ライフサイエンスコーパス: inflammatory cell

1 CTSC is expressed in the pancreas and in inflammatory cells.

2 m LPS-induced proteinuria and recruitment of inflammatory cells.

3 the inflammasome pathway, and recruitment of inflammatory cells.

4 attern molecules (DAMPs) and infiltration of inflammatory cells.

5 hed lesions and inhibits the infiltration of inflammatory cells.

6 al to identify lesions harbouring iron-laden inflammatory cells.

7 under normal conditions, restricts access of inflammatory cells.

8 may in part explain regional differences in inflammatory cells.

9 ritis pain independently of its functions in inflammatory cells.

10 veolar epithelial damage and accumulation of inflammatory cells.

11 y process promoting the recruitment of other inflammatory cells.

12 , which appear to be functional only in anti-inflammatory cells.

13 es are upregulated to promote recruitment of inflammatory cells.

14 nthase, and vascular/brain infiltration with inflammatory cells.

15 coupled receptors on acinar cells or through inflammatory cells.

16 d reduction in the number of osteoclasts and inflammatory cells.

17 ), IL-17, and IL-23 release from infiltrated inflammatory cells.

18 in plaque formation such as infiltration of inflammatory cells.

19 le cell types of gingival tissues, including inflammatory cells.

20 tion and inflammation by both structural and inflammatory cells.

21 could be upregulated by itself and IL-17 in inflammatory cells.

22 XCR4 receptor is expressed at the surface of inflammatory cells.

23 exhibited few collagen fibers among numerous inflammatory cells.

24 arked reduction in number of osteoclasts and inflammatory cells.

25 Atherosclerotic lesions exhibited inflammatory cells.

26 DBG/LV and DBG/HV presented almost no inflammatory cells.

27 nflammatory phenotype was mediated by immune/inflammatory cells.

28 nhanced steatohepatitis with infiltration of inflammatory cells.

29 rily via the accumulation of cholesterol and inflammatory cells.

30 lular HA matrix after division that recruits inflammatory cells.

31 was associated with reduced infiltration of inflammatory cells (14.1 +/- 1.6% vs. 21.3 +/- 1.5% of t

32 SPECT), or enhanced glycolytic flux seen in inflammatory cells ((18)F-FDG PET).

33 AA by promoting lesion chemokine expression, inflammatory cell accumulation, MAPK signaling, and cyto

34 Consistent with reduced lesion inflammatory cell accumulation, we find significant redu

35 The inflammatory cells activate hepatic stellate cells, whic

36 immune responses in PD, imaging evidence of inflammatory cell activation and evidence of immune dysr

37 lesions, and knocking down RIPK1 will reduce inflammatory cell activation and protect against the pro

38 By directly comparing inflammatory cell activation in a 4 mm ear injury during

39 ncreased baseline IFN production priming for inflammatory cell activation, immune response amplificat

40 is critical to promote the cytokine-induced inflammatory cell adhesion molecule (CAM) expression inc

41 iminished numbers of T cells and nonlymphoid inflammatory cells, along with reduced cytokine mediator

42 is correlated with increased infiltration of inflammatory cells and accelerated tumor growth in the b

43 parasitism, resulting in the recruitment of inflammatory cells and acute damage to the heart tissue.

44 ll inhibition (a) limits the infiltration of inflammatory cells and APC maturation at the graft site;

45 mmation, providing objective measurements of inflammatory cells and aqueous flare.

46 agonist FPS-ZM1 in mice, and the infiltrated inflammatory cells and cytokines were assessed by ELISA.

47 Inflammatory cells and cytokines were assessed in the bl

48 in, interferes with the interactions between inflammatory cells and ECs.

49 Contact between inflammatory cells and endothelial cells (ECs) is a cruc

50 Inflammatory cells and IL-17A(+), IL-17F(+), IL-21(+), I

51 monstrates that dynamic interactions between inflammatory cells and injectable biomaterials can induc

52 s associated with low levels of intrahepatic inflammatory cells and mediators of islet destruction, i

53 ized and compared the host immune responses (inflammatory cells and mediators) and the overall microb

54 a positive feedback loop between peripheral inflammatory cells and networked brain regions involved

55 A stability thereby promoting recruitment of inflammatory cells and production of proinflammatory cyt

56 CXCR4 antagonists mobilize inflammatory cells and promote infarct repair, but the c

57 vasculitis, with perivascular infiltrates of inflammatory cells and rare intravascular fibrin thrombi

