ライフサイエンスコーパス: inflamed

1 outpouching through the colonic wall, become inflamed.

2 at is remote from ischemic area also becomes inflamed.

3 ntitative and qualitative responses of human inflamed adipose tissue to IL-10 and provide a mechanist

4 Most individuals who are obese harbor inflamed adipose tissue, which resembles chronically inj

5 Oxysterols are increased in inflamed airways after allergen challenge and, through G

6 Chronic inflamed airways can lose tolerance over time to immunog

7 ion exchanger expressed in the epithelium of inflamed airways where it is thought to facilitate Cl(-)

8 g an inherent propensity to extravasate into inflamed and barrier sites.

9 m) showed the highest fluctuation within the inflamed and control groups.

10 lly over 4 weeks, resulting in a chronically inflamed and damaged lung.

11 ntial regulator of neutrophil recruitment to inflamed and damaged sites and plays prominent roles in

12 e human intestinal tract and is activated in inflamed and fibrotic tissue.

13 alpha Western blot/messenger RNA analysis of inflamed and healthy ankles to confirm our in vivo resul

14 onment surrounding periosteal pain fibers is inflamed and in turn activates trigeminovascular nocicep

15 The inflamed and incompetent neutrophil phenotype was also o

16 nism in Tollip alteration that underlies the inflamed and incompetent polarization of neutrophils lea

17 observed in measured HLA-A2 binding between inflamed and noninflamed cohorts.

18 We performed immunohistochemical analyses of inflamed and noninflamed regions of pancreatic tissue fr

19 n which sites of pressure or friction become inflamed and painful, thus significantly impacting quali

20 Although a subset of sarcomas appears inflamed and responsive to immune checkpoint blockade wi

21 Platelets can be found on the surface of inflamed and ruptured atherosclerotic plaques.

22 Asthmatic airways are inflamed and undergo remodelling.

23 rks under different experimental conditions (inflamed and uninflamed tissues in CD and UC).

24 neal transplantation, where the graft bed is inflamed and vascularized, immature APCs in the donor co

25 lPAG) is pronociceptive in naive and acutely inflamed animals, but its contributions in more prolonge

26 and a 45-fold elevation in ROS expression in inflamed ankles compared with the ankles of healthy cont

27 y differentiated Treg cells relocated to the inflamed aorta in atherosclerosis-prone low-density lipo

28 additional concomitant intussusceptions and inflamed appendix.

29 viral infection, ILC2 cells clustered within inflamed areas and acquired an ILC1-like phenotype.

30 e cells that naturally accumulate in painful inflamed areas.

31 d regulates the pathogenic remodeling of the inflamed arterial wall.

32 GM-CSF on (18)F-FDG uptake in normal versus inflamed arteries, using PET.

33 the number of pro-inflammatory Th17 cells in inflamed arthritic joints through TRAIL-induced apoptosi

34 alpha) and increases (18)F-FDG uptake within inflamed atheroma in vivo.

35 Inflamed atherosclerotic plaques can be visualized by no

36 ived cholesterol fecal excretion and reduces inflamed atherosclerotic plaques.

37 Inflamed BECs internalized myelin, which was routed to e

38 Moreover, myelin/MHC-II complexes on inflamed BECs stimulated the trans-endothelial migration

39 significantly distinguished noninflamed from inflamed biopsies (area under the curve, 0.74 and 0.70,

40 In humans, ESRP1 is downregulated in inflamed biopsies from inflammatory bowel disease patien

41 prised of CAR homing peptide that recognizes inflamed blood vessels and penetrates deep into the vess

42 Vascular permeability was twofold greater in inflamed blood vessels in Nrp2-deficient mice compared t

43 static function by securing the integrity of inflamed blood vessels to prevent bleeding from sites of

44 a result of their transmigration across the inflamed blood-spinal cord barrier.

45 entrations of aromatase and interleukin 6 in inflamed breast tissue and an increased number of macrop

46 ding confirmed that FmlH bound avidly to the inflamed, but not the naive bladder.

47 at arterial regions of atherosusceptible-SS inflamed by low-dose TNFalpha.

48 ing a primate, enables macrophage imaging in inflamed cardiovascular tissues.

49 he bowel wall, which can become infected and inflamed causing diverticulitis, with potentially severe

50 EVL/VASP-deficient activated T cells to the inflamed central nervous system of mice with experimenta

51 effect of the polyphenol-loaded carriers on inflamed chondrocytes.

