 ced incidence of collagen-induced arthritis (CIA).

75 mmune arthritis, collagen-induced arthritis (CIA).

76 s on established collagen-induced arthritis (CIA).

77 linical phase of collagen induced arthritis (CIA).

78 oplasmic iron-sulfur (FeS) cluster assembly (CIA) complex, which transfers critical FeS clusters to s

79 and cytosolic iron-sulfur cluster assembly (CIA) machineries carry out biogenesis of iron-sulfur (Fe

80 tosolic iron-sulfur (Fe-S) cluster assembly (CIA) pathway functions to incorporate inorganic Fe-S cof

81 through the cytosolic FeS cluster assembly (CIA) pathway.

82 A dedicated cytosolic Fe-S cluster assembly (CIA) system is required to assemble Fe-S clusters into c

83 the cytosolic iron-sulfur cluster assembly (CIA) system, converting it into cytosolic aconitase (c-a

84 ntified a cytoplasmic Fe-S cluster assembly (CIA) targeting complex composed of MMS19, CIAO1, and FAM

85 on with the cytosolic Fe-S cluster assembly (CIA) targeting complex composed of MMS19, FAM96B, and CI

86 the cytosolic iron-sulfur protein assembly (CIA) machinery required for maturation of [4Fe-4S] clust

87 the cytosolic iron-sulfur protein assembly (CIA) machinery, is crucial for Fe/S cluster insertion in

88 equires the cytosolic Fe-S protein assembly (CIA) machinery.

89 the cytosolic iron-sulfur protein assembly (CIA) machinery.

90 inis cytosolic iron-sulfur protein assembly (CIA) pathway includes the essential Cfd1-Nbp35 scaffold

91 tes with most known cytosolic Fe-S assembly (CIA) components.

92 complex with the cytoplasmic Fe-S assembly (CIA) proteins CIAO1, IOP1, and MIP18.

93 onent of the cytosolic iron-sulfur assembly (CIA) machinery.

94 nery and the cytosolic iron-sulfur assembly (CIA) system.

95 mAb to LAIR-1 also significantly attenuated CIA in the LAIR(+/+) mice.

96 TP-PA(-) women who were retested, 53% became CIA(-).

97 (-); more than half who were retested became CIA(-).

98 Our results indicated that the Boson CIA demonstrated strong discriminatory power in diagnosi

99 e damage and neutrophil infiltration in both CIA and CAIA models.

100 Sera were screened by CIA, and reactive samples underwent reflex testing with

101 The Advia-Centaur CIA and Trep-Sure EIA had signal strength cutoffs correl

102 uminescence immunoassay [CIA], Advia-Centaur CIA, and Trep-Sure EIA) and three manual assays (Trepone

103 S to 99.7% (99.0 to 99.9%) for Advia-Centaur CIA; negative agreement ranged from 86.3% (84.1 to 88.2%

104 However, for classical CIA, all elements in the loading vectors are nonzero, pr

105 ) and were categorized as "TP-PA confirmed" (CIA(+)/RPR(-)/TP-PA(+)) or "isolated CIA positive" (CIA(

106 designed cyclic analogues of alpha-conotoxin CIA, a potent muscle nicotinic acetylcholine receptor (n

107 Conversely, CIA joint inflammation and bone erosion are alleviated w

108 Finally, these cyclic CIA analogues were shown to be unique pharmacological to

109 When (Fe-S)(int) was added to cytoplasm, CIA utilized it for iron-sulfur cluster assembly without

110 Similar to mutant plants with defective CIA components, grxs17 loss-of-function mutants showed s

111 he perfect correlation between the developed CIA and commercial ELISA for the detection of various co

112 The developed CIA detected HFA in the range of 0.3 pg mL(-1)-20 ng mL(

113 -62 in protecting DBA/1 mice from developing CIA and mirrored its mechanism of action in downregulati

114 stamine resulted in significantly diminished CIA pathology and local markers of osteoclastogenesis.

115 h mice will develop clinical symptoms during CIA.