58 unohistochemistry, epithelial and submucosal inflammatory cells and remodelling markers were evaluate

59 in neurons is associated with activation of inflammatory cells and subsequent neuroinflammation foll

60 with a significantly reduced accumulation of inflammatory cells and the decreased production of proin

61 xpression also decreased the infiltration of inflammatory cells and the levels of IL-13 and IL-4 in O

62 n sodium homeostasis, such that the study of inflammatory cells and their secreted effectors has prov

63 iables covering clinical characteristics, IS inflammatory cells, and eicosanoids were considered in t

64 structures are composed of accumulations of inflammatory cells, and it has been shown that cytokines

65 re tissue homeostasis by functioning as anti-inflammatory cells, and macrophage-derived matrix metall

66 educed tumor angiogenesis and recruitment of inflammatory cells, and markedly decreased metastasis to

67 edema, infiltration of lung and pancreas by inflammatory cells, and plasma amylase activity compared

68 hyperresponsiveness, decreased the number of inflammatory cells, and reduced the production of cytoki

69 gocytes, tissue infiltration by non-resident inflammatory cells, and the production of pro-inflammato

70 tion of inflammation in the liver, the liver inflammatory cells, and their crosstalk with myofibrobla

71 ) decreases graft infiltration of alloimmune-inflammatory cells; and (d) prolongs allograft survival.

72 Inflammatory cells are important for tumor initiation an

73 ite adipose tissues (VWAT) were assessed for inflammatory cells as well as for differentially methyla

74 ent of Rho-family GTPases was higher in anti-inflammatory cells, but this disparity failed to account

75 roliferation, migration, and permeability of inflammatory cells by activating the mammalian target of

76 increased tumor uptake and reduced uptake in inflammatory cells compared with (S)-4-(3-(18)F-fluoropr

77 Infarct size, heart function, and inflammatory cell composition were analyzed in mouse mod

78 atory infiltrates identified were of chronic inflammatory cells, consisting of lymphocytes (n = 9), p

79 100 expression was inversely correlated with inflammatory cell content in patients.

80 evels of extracellular matrix, fibrotic, and inflammatory cell content were comparable in lesions in

81 icient mice (Ldlr(-/-)) significantly reduce inflammatory cell content within arterial plaques and li

82 l-3 expression significantly correlated with inflammatory cell count on endomyocardial biopsy (r=0.56

83 correlation between plasma Gal-3 levels and inflammatory cell count on endomyocardial biopsy was obs

84 Based on the analysis of inflammatory cell counts in induced sputum, asthmatic pa

85 led increased mean airway wall thickness and inflammatory cell counts in lungs from patients with COP

86 Osteoblast and inflammatory cell counts were counted on hematoxylin-eos

87 to-dry weight ratio, BAL protein levels, BAL inflammatory cell counts, pro-inflammatory cytokines, an

88 ial junction, a critical border region where inflammatory cells cross to promote disease progression.

89 pore-forming amino-terminal fragments causes inflammatory cell death (pyroptosis)(1).

90 brane pores, leading to cytokine release and inflammatory cell death (pyroptosis).

91 ischemic borderzone and increased markers of inflammatory cell death and DNA damage at 12 weeks post-

92 role of XLP-2 and VEO-IBD XIAP mutations in inflammatory cell death and provide a set of tools and f

93 n-1beta (IL-1beta) and IL-18 and inducing an inflammatory cell death called pyroptosis.

94 mbination of TNF-alpha and IFN-gamma induced inflammatory cell death characterized by inflammatory ce

95 s (MHV) activated the NLRP3 inflammasome and inflammatory cell death in the form of PANoptosis.

96 3-driven non-small-cell lung carcinomas from inflammatory cell death induced by SMAC-mimetic chemothe

97 Pyroptosis is the caspase-dependent inflammatory cell death mechanism that underpins the inn

98 e immune responses, inflammasome activation, inflammatory cell death pathways, and cytokine secretion

99 sdermin, the executioner protein of a highly inflammatory cell death reaction termed pyroptosis, whic

100 Pyroptosis is an inflammatory cell death response initiated by supramolec

101 suggest that blocking the cytokine-mediated inflammatory cell death signaling pathway identified her

102 and IL-18 in addition to inducing a type of inflammatory cell death termed "pyroptosis." Leukotriene

103 fate towards pyroptosis-a form of programmed inflammatory cell death that has major roles in health a

104 constitute a molecular pattern that induces inflammatory cell death upon sensing by ZBP1.