52 Treg accumulation in the inflamed CNS tissues is not affected by the lack of IL-2

53 In the inflamed CNS, myeloid cells are comprised of brain-resid

54 to inflammatory pathways activated in human inflamed colon and TNF-alpha-treated cells (false discov

55 In the inflamed colon of humans and mice, we found decreased le

56 STAT3 was activated (phosphorylated) in inflamed colon tissues from Mefv-/-, which also had incr

57 G2A(-/-) mice also had less IFN-gamma in inflamed colon tissues than wild-type mice.

58 ADP)ribose showed a positive staining in the inflamed colon.

59 numbers of IL-6-producing macrophages in the inflamed colonic lamina propria.

60 ificantly downregulated in IBD patients with inflamed colonic mucosa, and in trinitrobenzene sulphoni

61 were present in the linear and loose ECM of inflamed colons and polarized to the M1 phenotype.

62 ntracted structures were not observed in the inflamed colons of AKAP12 knockout (KO) mice.

63 istration of tegaserod increased motility in inflamed colons of guinea pigs and mice, whereas adminis

64 ated T cells, and distributed throughout the inflamed colons of mice with colitis.

65 quently, the proportion of M2 macrophages in inflamed colons was lower in AKAP12 KO mice than in WT m

66 To mimic an inflamed condition, RANKL upregulation in human mandibul

67 d in healthy corneas but was up-regulated in inflamed corneas by infiltrating macrophages.

68 crophages increased and remained elevated in inflamed corneas of IL-10(-/-) mice, indicating that IL-

69 enesis and faster egress of macrophages from inflamed corneas.

70 neutrophils and intravital microscopy of the inflamed cremaster muscle that CD95 mediates leukocyte s

71 airs leukocyte adhesion and extravasation in inflamed cremaster muscle venules in comparison with con

72 ng intravital confocal microscopy applied to inflamed cremaster muscles.

73 strongly increased in the interleukin-1beta inflamed cremaster.

74 Cytokine profiling in locally inflamed DRG showed increases in pro-inflammatory Type 1

75 In the inflamed EAE spinal cord however, the patterns of expres

76 In an LPS-induced inflamed ear murine model, HA-treated MSC demonstrated a

77 l and CD8 T cell infiltration was reduced in inflamed ear tissue, whereas CTLA-4(+)Foxp3(+) Treg freq

78 ill modulate the recruitment of monocytes to inflamed endothelial surface by altering the dynamics of

79 selectin extends from the plasma membrane of inflamed endothelium and serves to capture leukocytes fr

80 ponse to cytokines as well as restoration of inflamed endothelium into a quiescent state.

81 orporated into liposomes, designed to target inflamed endothelium, shows reduced atherosclerosis and

82 rs with intracellular adhesion molecule 1 on inflamed endothelium.

83 ascular permeability, and extravasate across inflamed endothelium.

84 Reduced IL-33 in the Sm Egg-inflamed environment was shown to contribute to the fail

85 Inflamed environments are typically hypercellular, rich

86 regulates the bioavailability of cortisol in inflamed environments by fine-tuning the RCL proteolysis

87 ty of bacteria to persist within chronically inflamed environments.

88 ms underlying GR actions for modulating the "inflamed epigenome."

89 sition of microparticles by neutrophils onto inflamed epithelium: a new mechanism to disrupt epitheli

90 e of HIFs in myeloid cell migration into the inflamed eye.

91 dispensable for leukocyte migration into the inflamed eye.

92 ad no impact on myeloid trafficking into the inflamed eye.

93 pain control, and avoidance of surgery in an inflamed eye.

94 al management purposes, with patients having inflamed eyes being treated with systemic immunomodulato

95 Subclinical retinal thickening of mildly inflamed eyes with IU can occur though bearing no functi

96 stigation of inflammatory cells recruited to inflamed G2A(-/-) colons showed significantly more TNF-a

97 Fewer CD4(+) lymphocytes were recruited to inflamed G2A(-/-) colons, and fewer colonic lymphocytes

98 rized by the presence or absence of a T-cell-inflamed gene signature.

99 The T cell-inflamed GEP contained IFN-gamma-responsive genes relate

100 The T cell-inflamed GEP has been developed into a clinical-grade as

101 s and eventually defining a pan-tumor T cell-inflamed GEP in 220 patients with 9 cancers.