116 fied with traditional screening methods (eg, CIA-positive, rapid plasma regain (RPR)-negative).

117 Blockade of NKG2D ameliorated established CIA, with significant reductions in clinical scores and

118 to, all flours, doughs, and breads exhibited CIA.

119 he best performance compared to the existing CIA method in terms of feature selection and recovery of

120 In addition, the FBXL5-CIA-targeting complex interaction is regulated by oxygen

121 B6.DR1/LAIR-1(+/+) mice were challenged for CIA and mean severity scores were recorded thrice weekly

122 rmularity with a user-friendly interface for CIA function and newly developed search function Isotopi

123 rin is expressed on synovial Th17 cells from CIA mice and its neutralization with a specific mAb sign

124 tic cells, was important for protection from CIA.

125 daptor that recruits apo-Rli1 to the generic CIA machinery.

126 s the potential utility of the developed HFA CIA for clinical diagnosis.

127 How CIA and FBXL5 collaborate to maintain cellular iron home

128 Abnormalities of the common iliac (CIA), external iliac (EIA), and femoral arteries were cl

129 d a new Boson chemiluminescence immunoassay (CIA) and evaluated its application with cross-sectional

130 um treponemal chemiluminescence immunoassay (CIA) specimens cause clinical uncertainty.

131 t such as the chemiluminescence immunoassay (CIA), followed by testing of CIA-positive (CIA(+)) speci

132 gram sensitive chemiluminescent immunoassay (CIA) was developed for the detection of human fetuin A (

133 DVIA Centaur (chemiluminescence immunoassay [CIA]); (2) Bioplex 2200 (microbead immunoassay); (3) flu

134 BIA], Liaison chemiluminescence immunoassay [CIA], Advia-Centaur CIA, and Trep-Sure EIA) and three ma

135 h treponemal chemiluminescence immunoassays (CIA) identifies patients with discordant serology who ar

136 Impaired CIA activity, as noted by reduced c-acon activity, was a

137 In CIA mice, (99m)Tc-NbV4m119 accumulation in arthritic les

138 une responses and its mechanism of action in CIA pathogenesis.

139 stigate arthritis development in STIA and in CIA under dexamethasone treatment.

140 creased levels of IL-27 relieve arthritis in CIA mouse ankles.

141 fied by enzyme-linked immunosorbent assay in CIA mouse ankles locally expressing adenoviral IL-27 as

142 creased in mice that received the T cells in CIA, and levels of these T cells were increased in the s

143 gulator of inflammatory joint destruction in CIA.

144 phosphatase were significantly diminished in CIA-challenged and even unchallenged fXIIIA(-/-) mice re

145 Arthritis subsided more efficiently in CIA mice injected with mcTNFR2MSCs than in those injecte

146 hed RANKL positive cells and bone erosion in CIA mice.

147 Furthermore, inhibition of HDAC1 in CIA resulted in reduced joint swelling, cartilage and bo

148 Tc-NbV4m119 visualizes joint inflammation in CIA.

149 mmunoregulatory effects of PAD inhibition in CIA are complex, but primarily mediated by transcription

150 joints and to a reduction of IL-17 levels in CIA mice.

151 cted periarticular and systemic bone loss in CIA mice by maintaining trabecular bone structure.

152 e inflammation-induced systemic bone loss in CIA mice by reducing osteoclast precursors and promoting

153 une and subsequent inflammatory processes in CIA.

154 get molecules were greatly down-regulated in CIA mouse ankles receiving forced expression of IL-27.

155 indicate that SAP plays an essential role in CIA because of Fyn-independent and Fyn-dependent effects

156 d RA patients, whereas knockdown of Snail in CIA joints prevents cartilage invasion and joint damage.

157 is an evolutionarily conserved key target in CIA pathobiology.

158 It has been also shown that in CIA the concentration of 3-HAA was increased in the kidn

159 ction in RA, we used anti-TLR5 Ab therapy in CIA mice.