105 Altogether, our findings show that inflammatory cell death, PANoptosis, is induced by coron

106 ced inflammatory cell death characterized by inflammatory cell death, PANoptosis.

107 retion of IL-1beta and IL-18 and induces the inflammatory cell death, pyroptosis, via gasdermin D.

108 of inflammatory cytokines, and induction of inflammatory cell death, pyroptosis.

109 plexes that couple cytokine release with pro-inflammatory cell death.

110 Gasdermin D is an executioner of inflammatory cell death.

111 NOD2 phenotype also lower the threshold for inflammatory cell death.

112 as a ROS-sensitive, caspase independent, non-inflammatory cell-death pathway and was important for pr

113 /threonine-protein kinase 3 (RIPK3)-mediated inflammatory cell deathafter coronavirus infection.

114 pancreatitis and much greater in the later, inflammatory cell-dependent phase of the disease.

115 t cardiac endothelial cells established that inflammatory cell-derived Sulf2 and endothelial cell-aut

116 co-expressed in LA revealed numerous immune/inflammatory cells dominated by a myeloid phenotype, in

117 xia emanates from a combination of recruited inflammatory cells (e.g., neutrophils, eosinophils, and

118 er cells, as well as surrounding stromal and inflammatory cells, engage in well-orchestrated reciproc

119 sympathetic neuro-immune modulation and anti-inflammatory cell enrollment as well as prevents oxidati

120 In acute inflammatory cell extracts from exercised mice, we found

121 Data indicate that NF-kappaB activation in inflammatory cells facilitates the development of MS.

122 apture and transport these lipids to promote inflammatory cell fate decisions.

123 ing context-dependent signals that determine inflammatory cell fate decisions.

124 tivation of complement, and interaction with inflammatory cells (fifth dimension).

125 resistin, is upregulated in macrophage-like inflammatory cells from lung tissues of patients with id

126 = 114), blister fluid (n = 23), and primary inflammatory cells from patients with BP were used to in

127 t regulate cellular events required to clear inflammatory cells from sites of infection or injury to

128 drugs (colchicine and metformin) that alter inflammatory cell function and signalling pathways chara

129 Fibrin can modify multiple aspects of inflammatory cell function by engaging leukocytes throug

130 esion molecule-1) and tissue infiltration of inflammatory cells (Gr-1).

131 tromal compartment composed of immune cells, inflammatory cells, growth factors, extracellular matrix

132 ls interface with a greater number of cells, inflammatory cells have the largest contact area suggest

133 t with sloughed tracheobronchial tissues and inflammatory cells in a background of dense mucin.

134 of proinflammatory genes and recruitment of inflammatory cells in a manner that was dependent on HIF

135 e adipocyte cell sizes, increased numbers of inflammatory cells in adipose and liver tissue, and stea

136 Inflammatory cells in bronchoalveolar lavage (BAL) fluid

137 often linked with inflammation, the role of inflammatory cells in contraction of blood clots and thr

138 /CT that is retained by metabolically active inflammatory cells in granulomas, but lacks specificity

139 then analyzed the gene expression pattern of inflammatory cells in HCC tumor samples.

140 red to be associated with the recruitment of inflammatory cells in human airways regardless of the or

141 enhance inflammation, specific signatures of inflammatory cells in humans are missing.

142 ADAMTS5 is associated with interstitial inflammatory cells in IgAN and other kidney lesions and

143 ents, suggesting the imbalance of immune and inflammatory cells in IgG4-related disease.

144 s also often correlate with axons, glial, or inflammatory cells in models where axonal degeneration o

145 in function, the specific role of immune and inflammatory cells in neurodegenerative diseases remain

146 The virus-induced inflammatory cells in patients with COPD were positively

147 However, analyses of inflammatory cells in PD with human periodontal tissue h

148 ondrial interactions and between mesenchymal inflammatory cells in PH.

149 n airway epithelial cells and lamina propria inflammatory cells in severe asthma compared with health

150 ate immune cells and other compartmentalized inflammatory cells in the brains and spinal cords of peo

151 ngth and decreased alveolar protein leak and inflammatory cells in the bronchoalveolar lavage fluid.

152 s derived from fetal liver are the major pro-inflammatory cells in the developing fetus.

