ライフサイエンスコーパス: inflammatory cell

1 y process promoting the recruitment of other inflammatory cells.

2 coupled receptor G2A on myeloid and lymphoid inflammatory cells.

3 M-derived tdT+ cells in injured kidneys were inflammatory cells.

4 , removal of myofibroblasts, and the role of inflammatory cells.

5 , whereas in TCMR, this may be controlled by inflammatory cells.

6 vere in regions of extravasated perivascular inflammatory cells.

7 tive in vivo detection of cell therapies and inflammatory cells.

8 coupled receptors on acinar cells or through inflammatory cells.

9 rate, but no change in other myeloid-derived inflammatory cells.

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

11 les that can transport inflammatory cargo to inflammatory cells.

12 iding with a local increase in the number of inflammatory cells.

13 regulate calcium signaling and migration of inflammatory cells.

14 area, collagen area, and submucosal effector inflammatory cells.

15 and did not demonstrate increased numbers of inflammatory cells.

16 y polarization and intestinal homing of many inflammatory cells.

17 ated their impact on phagocytosis in myeloid inflammatory cells.

18 These foreign materials were surrounded by inflammatory cells.

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

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

21 in plaque formation such as infiltration of inflammatory cells.

22 es are upregulated to promote recruitment of inflammatory cells.

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

24 tion and inflammation by both structural and inflammatory cells.

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

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

27 exhibited few collagen fibers among numerous inflammatory cells.

28 arked reduction in number of osteoclasts and inflammatory cells.

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

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

31 duce pancreatitis, parenchymal or periductal inflammatory cell accumulation, ductal hyperplasia, or d

32 dent of weight loss, decreases perilymphatic inflammatory cell accumulation, improves lymphatic funct

33 animals and decreases perilymphatic iNOS and inflammatory cell accumulation.

34 ed by the infiltration and transmigration of inflammatory cells across the endothelium to infected ti

35 The inflammatory cells activate hepatic stellate cells, whic

36 additional useful applications to block pro-inflammatory cell activation events but complicates how

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

38 tive molecule commonly secreted by recruited inflammatory cells, allowing for paracrine signaling at

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

40 re accelerated, and sequestrum formation and inflammatory cell and TNF-alpha infiltration were signif

41 he skin lesions, with a diminished influx of inflammatory cells and a reduced epidermal hyperprolifer

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

43 ngs also demonstrated marked infiltration of inflammatory cells and activation of NF-kappaB.

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

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

46 ity supplying the bone marrow (BM) increases inflammatory cells and decreases angiogenic cells, littl

47 incle was highly expressed in hepatic innate inflammatory cells and endothelial cells in both mice an

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

49 expression was mainly found in infiltrating inflammatory cells and in the glomeruli.

50 rivers and other somatic alterations recruit inflammatory cells and induce changes in normal cells to

51 A, whereas nonspecific DEGs are expressed by inflammatory cells and induced by IFN-gamma and tumor ne

52 g in decreased perilymphatic accumulation of inflammatory cells and inducible nitric oxide synthase e

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

54 plays a pivotal role in distinct immune and inflammatory cells and is expressed in eosinophils and l

55 CCR9 mediates the chemotaxis of inflammatory cells and participates in the pathological

56 is a wealth of information about the role of inflammatory cells and pathways during acute injury and

57 sses the current limitations of studies, the inflammatory cells and pathways linked to emerging pheno

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

59 f other tracers, including those that target inflammatory cells and proteolytic enzymes (eg, integrin

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

61 tes to hypertension by increasing peripheral inflammatory cells and their extravasation into the brai

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

63 We also observed a remarkable influx of inflammatory cells and upregulation of cytokines in kidn

64 tinal) from infiltrating bone marrow-derived inflammatory cells and were made diabetic using streptoz

65 nature, increased collagen deposition, fewer inflammatory cells, and improved indices of angiogenesis

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

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

68 in vitro and to analyze how gut microbiome, inflammatory cells, and peristalsis-associated mechanica

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

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

71 ty of LCs and challenge the notion that some inflammatory cells are a population of monocyte-derived

72 ve, stroma-rich tumours with infiltration of inflammatory cells are even more aggressive.

73 The viability and integrity of the inflammatory cells are maintained during the acoustoflui

74 an inflammatory lipotoxic disorder, but how inflammatory cells are recruited and activated within th

75 ice in situations where mesenchymal cells or inflammatory cells are significantly increased in the pa

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

77 receptor axes regulating the trafficking of inflammatory cells at all stages of the disease.