160 Serum and local TNF in CIA paws and C. rodentium colons were significantly incr

161 al studies, flagellin postonset treatment in CIA and local TLR5 ligation in vivo provoke homing and o

162 Vascularization in CIA was determined by immunohistochemical analysis and d

163 differentiation and joint vascularization in CIA.

164 Chicken type II collagen was used to induce CIA in mice, which were then treated with an anti-human

165 y trypsin (TIA) and chymotrypsin inhibitory (CIA) activities were determined in the extracts of wheat

166 The purpose of this study was to investigate CIA using computational analysis.

167 ve on CIA, of which 133 (11.3%) had isolated CIA reactivity.

168 irmed" (CIA(+)/RPR(-)/TP-PA(+)) or "isolated CIA positive" (CIA(+)/RPR(-)/TP-PA(-)).

169 Mice lacking CIA-DC-derived IL-22BP exhibited diminished expression o

170 composition and interactions within the late CIA complex.

171 (4) INNO-LIA (line immunoassay); (5) LIAISON CIA; (6) Treponema pallidum particle agglutination assay

172 BioPlex MBIA and Liaison CIA had signal strength cutoffs correlating with >/=99%

173 smic iron-sulfur protein assembly machinery (CIA).

174 s may provide a promising strategy to manage CIA.

175 Compared to that in wild-type mice, CIA in Crp-/- mice progressed more rapidly and was more

176 They were mild (CIA and EIA mean severity, 19% +/- 7 and 26% +/- 11, res

177 (against U1), resembling human RA and murine CIA.

178 etained the low nanomolar activity of native CIA toward muscle-type nAChRs but showed greatly improve

179 To identify new CIA proteins we employed systematic protein interaction

180 We propose a novel CIA method that uses l1-penalization to induce sparsity

181 ively, viperin maturation represents a novel CIA pathway with a minimal requirement of the CIA-target

182 We found that a certain amount of CIA was essential for the model to reproduce reported ef

183 used to noninvasively monitor the course of CIA in mice.

184 nduced hair follicle damage or the degree of CIA, respectively.

185 nd that SAP was essential for development of CIA in response to collagen immunization.

186 ombin(WE) also suppressed the development of CIA in wild-type mice.

187 We found evidence of CIA, TPPA, and FTA Abs seroreversion.

188 key morphological and functional features of CIA, whereas recombinant Shh protein partially rescued h

189 before and up to 18 days after induction of CIA by immunization with type II collagen.

190 Furthermore, induction of CIA led to significantly elevated numbers of Iba-1-expre

191 ion (early) and during development (late) of CIA strongly suppressed clinical and histological signs

192 Here, we show that in a mouse model of CIA, the downregulation of Shh signaling in the hair mat

193 treatment with flagellin after the onset of CIA exacerbated joint inflammation; in contrast, inflamm

194 hermore, treatment with ASCs at the onset of CIA significantly reduced clinical symptoms and joint pa

195 increased incidence and an earlier onset of CIA that was associated with a more pronounced inflammat

196 can amplify disease severity after onset of CIA.

197 Th17 cell activation in the pathogenesis of CIA, suggesting that its blockade can be beneficial for

198 filament model, which allowed predictions of CIA-dependent muscle behavior.

199 of twitch tension show that the presence of CIA increases peak tension while profoundly delaying rel

200 oval of SAP expression during progression of CIA attenuated disease severity.

201 partially interfered with the progression of CIA.

202 Strategies for reconciliation of CIA and IPA assignments were discussed.

203 This link might contribute to recovery of CIA machinery efficiency to mature cytosolic and nuclear

204 identifies CD73 as an important regulator of CIA in mice.

205 controlling the development and severity of CIA mostly depends on CD39/CD73 signals and partially de

206 The results demonstrated that suppression of CIA by A9 is dependent on T cells.

207 ce immunoassay (CIA), followed by testing of CIA-positive (CIA(+)) specimens with the rapid plasma re

208 und to be upregulated in synovial tissues of CIA mice.