153 e no differences (P > 0.05) in the number of inflammatory cells in the endometrium between areas with

154 The recruitment and activation of inflammatory cells in the liver delineates the transitio

155 but not before shock, caused recruitment of inflammatory cells in the lung, increased vascular perme

156 s to prolonged recruitment and activation of inflammatory cells in the respiratory mucosa.

157 he infiltration of T cell subsets, and other inflammatory cells, in the eyes.

158 Histology showed infiltration of inflammatory cells including neutrophils and T lymphocyt

159 meliorate EAU by inhibiting the migration of inflammatory cells, indicating a potential novel therapy

160 ompared to control-RWE, as indicated by lung inflammatory cell infiltrate and mediators, mucus hypers

161 illi, loss of crypt architecture and intense inflammatory cell infiltrate as well as increased GFAP a

162 Synovial NK cells promote a neutrophilic inflammatory cell infiltrate, and persistent arthritis,

163 fferentiated epithelial cells within a dense inflammatory cell infiltrate.

164 filtrate in IgG-treated tumors and increased inflammatory cell infiltrates in anti-CD47 treated tumor

165 ce of neuronal cell toxicity or induction of inflammatory cell infiltrates was observed.

166 marker CK19 vs. control subjects, and islet inflammatory cell infiltrates, independently of the seve

167 tionally, the excised tumors were scored for inflammatory cell infiltrates.

168 , MIP-1alpha, MIP-2, RANTES, and TNF-alpha), inflammatory cell infiltration (CD3 + T cells, macrophag

169 lung pathology scores and alleviated airway inflammatory cell infiltration after adoptive transfer i

170 + Gen group demonstrated the attenuation of inflammatory cell infiltration and H. pylori colonizatio

171 istological analysis revealed that EP favors inflammatory cell infiltration and junctional epithelium

172 6 weeks of age, LivKO mice showed increased inflammatory cell infiltration and proinflammatory gene

173 of periapical inflammation via induction of inflammatory cell infiltration and prolonged cell surviv

174 significantly inhibits pathways that lead to inflammatory cell infiltration and the production of inf

175 tissue displayed increased tissue damage and inflammatory cell infiltration at early time points duri

176 ardiac microvascular perfusion and increases inflammatory cell infiltration in mouse MI/R.

177 ocyte chemoattractant protein 1]), increases inflammatory cell infiltration in the kidney, reduces te

178 , gingival tissues showed significantly more inflammatory cell infiltration in the WT ligated but not

179 nflammatory cardiomyopathy, characterized by inflammatory cell infiltration into the myocardium and a

180 Fibrosis follows UUO, but inflammatory cell infiltration mostly depends upon Notch

181 ent indicated that deletion of TSP-1 reduced inflammatory cell infiltration of muscle fibers, but onl

182 atory cytokines and chemokines and decreased inflammatory cell infiltration of the heart, as well as

183 ns, these animals showed strikingly improved inflammatory cell infiltration versus WT.

184 In stress models, inflammatory cell infiltration was initially lower in kn

185 Inflammatory cell infiltration was observed in both MG a

186 e proliferation of pulmonary vascular cells, inflammatory cell infiltration, and regresses establishe

187 s SMC apoptosis, degrades versican, promotes inflammatory cell infiltration, and thus contributes to

188 nt loss of alveolar bone volume and enhanced inflammatory cell infiltration, as well as an increased

189 iflozin attenuates ISO-mediated increases in inflammatory cell infiltration, collagen deposition and

190 ive DNA repair, melanocyte proliferation, or inflammatory cell infiltration, did not explain melanoma

191 issue samples were analyzed for vascularity, inflammatory cell infiltration, growth pattern, and tumo

192 damage due to elevated pulmonary congestion, inflammatory cell infiltration, iron overload, and secre

193 had markedly reduced weight loss, pulmonary inflammatory cell infiltration, mucus production, and ai

194 sive dilated cardiomyopathy characterized by inflammatory cell infiltration, necrosis, and cardiac fi

195 istopathologic analysis was used to evaluate inflammatory cell infiltration, numbers of osteoblasts a

196 ore, anti-mmu-miR-2137 significantly reduced inflammatory cell infiltration, osteoclast activity, and

197 D-fed low-fitness LCR rats displayed greater inflammatory cell infiltration, serum alanine transamina

198 r stages of the disease are characterized by inflammatory cell infiltration, tissue destruction and n

199 c group exhibited dermal disorganization and inflammatory cell infiltration, which were improved in t

200 pendent on the presence of cGAS, as was skin inflammatory cell infiltration.