102 e to reduction of IL-6 immunolabeling in the inflamed gingival mucosa.

103 ed that monocytes patrol both uninflamed and inflamed glomeruli using beta2 and alpha4 integrins and

104 to investigate NET formation in the acutely inflamed glomerulus.

105 te approximately 90%, the rejection rates in inflamed graft beds or high-risk recipients often exceed

106 urvival in corneal allograft recipients with inflamed graft beds.

107 reduction of Salmonella colonization in the inflamed gut was accompanied by expansion of Lactobacill

108 petition among the Enterobacteriaceae in the inflamed gut.

109 a to outcompete commensals and thrive in the inflamed gut.

110 gastroenteritis in humans and thrives in the inflamed gut.

111 ta, some of these organisms can bloom in the inflamed gut; expansion of enterobacteria is a hallmark

112 eic corneal transplantation was performed on inflamed host beds.

113 Galectin-8 is markedly upregulated in inflamed human and mouse corneas, and galectin-8 inhibit

114 Mice carrying inflamed human arteries were treated with tofacitinib or

115 macrophages and mesenchymal stromal cells in inflamed human pulp tissues.

116 By using a tumor model resembling non-T cell-inflamed human tumors, we assessed whether adoptive T ce

117 Inflamed ileal tissues and PBMCs from patients with CD h

118 ially expressed transcripts (DETs) unique to inflamed ileocolonic tissue from symptomatic ASD(IC+) ch

119 d, to a lesser degree, the arterial wall are inflamed in HIV, inflammation in these tissues is not cl

120 review describes how adipose tissue becomes inflamed in obesity, summarizes ways these mechanisms im

121 co-existing host and bacterial elastases in inflamed/infected tissues remain unknown.

122 Inflamed intestinal tissues and intestinal macrophages f

123 we show that, relative to healthy controls, inflamed intestinal tissues from patients with IBD expre

124 ) 17 cell pathway molecules are increased in inflamed intestinal tissues of patients with IBD.

125 EcN limits the growth of competitors in the inflamed intestine, including commensal E. coli, adheren

126 hils infiltrate the serosa and mucosa of the inflamed intestines.

127 cate a monocytic origin of CD11c(+) cells in inflamed islets and suggest that therapeutic regulatory

128 Ccl5 and Ccl8 were persistently elevated in inflamed islets and the influx of CD11c(+) cells was par

129 and it is also up-regulated in beta cells of inflamed islets from non-obese diabetic mice.

130 CD11c(+) cells in inflamed islets resembled classical dendritic cells base

131 cursors could give rise to CD11c(+) cells in inflamed islets.

132 The uptake of radiolabeled 28H1 in inflamed joints (percentage injected dose) correlated wi

133 Of note, RvD3 levels were reduced in inflamed joints from mice with delayed-resolving arthrit

134 (99m)Tc-NbV4m119 accumulated in inflamed joints of WT, but not CRIg(-/-) mice with CIA a

135 e synovium, possibly by expressing CXCL10 in inflamed joints.

136 ercentage injected dose per gram in severely inflamed joints.

137 s the major cellular source of IL-17F in the inflamed kidney.

138 Given its survival in inflamed lesions, the ability to sense and overcome oxid

139 sident memory T cells well beyond clinically inflamed lesions.

140 strated an active molecular clock within the inflamed limbs and highlighted the resident inflammatory

141 rough endothelium into a model mimicking the inflamed liver microenvironment did not affect Treg stab

142 he immunoregulatory function of ILC2s in the inflamed liver remains elusive.

143 Analysis of chronically inflamed liver tissue demonstrated accumulation of SCARF

144 ve macrophages are highly accumulated in the inflamed liver, and chemical inhibition of ETAR signalin

145 8 T cells are the main source of IL-2 in the inflamed liver.

146 vel mechanism of OxPAPC-assisted recovery of inflamed lung endothelium.

147 oxp3(+) Tregs are rapidly mobilized into the inflamed lung tissues.

148 The uptake ratio of infected lung over inflamed lung was 8.5 and 1.7 for (18)F-FDS and (18)F-FD

149 tor T cells within the interstitial space of inflamed lungs are incompletely understood.

150 and 10.6+/-0.3h (R(2)=1.000) for healthy and inflamed lungs respectively (n=3).