78 e showed reduced numbers of monocyte-derived inflammatory cells at the infection site, impaired IFNga

79 ic cue for cytolysis from recruited sentinel inflammatory cells before shedding.

80 ells-dependent inflammatory process attracts inflammatory cells but also generates changes in the api

81 ndothelial cells only- increases circulating inflammatory cells, but decreases their aortic infiltrat

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

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

84 (AT1) receptors in the kidney or circulating inflammatory cells can have opposing effects on the gene

85 Thus, in these highly inflammatory cells, changes in Morrbid levels provide a

86 were less contaminated with mesenchymal and inflammatory cells, compared to UEA-I purified acinar ce

87 100 expression was inversely correlated with inflammatory cell content in patients.

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

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

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

91 ERp57 resulted in a significant decrease in inflammatory cell counts and airways resistance in a mur

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

93 f upper airway specimens identifies specific inflammatory cells, cytokine signatures, and fibrotic ai

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

95 ammatory cytokines IL-1beta and IL-18 and an inflammatory cell death called pyroptosis.

96 IL-1beta and IL-18 and the initiation of an inflammatory cell death pathway termed pyroptosis.

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

98 d not secrete IL-1beta and exhibited reduced inflammatory cell death, referred to as pyroptosis.

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

100 essential role in inflammatory signaling and inflammatory cell death.

101 AM pyroptosis, a type of caspase-1-dependent inflammatory cell death.

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

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

104 neoplasia to image the interactions between inflammatory cells drawn to a wound, and to adjacent pre

105 uced tissue remodeling by 50%, and decreased inflammatory cells (e.g. eosinophils down by 54%)/inflam

106 hich results from a combination of recruited inflammatory cells (e.g., neutrophils and monocytes), th

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

108 erative disease Duchenne muscular dystrophy, inflammatory cells enter muscles in response to repetiti

109 ion of microglia/astrocytes, infiltration of inflammatory cells, expression of chemokines/cytokines,

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

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

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

113 inflamed limbs and highlighted the resident inflammatory cells, fibroblast-like synoviocytes (FLSs),

114 rated from a SSAW field to actively transfer inflammatory cells from a solution containing residual D

115 For sputum analysis, the transfer of inflammatory cells from liquefied sputum samples to a cu

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

117 n and facilitates immunophenotyping of major inflammatory cells from sputum samples.

118 on is a critical step because it removes the inflammatory cells from the presence of residual dithiot

119 High PD-L1 expression by inflammatory cells from the tumor microenvironment also

120 PD-L1 expression was assessed in tumour and inflammatory cells from tumour biopsies provided at stud

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

122 matory cytokines and greater accumulation of inflammatory cells in A2AR(-/-) mice than wild-type (WT)

123 nflammatory responses and chemoattraction of inflammatory cells in asthma.

124 ins unknown whether nestin(+) cells regulate inflammatory cells in chronic inflammatory diseases, suc

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

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

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

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

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

130 uppressing infiltration of multiple kinds of inflammatory cells in infarcted heart.

131 s showed a lack of injury or infiltration of inflammatory cells in livers of Liv-Ikk2ca mice.

132 myelinated and remyelinated fibers and fewer inflammatory cells in lumbar motor roots, as well as in

133 peritoneal macrophages and monocyte-derived inflammatory cells in lungs and spleen.

134 ammatory response and limits infiltration of inflammatory cells in peri-infarct ventricular tissue, i

135 ondrial interactions and between mesenchymal inflammatory cells in PH.

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

137 Macrophages are essential inflammatory cells in skin wound regeneration.

138 SLC8A1, was expressed in spindle-shaped and inflammatory cells in the aneurysm wall.

139 e presence and accumulation of MPO-secreting inflammatory cells in the brain (r = 0.93).

140 ier integrity, and increased infiltration of inflammatory cells in the CNS.

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

142 vides important new insight into the role of inflammatory cells in the genesis of vascular dementia.

143 In bronchial tissue, uPAR was elevated in inflammatory cells in the lamina propria (P = 0.0019), b

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

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

146 levels of essential lipids to be related to inflammatory cells in the stroma, while cancerous areas

147 affect the maturation and differentiation of inflammatory cells in the tumor microenvironment.

148 ression and a reduced number of infiltrating inflammatory cells in vivo.