209 erexpressed in synovial cells and tissues of CIA rats and RA patients, whereas knockdown of Snail in

210 Dexamethasone treatment of CIA mice reduced (99m)Tc-NbV4m119 accumulation as compar

211 Treatment of CIA with PLP-LCL significantly suppressed joint swelling

212 in Treg frequencies after IL-33 treatment of CIA.

213 sue inflammation and damage were assessed on CIA up to 47 days following immunization.

214 women considered susceptible to RV based on CIA results tested positive for RV antibodies by IB/Nt.

215 reversed the protective effect of G-MSCs on CIA.

216 261 specimens, 1171 (4.1%) were reactive on CIA, of which 133 (11.3%) had isolated CIA reactivity.

217 mutants defective in either Fe-S cluster or CIA targeting complex binding blocks Fe-S cluster assemb

218 19 revealed that CIA1, but none of the other CIA factors, is predominantly required for (55)Fe/S clus

219 ions demonstrate that our proposed penalized CIA methods achieve the best or close to the best perfor

220 tive serology may represent a false-positive CIA in low-prevalence populations.

221 (CIA), followed by testing of CIA-positive (CIA(+)) specimens with the rapid plasma reagin test (RPR

222 RPR(-)/TP-PA(+)) or "isolated CIA positive" (CIA(+)/RPR(-)/TP-PA(-)).

223 linical species and robust efficacy in a rat CIA model.

224 toff ratio was similar for isolated reactive CIA sera and sera that were reactive on either FTA Abs o

225 20 patients (55%) with an isolated reactive CIA specimen who underwent medical record review had pre

226 Isolated reactive CIA specimens may represent true T. pallidum infection a

227 ts (66 of 82 [80.5%]) with isolated reactive CIA specimens were from high-prevalence populations.

228 a subset of subjects with isolated reactive CIA specimens.

229 y on the CIA were deemed "isolated" reactive CIA samples.

230 Recently CIA has been used for an integrative analysis of multipl

231 Anti-IL-7 Ab treatment significantly reduces CIA monocyte recruitment and osteoclast differentiation

232 , which can be further manipulated to rescue CIA.

233 linical significance of discordant serology (CIA(+)/RPR(-)) for maternal and neonatal outcomes is unk

234 tected, developing significantly less severe CIA and PIA.

235 tment with stimulating LAIR-1 Abs suppresses CIA whereas B6.DR1/LAIR-1(-/-) mice develop more severe

236 nct subset of intestinal cDCs, which we term CIA-DCs.

237 Our analyses suggest that CIA is present in cardiac muscle under normal conditions

238 The CIA study in DBA/1J mice indicated that compounds led to

239 The CIA, EIA, and femoral lesion classification may help to

240 l iron-sulfur cluster assembly (ISC) and the CIA machineries.

241 idence of a possible direct link between the CIA machinery and the mitoNEET cluster transfer repair p

242 served C-terminal tryptophan for binding the CIA targeting complex, the deca-GX3 motifs in both Yae1

243 rize how Fe-S assembly is facilitated by the CIA targeting complex.

244 n which XPD acquires a Fe-S cluster from the CIA targeting complex before assembling into TFIIH.

245 Angiography depicted 28 abnormalities in the CIA (27 stenoses, one dissection), 185 in the EIA (17 th

246 icantly reduced arthritis progression in the CIA and delayed-type hypersensitivity arthritis models.

247 racts with Fe-S apoproteins and MMS19 in the CIA complex but not with the individual proteins.

248 n of osteoclasts, and vascularization in the CIA effector phase.

249 locks the proteolytic capacity of uPA in the CIA model and the delayed-type hypersensitivity arthriti

250 tis and autoimmunity by treating mice in the CIA model with Cl-amidine on days 0-35.

251 In the CIA model, the impact of anti-uPA treatment was on par w

252 In the CIA pathway, CIA1 cooperates with CIA2A, CIA2B, and MMS1

253 Fe/S target protein is unprecedented in the CIA pathway.

254 None of the CIA components downstream of Dre2 was required for RNR c

255 Fe-S cluster, or along with knockdown of the CIA factors NUBP2 or FAM96A, reduced cell viability.

256 rming that MMS19 is a central protein of the CIA machinery that brings Fe-S cluster donor proteins an

257 cluster chaperone in the early stage of the CIA machinery.