151 olong their presence in both the healthy and inflamed lungs.

152 contact with the high endothelial venule in inflamed lymph node.

153 In inflamed lymph nodes, Ag-specific CD4(+) and CD8(+) T ce

154 wed us to discriminate between malignant and inflamed lymph nodes, whereas [(18)F]FDG-PET failed to d

155 prior to cognate Ag-induced TCR signaling in inflamed lymph nodes; however, the molecular mechanisms

156 We found that miR-124-3p promoted the anti-inflamed M2 polarization in microglia, and microglial ex

157 dicate that CAPN6 promotes atherogenicity in inflamed macrophages by disturbing CWC22/EJC systems.

158 the process of leukocyte recruitment to the inflamed microcirculation.

159 es by antibody-guided LIGHT creates a T cell-inflamed microenvironment and overcomes tumor resistance

160 concert with local mechanisms to sustain the inflamed microenvironment and promote tumor growth.

161 However, whether quantifying T cell-inflamed microenvironment is a useful pan-tumor determin

162 matory bone erosion, thrives within a highly inflamed milieu and disseminates to distant sites, such

163 med the selective release of morphine in the inflamed milieu.

164 a mechanism of Nur77-dependent clearance of inflamed mitochondria to alleviate inflammation.

165 SRP of inflamed moderate pockets during 6-month PMT, with or wi

166 multinucleated cells at the bone surface of inflamed mouse joints.

167 multinucleated giant cells are formed in the inflamed mouse peritoneum during the resolution phase of

168 and F4/80(+) macrophages was observed in the inflamed mucosa along with reduction in the mRNA levels

169 erexpressed MFSD2A not only localized to the inflamed mucosa but also restored the ability of the end

170 r regulating PMN trafficking and function in inflamed mucosa.

171 -/-) neutrophils were unable to migrate into inflamed murine cremaster muscle venules, instead persis

172 41 in the infected muscles compared with the inflamed muscles was clearly observed in the PET/CT imag

173 Infected or inflamed muscles were dissected, homogenized, and cultur

174 nd antibody production within pathologically inflamed non-lymphoid tissues.

175 gain the ability to access both healthy and inflamed nonlymphoid tissues.

176 atients maintain what grossly looks like non-inflamed, normal skin in the face of massive inflammator

177 Incubation of inflamed Ob visceral adipose tissues and human macrophag

178 ingly, matrix stiffness in the range seen in inflamed or fibrotic lung is required to sensitize the T

179 ivity may be important for T cells to access inflamed or injured tissues with abrupt topographical ch

180 th monocytic and lymphocytic infiltration of inflamed or tumor-bearing lung.

181 in-positive lymphatic vessels within acutely inflamed orbital fat tissue.

182 ary lymphoid tissue (TLT) can form within an inflamed organ, including the CNS.

183 fic requirements for Treg migration into the inflamed organs and the positioning of these cells withi

184 conditions involving migration of T cells to inflamed organs.

185 dentified proinsulin-responding T cells from inflamed pancreatic islets of organ donors with recent-o

186 We identified hundreds of T cells from inflamed pancreatic islets of three young organ donors w

187 BCL3 is up-regulated in inflamed pancreatic or biliary tissues from mice and pat

188 iated with lower all-cause mortality risk in inflamed patients (HR [95% CI] for Q1: 5.63 [4.25 to 7.4

189 rotective effect of high BMI was observed in inflamed patients, this effect was mitigated in noninfla

190 e for dysregulated endogenous RvD3 levels in inflamed paw joints and its potent actions in reducing m

191 beta-endorphin levels increased in the inflamed paw, and this increase and the antihyperalgesic

192 heres (MMs) are being used to treat residual inflamed periodontal pockets during periodontal maintena

193 Prostaglandin (PG)E2 accumulates in inflamed periodontal tissue and induces receptor activat

194 bundance of genetic alterations and a T-cell-inflamed phenotype.

195 ected by transforming viruses or chronically inflamed, pointing toward extrinsic causes for transform

196 pulp stem cells (DPSCs) can be isolated from inflamed pulp derived from carious teeth with symptomati

197 In addition, chronically inflamed Rab27DKO mice had a blunted response to bacteri

198 ral opioid receptors to produce analgesia in inflamed rat paws without major side effects such as sed

199 -25% of individuals, the diverticulae become inflamed, resulting in diverticulitis.