201 es of lung vascular permeability, edema, and inflammatory cell infiltration.

202 load, decreased corneal edema, and decreased inflammatory cell infiltration.

203 mucosal dendritic cells, inducing immune and inflammatory cell infiltration.

204 of hBD2 significantly reduced the influx of inflammatory cells into the bronchoalveolar lavage fluid

205 critical role in regulating infiltration of inflammatory cells into the retina.

206 Rlow that contributes to the infiltration of inflammatory cells into the tracheal mucosa.

207 IVCM shows that inflammatory cells invade only the stroma during an acut

208 mature intracellular protease activation and inflammatory cell invasion.

209 To characterize the inflammatory cells involved in osteoarthritis, synovial

210 Recruitment of inflammatory cells is a major feature of alcoholic liver

211 quencing (scRNA-seq) was performed on airway inflammatory cells isolated from sex-mismatched lung tra

212 ce had decreased airway resistance and fewer inflammatory cells, less severe histopathology, and lowe

213 ar smooth muscle cells, cardiac myocytes and inflammatory cells, like monocyte/macrophages, cellular

214 anied by high numbers of red blood cells and inflammatory cells (macrophage surface glycoproteins bin

215 ular protease activation and infiltration of inflammatory cells, mainly neutrophil granulocytes and m

216 Inflammatory cells multitask at the wound site by facili

217 of histamine-secreting bacteria also reduced inflammatory cell numbers in bronchoalveolar lavage (BAL

218 st cell number was higher and osteoclast and inflammatory cell numbers were lower in the P group comp

219 Microglia are resident inflammatory cells of the CNS and have important roles i

220 .78, p < 0.001) or honeycomb distribution of inflammatory cells (OR 5.24, 95% CI: 1.44-19.06, p = 0.0

221 s of function of IDO in smooth muscle cells, inflammatory cells, or cardiomyocytes does not affect ca

222 We show an additional set of multiple inflammatory cell pathways involved in virus-associated

223 rate asthma, an almost equal distribution of inflammatory cell patterns, the lowest concentrations of

224 g to neutrophilic versus nonneutrophilic BAL inflammatory cell patterns.

225 The mean number of inflammatory cells per mm(2) in the 20-Gy group was sign

226 nents of the RAS signaling cascade influence inflammatory cell phenotype and function with unpredicta

227 The virus-induced inflammatory cell phenotypes observed in COPD positively

228 Bronchial mucosal inflammatory cell phenotypes were determined at preinfec

229 liber, extent of injury, C4d positivity, and inflammatory cell phenotyping.

230 We investigated whether different inflammatory cell population and cytokine profiles in le

231 by regulating blood-derived and local brain inflammatory cell populations involved in beta-amyloid c

232 d obesity is associated with accumulation of inflammatory cells predominantly in visceral adipose dep

233 led pentixafor to detect CXCR4 expression on inflammatory cells present in atherosclerotic plaques of

234 Finally, inflammatory cell recruitment and cytokine generation in

235 Attenuation of inflammatory cell recruitment and cytokine production by

236 MCP-1 regulates inflammatory cell recruitment and differentiation of mac

237 Intra-prostatic inflammatory cell recruitment and expansion can ultimate

238 mber, improved ATP production, and decreased inflammatory cell recruitment and pulmonary oedema in ag

239 o C3aR-deficient mice rescues the defects in inflammatory cell recruitment and regeneration.

240 mor growth, inhibited tumor angiogenesis and inflammatory cell recruitment and, most importantly, pre

241 ntify ALS patients with an altered course of inflammatory cell recruitment at the diseased central ne

242 eting DR cells may be useful to mitigate the inflammatory cell recruitment in AH.

243 lation with pyridostigmine (PY) induces anti-inflammatory cell recruitment soon after myocardial infa

244 ed in reduced airway hyperresponsiveness and inflammatory cell recruitment to the lung.

245 r with Src42A and Draper to ensure effective inflammatory cell recruitment to wounds.

246 The generalized impairment in inflammatory cell recruitment was associated with compen

247 rkers of adiposity, endothelial dysfunction, inflammatory cell recruitment, and cardiac stress and in

248 nterleukin-6 release, complement activation, inflammatory cell recruitment, and demyelination.

249 te the production of matrix metalloprotease, inflammatory cell recruitment, and dendritic cell matura

250 phagy, mitochondrial dysfunction, apoptosis, inflammatory cell recruitment, profibrotic signaling, an

251 ein kinase signaling, tumor angiogenesis and inflammatory cell recruitment.