258 h Ccdc117's interaction with elements of the CIA pathway and the facilitation of DNA replication duri

259 ins Yae1 and Lto1 as binding partners of the CIA targeting complex.

260 IA pathway with a minimal requirement of the CIA-targeting factors and represents a new paradigm for

261 hrough ubiquitination and degradation of the CIA-targeting protein MMS19.

262 ly depends on ISC machineries and not on the CIA or CIAPIN1.

263 Samples reactive only on the CIA were deemed "isolated" reactive CIA samples.

264 y exclusive fashion with either TFIIH or the CIA targeting complex.

265 GE-F1-NSE1 E3 ubiquitin ligase regulates the CIA pathway through ubiquitination and degradation of th

266 However, the mechanisms regulating the CIA pathway are unknown.

267 We demonstrate that the CIA-targeting complex promotes the ability of FBXL5 to d

268 Thus, flux through the CIA pathway can be regulated by degradation of the subst

269 cytosolic monothiol GRXs associate with the CIA complex, as in other eukaryotes, and contribute to,

270 ndicate that the association of XPD with the CIA targeting complex occurs in the cytoplasm, whereas i

271 At the same time, CIA had minimal effect on the rate of force redevelopmen

272 ve, TP-PA--negative patients seroreverted to CIA-negative.

273 Susceptibility to CIA, a disease that resembles RA in humans, was compared

274 t mice are significantly more susceptible to CIA than wild-type mice.

275 lls was elevated in LACC1 KO mice undergoing CIA as well as aged mice compared with WT controls.

276 Of 21,623 assays, 439 (2%) were CIA-positive and 255/439 (58%) were RPR-negative; subseq

277 ere CIA(+)/RPR(-)/TP-PA(-) and 38 (20%) were CIA(+)/RPR(-)/TP-PA(+).

278 Of 194 pregnant women, 156 (80%) were CIA(+)/RPR(-)/TP-PA(-) and 38 (20%) were CIA(+)/RPR(-)/T

279 pregnant women with discordant serology were CIA(+)/RPR(-)/TP-PA(-); more than half who were retested

280 yphilis during pregnancy than women who were CIA(+)/RPR(-)/TP-PA(-) (all P < .005).

281 However, it had no effect on disease when CIA was clinically established.

282 horylation of IRP1 at Ser-138 increased when CIA was inhibited and was required for iron rescue.

283 importance of FBXL5 for regulating IRP1 when CIA is impaired.

284 ed more rapidly and was more severe, whereas CIA in CRP-Tg mice was dramatically attenuated.

285 While CIA assigns elemental formulas for compounds containing

286 ed joints of WT, but not CRIg(-/-) mice with CIA and STIA.

287 s indicate that ES-62 treatment of mice with CIA leads to unique multisite manipulation of the initia

288 Infusion of G-MSCs in DBA/1J mice with CIA significantly reduced the severity of arthritis, dec

289 Mice with CIA were treated with the TLR-5 agonist flagellin to doc

290 In the knees of mice with CIA, (99m)Tc-NbV4m119 was found to accumulate even befor

291 Moreover, in the livers from mice with CIA, concentration of tryptophan and kynurenine was decr

292 In mice with CIA, MMR expression was detected on cells from the bone

293 human/mouse DR5-transgenic Ubc.Cre mice with CIA, transgenic DR5 was most highly expressed on CD11b+

294 FAP antibody 28H1 was performed in mice with CIA.

295 obtained from various organs from mice with CIA.

296 o down-regulate IL-17 responses in mice with CIA.

297 ryptophan, kynurenine and 3-HAA in mice with CIA.

298 analysis of joint inflammation in mice with CIA.

299 Rats with CIA developed significant mechanical hypersensitivity, w

300 and spinal microglial response in rats with CIA.