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

150 tion as evidenced by reduced infiltration of inflammatory cells including eosinophils, dendritic cell

151 show significantly enhanced infiltration of inflammatory cells, including eosinophils and lymphocyte

152 The IL-33R, ST2, is expressed on several inflammatory cells, including eosinophils, and is best c

153 ed in airway recruitment of Gal-1-expressing inflammatory cells, including eosinophils, as well as in

154 ill summarize the contributions of different inflammatory cells, including hepatic macrophages, T and

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

156 s cellulose parasite with an extensive mixed inflammatory cell infiltrate in the surrounding tissue.

157 experiment, NPRM-bLXA4 dramatically reduced inflammatory cell infiltrate into chronic periodontal di

158 erized by myofibroblast proliferation and an inflammatory cell infiltrate.

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

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

161 numbers of mucus-producing goblet cells and inflammatory cell infiltrates were reduced.

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

163 s exhibited progressive fibrosis and chronic inflammatory cell infiltrates.

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

165 e dust mite antigen, Zbtb46-negative CD64(+) inflammatory cells infiltrating the lung were substantia

166 ne level (PBL) loss and histomorphometry for inflammatory cell infiltration and collagen density.

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

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

169 er that controls the magnitude and extent of inflammatory cell infiltration by suppressing canonical

170 Autoantibody deposition and inflammatory cell infiltration in target organs such as

171 Despite the high levels of viral antigen and inflammatory cell infiltration in the liver, the charact

172 ted CXCL12-induced morphological changes and inflammatory cell infiltration in the mouse lung, and pr

173 Osteoclast density and inflammatory cell infiltration in the RvE1 groups were l

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

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

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

177 M) mice do not have increased adipose tissue inflammatory cell infiltration or greater expression of

178 d VEGF release were drastically reduced, and inflammatory cell infiltration was abrogated nearly comp

179 Inflammatory cell infiltration was observed in both MG a

180 In the induction phase, PBL and inflammatory cell infiltration were significantly reduce

181 In the recovery phase, PBL and inflammatory cell infiltration were significantly reduce

182 i-fibrotic effects through its inhibition of inflammatory cell infiltration, alveolar structure disru

183 sodium exhibited severe colitis, had greater inflammatory cell infiltration, and an increased presenc

184 toantibody binding is followed by a lesional inflammatory cell infiltration, and the overall clinical

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

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

187 zation, medial hypertrophy, and perivascular inflammatory cell infiltration, associated with raised p

188 We demonstrated that IP deficiency increased inflammatory cell infiltration, eosinophilia, and IL-5 a

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

190 sease characterized by synovial hyperplasia, inflammatory cell infiltration, irreversible cartilage a

191 elopment in AdAPN mice by suppressing aortic inflammatory cell infiltration, medial degeneration and

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

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

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

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

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

197 including IL-8 and CCL20, and reduce further inflammatory cell infiltration.

198 umors featuring Akt activation and extensive inflammatory cell infiltration.

199 tissue attachment, and the surface area with inflammatory cell infiltration.

200 jury, apoptosis, renal oxidative stress, and inflammatory cell infiltration.

201 ulein and L-arginine induction, with obvious inflammatory cells infiltration.

202 13 and IL-4 production from splenocytes, and inflammatory cell infiltrations in the lesions 48 h afte

203 constriction, airway hyperresponsiveness and inflammatory cell influx suggesting the presence of a no

204 had bronchial hyperreactivity and increased inflammatory cell influx when infected with RSV compared

205 nduced hypothermic response, infiltration of inflammatory cells into the airway, and lung inflammatio

206 the adjuvants led to an influx of activated inflammatory cells into the muscle but to little systemi

207 capillaries and the increase of infiltrating inflammatory cells into the retina (F4/80(+)) (preventio

208 was associated with reduced infiltration of inflammatory cells into the retina and decreased numbers

209 sted that IL-1 contributed to recruitment of inflammatory cells into the skin.

210 Burn injury caused mobilization of human inflammatory cells into the systemic circulation.

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

212 Our study demonstrates that inflammatory cells invading the brain lead to secondary

213 a dynamic vascular disease characterized by inflammatory cell invasion and extracellular matrix degr

214 cadherin-11 is upregulated during tumour and inflammatory cell invasion, but the mechanisms underlyin

215 mature intracellular protease activation and inflammatory cell invasion.

216 Neutrophils are the predominant inflammatory cell involved in periodontitis and have pre

217 To characterize the inflammatory cells involved in osteoarthritis, synovial

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

219 ression by either neoplastic or intratumoral inflammatory cells is related to tumor aggressiveness an

220 rface response while the secondary influx of inflammatory cells leading to the recruitment and activa

221 s of micro-computed tomography, infiltrating inflammatory cells measured by quantitative histology, a

222 nestin expression marks cells that regulate inflammatory cell migration during atherosclerosis.