200 CD68(+) percentage (maxCD68(+)) in the most inflamed section/plaque.

201 to be maximum colonic wall thickness in the inflamed segment (hazard ratio [HR], 1.07 per every mill

202 difference in maximum wall thickness in the inflamed segment (HR, 1.05 per millimeter; P = .016) and

203 lved segments, maximum wall thickness in the inflamed segment, severity of diverticulosis, presence o

204 t the source of periostin and VCAM-1 was the inflamed sheep liver tissue.

205 e analog) and by local administration at the inflamed site of monoclonal antibody 3-E7, which recogni

206 mmation by preventing macrophage egress from inflamed sites and is required for osteoclast differenti

207 phocyte homing and neutrophil recruitment to inflamed sites are normal.

208 t interleukin-23-interleukin-17 signature at inflamed sites in humans with LAD1 and in mouse models o

209 s diverted Tfh cells from systemic (non-gut) inflamed sites such as the lung into the gut-associated

210 chemokine receptors that direct migration to inflamed sites, such as CCR2, CX3CR1, and CCR5, in TPH c

211 pographic commitment of T cells for skin and inflamed sites.

212 nd an increase in macrophage accumulation at inflamed sites.

213 Drug-specific clones from inflamed skin (n = 96, 83% CD4(+)) secreted a similar pr

214 rin and relocated from the peritoneum to the inflamed skin and intestine upon innate stimulation, ind

215 VL/VASP double-knockout (dKO) T cells to the inflamed skin and secondary lymphoid organs.

216 l B1 cells preferentially migrating into the inflamed skin of mice.

217 e observed in squamous cancer subsets and in inflamed skin of transgenic mice overexpressing DeltaNp6

218 hese findings suggest that pain arising from inflamed skin reflects a dramatic shift in the balance o

219 Histopathology analyses of the inflamed skin revealed intrafollicular and perifollicula

220 tions with stationary MCs before leaving the inflamed skin to draining lymph nodes.

221 es to the Treg gene program between adjuvant-inflamed skin types, suggesting a lack of selective recr

222 -specific T cells were cloned from blood and inflamed skin, and cellular phenotype and function were

223 ollients that are used to treat pruritic and inflamed skin, and/or whether the impaired skin barrier

224 role for PLCepsilon1 in T-cell migration to inflamed skin, but not for cytokine secretion and prolif

225 lex interactions between various cells in AD inflamed skin, it is difficult to dissect the precise an

226 tion of CD25 expression, specifically in the inflamed skin.

227 that CCR6 mediates monocyte trafficking into inflamed skin.

228 rast, Tregs accumulated poorly in the Sm Egg-inflamed skin.

229 lprotectin and Toll-like receptor (TLR) 4 in inflamed skin.

230 reduced the number of gammadeltaT17 cells in inflamed skin.

231 tour was higher in dysplasia than control or inflamed specimens, indicating transition from flat to a

232 Periodontal inflamed surface area (PISA) and FMD were assessed in al

233 cterized by double immunofluorescence in the inflamed synovium from patients with rheumatoid arthriti

234 This cell actively invades inflamed target tissue and further terminates an ongoing

235 iminate effector autoreactive T cells in the inflamed target tissue, the CD8alphaalpha(+) AP-NK cell

236 * constitutes the major CRP species in human-inflamed tissue and allows binding of complement factor

237 While classical monocytes extravasate into inflamed tissue and give rise to macrophages or dendriti

238 that CKD impairs leukocyte recruitment into inflamed tissue and host defense in mice and humans.

239 activity dampens neutrophil recruitment into inflamed tissue and is required for survival of myocardi

240 PAPC) and its derivatives were identified in inflamed tissue by mass spectrometry and binding assays.

241 activation of opioid receptors in peripheral inflamed tissue can reduce pain without central adverse

242 (ASD(IC+)) compared to anatomically similar inflamed tissue from typically developing children with

243 on of activated regulatory T (Treg) cells to inflamed tissue is crucial for their immune-modulatory f

244 -kappaB signaling and is associated with the inflamed tissue state observed in human celiac disease.

245 identify and profile ILCs across healthy and inflamed tissue types.

246 Having arrived in inflamed tissue, aged neutrophils were found to exhibit

247 t membrane for successful extravasation into inflamed tissue, but this process is incompletely unders

248 (+) T-cell phenotypes present in chronically inflamed tissue.