252 inflammation, decreased lung infiltration of inflammatory cells, reduced NETosis activity, and more l

253 hat JAK3 inhibition enhances infiltration of inflammatory cells, reduces expression of Wnt3a and Dvl3

254 Within a healing skin wound, recruited inflammatory cells release a multitude of bacteriocidal

255 EMA3F, we investigated the role of SEMA3F in inflammatory cell retention within inflamed tissues.

256 oblasts suggests roles in matrix deposition, inflammatory cell retention, and connective tissue cell

257 utaneous injury is a coordinated response of inflammatory cells, secreted factors, and biologically a

258 ressed by macrophages and essential for anti-inflammatory cell signaling and regulation of cytokine e

259 the approximate threshold for eliciting anti-inflammatory cell signaling in macrophages ( approximate

260 red brain injury exhibit an induction of pro-inflammatory cell signaling, a robust activation of adap

261 Together these data demonstrate inflammatory cells significantly contribute to scar elec

262 Finally, the main inflammatory cell subpopulations that are present in the

263 Transgenic lines expressing luciferase in inflammatory cell subsets (myeloid cells, T cells, and B

264 nalysis reveals a specific shift from highly inflammatory cell subsets toward a resting state upon de

265 ecruit leukocytes, and the identification of inflammatory cell subtypes in lesions spurred the unrave

266 ls are the resident macrophage in the liver, inflammatory cells such as infiltrating macrophages, T l

267 mechanistic insights into Pf drug action on inflammatory cells such as neutrophils.

268 n and mast cells induce IL-6 production from inflammatory cells such as skin fibroblasts and promote

269 Type 2 cytokines activate inflammatory cells that are implicated in the pathogenic

270 e course and severity are mostly governed by inflammatory cells that drive local and systemic immune

271 in part, from the induction and expansion of inflammatory cells that include myeloid-derived suppress

272 s with the unique subsets of myeloid-derived inflammatory cells that infiltrate sites of infection.

273 Neutrophils are major inflammatory cells that rapidly infiltrate wounds to pro

274 n skin biology, including the recruitment of inflammatory cells, the alteration of the skin microbiom

275 drugs may lead to stimulations of immune or inflammatory cells, three forms of DHR were discriminate

276 These data suggest that the inflammatory cells through their expression of tissue fa

277 ur results demonstrate an essential role for inflammatory cells to regulate a regenerative response.

278 llergic airway inflammation increases FAO in inflammatory cells to support the production of cytokine

279 f effector T cell responses and migration of inflammatory cells to the CNS.

280 The contribution of inflammatory cells to the electrophysiological propertie

281 l as the expression of chemokines attracting inflammatory cells to the nasal mucosa.

282 g to extensive migration and infiltration of inflammatory cells to the ocular surface.

283 tcecal ligation and puncture) recruitment of inflammatory cells to the peritoneum, or improve phagocy

284 Inflammatory cell trafficking after MI is controlled by

285 flective cellular structures consistent with inflammatory cells transiently occupied the anterior to

286 , CTSD is expressed in pancreatic acinar and inflammatory cells, undergoes subcellular redistribution

287 though we observed an increase of peripheral inflammatory cells, we did not detect differences in ery

288 chemoattractive effects of CCL2 and CCL21 on inflammatory cells were inhibited by MSC-Exo.

289 ung ILC2, IL-5 and IL-13 production, and BAL inflammatory cells were measured on day 5 of Alt Ext cha

290 xposure, higher bronchoalveolar lavage fluid inflammatory cells were observed in all mice (KKAy > KK

291 Inflammatory cells were observed with CD3 biomarker in n

292 s of subepithelial interferon/PRR-expressing inflammatory cells were related to greater viral load, a

293 esence of myeloperoxidase (MPO) derived from inflammatory cells, which are active participants in wou

294 imental peripheral factors, including immune/inflammatory cells, which contribute to motor neuron dys

295 ug interactions with receptors or enzymes of inflammatory cells, which may lead to their direct activ

296 V565 tissue penetration and association with inflammatory cells, while decreased phosphoproteins afte

297 microcirculation impairment, infiltration of inflammatory cells with local production of proinflammat

298 dominated by an interstitial accumulation of inflammatory cells with minimal-to-absent fibrosis.

299 was detected in tubular epithelial cells and inflammatory cells within the grafts.

300 Colchicine led to an increase in inflammatory cells within the renal parenchyma.