223 Here, we show that nestin(+) cells direct inflammatory cell migration during chronic inflammation.

224 n addition to its well-characterized role in inflammatory cell migration, DP2 might contribute to air

225 ere collected 4 hours after injury and human inflammatory cell mobilization analyzed using flow cytom

226 Inflammatory cells multitask at the wound site by facili

227 epidermis, which triggers the recruitment of inflammatory cells needed to support skin carcinogenesis

228 by weight loss, bronchoalveolar lavage (BAL) inflammatory cell number, cytokine concentration, protei

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

230 wn about the reciprocal impact of BM-derived inflammatory cells on neuroinflammation in hypertension.

231 a (IKKbetaca) in epithelial cells but not in inflammatory cells or the surrounding stroma (IKKbetaca

232 Inflammatory cells orchestrate postischemic cardiac remo

233 is generally achieved by rapid migration of inflammatory cells out of circulation, through modified

234 Within hours, there is an infiltration by inflammatory cells, particularly Th2 T lymphocytes, eosi

235 The mechanism(s) by which inflammatory cells persist in VZV-infected arteries is u

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

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

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

239 A expression in sputum supernatants with the inflammatory cell profile and disease severity in asthma

240 ytokine levels (ELISA and quantitative PCR), inflammatory cell profile, and AHR (flexiVent) were asse

241 posed of fibrous tissues, myofibroblasts and inflammatory cell proliferation with obscure etiology.

242 eight gain and accumulation of perilymphatic inflammatory cells (r = 0.9872, P < 0.0005) and expressi

243 Investigation of inflammatory cells recruited to inflamed G2A(-/-) colons

244 tor 1 (TNFR1)/TNFR2 (TNFR1R2) with increased inflammatory cell recruitment and bacterial load in the

245 pid signaling also correlated with increased inflammatory cell recruitment and CSF1R signal transduct

246 Attenuation of inflammatory cell recruitment and cytokine production by

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

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

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

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

251 umor cell-intrinsic PI3'-lipid signaling and inflammatory cell recruitment has remained enigmatic.

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

253 ence or blockade of functional VAP-1 reduced inflammatory cell recruitment to the liver and attenuate

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

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

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

257 e lung resulted in enhanced mucus secretion, inflammatory cell recruitment, and cytokine production i

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

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

260 ed IgE production, chemokine expression, and inflammatory cell recruitment.

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

262 To this end, we hypothesized that the human inflammatory cell response to injury could be selectivel

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

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

265 PC-cleaved form of fV are cofactors for anti-inflammatory cell signaling by aPC in the context of end

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

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

268 d peptides (EDPs), which are chemotactic for inflammatory cells such as monocytes.

269 tment has been ascribed to changes in dermal inflammatory cells, such as activation of Th2 cells and

270 osis warrants targeted treatment of specific inflammatory cells that aggravate the disease.

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

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

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

274 and counterbalance of subsets of immune and inflammatory cells that interact through interleukins, i

275 uppressor cells (MDSCs) are highly prevalent inflammatory cells that play a key role in tumor develop

276 herefore a key reprogrammer of metabolism in inflammatory cells that promotes inflammatory gene expre

277 Reduced infiltration of inflammatory cells, that is, CD3(+) lymphocytes and F4/8

278 oxidative stress increased necrotic death of inflammatory cells, thereby resulting in lethal damage t

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

280 The exact contribution of inflammatory cells to a TBI lesion is dictated by their

281 We investigated whether radiation causes inflammatory cells to acquire an immune-suppressive phen

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

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

284 of iPLA2beta may decrease the recruitment of inflammatory cells to the heart to manage parasite accum

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

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

287 However, purines are also essential for inflammatory cell trafficking in animal models of allerg

288 his review we revisit classical paradigms of inflammatory cell trafficking in the context of recent s

289 In another critical inflammatory cell type, Th17 cells, HIF1alpha acts via t

290 o modulate the communication between KCs and inflammatory cells under co-culture conditions.

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

292 an acoustofluidic platform for transferring inflammatory cells using standing surface acoustic waves

293 mune-system predominantly reflecting the pro-inflammatory cell wall beta-glucans.

294 endothelial proliferation and subendothelial inflammatory cells were found in sections of all infecte

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

296 condary processes, including infiltration of inflammatory cells, which can exacerbate brain inflammat

297 n as well as recruitment and infiltration of inflammatory cells, which in turn triggers further endot

298 exposed ECs activate airway DCs and effector inflammatory cells, which together induce a HDM-specific

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

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