249 trafollicular plasmablast development within inflamed tissue.

250 , anti-myelin B cells were excluded from the inflamed tissue.

251 moting immune effector-cell trafficking into inflamed tissue.

252 ead to enhanced recruitment of leukocytes to inflamed tissue.

253 tion, and proinflammatory gene expression in inflamed tissues and concomitantly downregulated annexin

254 ed immunities following their recruitment to inflamed tissues and lymphoid organs.

255 e a mechanism to explain Treg dysfunction in inflamed tissues and suggest that IL-2 supplementation,

256 ocyte contact with adhesion molecules in non-inflamed tissues and that downregulation of endomucin is

257 erstanding of innate immune cell function in inflamed tissues and their subsequent interactions with

258 Further, because hypoxic inflamed tissues are associated with the overexpression

259 ion, including their ability to migrate into inflamed tissues during autoimmune disease.

260 ponsive cell and accumulated in peripherally inflamed tissues during TLR9-driven inflammation.

261 Thus, the magnitude of the Treg response in inflamed tissues is controlled at two interdependent lev

262 how these cells are sustained in chronically inflamed tissues remains unclear.

263 and acutely enhances (18)F-FDG uptake within inflamed tissues such as atherosclerotic plaques in vivo

264 (CBG) delivers anti-inflammatory cortisol to inflamed tissues upon elastase-based proteolysis of the

265 ironment), tissue level (e.g., cancerous and inflamed tissues), and cellular level (e.g., sub-cellula

266 ransendothelial migration of leukocytes into inflamed tissues, but the mechanisms by which shear is s

267 onocyte-derived macrophages are recruited to inflamed tissues, where they produce proinflammatory cyt

268 s on innate and adaptive immune responses in inflamed tissues.

269 extravasation of circulating leukocytes into inflamed tissues.

270 essed in the endothelium of some chronically inflamed tissues.

271 ar neutrophils, and dendritic cells into the inflamed tissues.

272 CR5, responsible for their homing to sterile inflamed tissues.

273 tokines were also found to be induced in the inflamed tissues.

274 to homeostasis and are also produced in non-inflamed tissues.

275 igration and recruitment of neutrophils into inflamed tissues.

276 al to facilitate adhesion of leukocytes into inflamed tissues.

277 r, in governing the mechanical properties of inflamed tissues.

278 ve oxygen species (ROS) that are produced in inflamed tissues.

279 tissue/organ-associated and migrate to local inflamed tissues/organs to suppress the autoimmune respo

280 eling revealed PD-1/CYT expression (i.e., an inflamed tumor microenvironment) as the most impactful f

281 gene expression for the presence of a T-cell-inflamed tumor microenvironment, which correlates with c

282 immune evasion or simply correlates with an inflamed tumor microenvironment.

283 delay and prolonged survival only in T-cell-inflamed tumor models of head and neck cancers.

284 Furthermore, targeting non-T cell-inflamed tumor tissues by antibody-guided LIGHT creates

285 trigger immune infiltration into non-T-cell-inflamed tumors in the hope of rendering them immunother

286 nresponsive patients tend to have non-T-cell-inflamed tumors that lack markers associated with the ac

287 ades and other immunotherapies in non-T cell-inflamed tumors.

288 by CD103(+) dendritic cells (DCs) in T cell-inflamed tumors.

289 F9/Yde/Fml pilus for UPEC persistence in the inflamed urothelium.

290 CLA/ESL mediates adhesion of T cells to inflamed vascular endothelium.

291 wed that these vesicles can selectively bind inflamed vasculature because they possess intact targeti

292 r example employ membrane proteins to target inflamed vasculature, locally increase vascular permeabi

293 To target inflamed vasculature, nanoparticles are commonly enginee

294 cells represents a novel Th17 marker in the inflamed VAT, which also confers protection against ATP-

295 In inflamed vessels of the mesenteric circulation, VWF recr

296 a mechanistic basis for the role of CD2AP in inflamed vessels, identifying this adaptor protein as a

297 n SSRBC infusion inhibited SSRBC adhesion in inflamed vessels, prevented the progression of vasoocclu

298 he mouse model, they can be localised within inflamed vessels, suggesting their involvement in vascul

299 f myeloid cells through factors presented by inflamed vessels.

300 We compared gene expression signatures in inflamed vs noninflamed intestinal and rectal tissues co