ライフサイエンスコーパス: inflammatory

1 Remarkably, all these inflammatory actions by activated platelets were abrogat

2 Anti-inflammatory activity was observed in casein hydrolysate

3 ndant serine/threonine phosphatase with anti-inflammatory activity.

4 owledge, the external application of an anti-inflammatory agent in animals.

5 populations experience recurrent exposure to inflammatory agents that catalyze fluctuations in the co

6 erations of host transcripts associated with inflammatory and acute-phase responses, coagulative acti

7 n resulted in rapid deployment of both a pro-inflammatory and an immunosuppressive response in the sk

8 active than AGN 211377, but pronounced anti-inflammatory and angiostatic effects were achieved by ad

9 Lutein is a carotenoid presenting known anti-inflammatory and antioxidant properties.

10 Anti-inflammatory and bronchodilator treatments are the mains

11 To better define serum inflammatory and cardiovascular risk proteins, we used a

12 roids) are steroid hormones with potent anti-inflammatory and immune modulatory profiles.

13 lobal regulatory changes that impact hepatic inflammatory and lipid metabolic pathways, providing new

14 omplement-driven networks in a wide range of inflammatory and neurodegenerative disorders and cancer.

15 uccess in therapies targeting the downstream inflammatory and oxidative effects of CO poisoning.

16 rotein C functions as an anticoagulant, anti-inflammatory and regenerative factor.

17 sident macrophages and the induction of anti-inflammatory and tissue repair genes in the lungs after

18 Exudates were collected 6 h (inflammatory) and 24 h (resolving) following carrageenan

19 ssion could provide a new target for an anti-inflammatory approach in diabetic vascular disease.

20 ere WAS manifesting as cutaneous vasculitis, inflammatory arthropathy, intermittent polyclonal lympho

21 ostic tests in DED are tear film osmolarity, inflammatory biomarkers, and meibomian gland imaging.

22 as studied in blood samples of patients with inflammatory bowel disease (IBD) receiving anti-TNF ther

23 is (OA)) or chronic inflammatory conditions (inflammatory bowel disease (IBD)) can be identified.

24 ith familial adenomatosis polyposis (FAP) or inflammatory bowel disease (IBD).

25 pus erythematosus (SLE), Sjogren's syndrome, inflammatory bowel disease and multiple sclerosis.

26 Moreover, DC-LMP1/CD40 chimeras developed inflammatory bowel disease characterized by massive tran

27 s of Crohn's disease, ulcerative colitis, or inflammatory bowel disease unclassified before the age o

28 with IBD (1646 with CD, 583 with UC, and 116 inflammatory bowel disease unclassified) and 5002 indivi

29 t of rheumatologic conditions, malignancies, inflammatory bowel disease, dermatologic conditions, or

30 atory diseases, such as allergy, asthma, and inflammatory bowel disease.

31 phages may contribute to the pathogenesis of inflammatory bowel disease.

32 ptophan and its metabolites in patients with inflammatory bowel diseases (IBD), and study their assoc

33 Inflammatory bowel diseases (IBD), including Crohn's dis

34 teractions are altered during development of inflammatory bowel diseases (IBDs).

35 Strategies for management of inflammatory bowel diseases are shifting from simple con

36 BACKGROUND & AIMS: Diarrhea associated with inflammatory bowel diseases has been associated with inc

37 ls and intestinal tissues from patients with inflammatory bowel diseases vs controls, we found that r

38 tral pathological feature of colitis and the inflammatory bowel diseases.

39 ne expression patterns associated with human inflammatory bowel diseases.

40 ncatecholaminergic support in the setting of inflammatory cardiovascular dysfunction.

41 me allows for the cleavage and activation of inflammatory caspases.

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

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

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

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

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

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

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

49 es are upregulated to promote recruitment of inflammatory cells.

50 y process promoting the recruitment of other inflammatory cells.

51 ntrinsic contractile activity and associated inflammatory changes.

52 ell-source for new neurons in infectious and inflammatory colitis.

53 r MS-444 in AOM/DSS mice, a model of IBD and inflammatory colon cancer, augmented DSS-induced weight

54 erize the immunohistopathology of this novel inflammatory condition.

55 ritis (PsA), osteoarthritis (OA)) or chronic inflammatory conditions (inflammatory bowel disease (IBD

56 ulcerative colitis (UC), are complex chronic inflammatory conditions of the gastrointestinal tract th

57 can reverse back to the immune system under inflammatory conditions via the production of an interge

58 By contrast, under inflammatory conditions, estrogen effects depend upon st

59 Although FetA is involved in numerous inflammatory conditions, its potential role in allergy i

60 t can act as an adjuvant in the treatment of inflammatory conditions.

61 e function with therapeutic implications for inflammatory conditions.

62 ysiological state of blood vasculature under inflammatory conditions.

63 aintenance of Th17 effector responses in the inflammatory contexts of both acute infection and chroni

64 riming and elevated T cell expression of the inflammatory cytokine GM-CSF, concomitant with pancreati

65 enhancing the release of the regulatory/anti-inflammatory cytokine IL-10.

66 , as well as a plasmatic increase of the pro-inflammatory cytokine IL-1beta.

67 o seizures and have high brain levels of the inflammatory cytokine IL-1beta.

68 articles with strong interferon and mild pro-inflammatory cytokine induction may qualify as vaccine a

69 xpression, while monocytes expressed the pro-inflammatory cytokine interleukin-1beta (IL-1beta).

70 cells require sustained Ca(2+) signaling for inflammatory cytokine production and the killing of targ

71 ate, colonic infiltration of neutrophils and inflammatory cytokine production are impaired in M-ILK-d

72 wever, this can be reversed by inhibition of inflammatory cytokine production that can be used to pro

73 st that peripheral tumors elicit central pro-inflammatory cytokine production, in turn leading to dep

74 ciated with diminished Vdelta2(+) T cell pro-inflammatory cytokine production.

75 Despite having significantly reduced inflammatory cytokine responses to LPS and bacterial inf

76 JAK1 is a critical effector of pro-inflammatory cytokine signaling and plays important role

77 or miR-718 in controlling TLR4 signaling and inflammatory cytokine signaling through a negative feedb

78 Levels of anti-inflammatory cytokine TGF-beta remained practically unaf

79 enged with LPS had exacerbated levels of pro-inflammatory cytokines and exhibited significantly worse

80 st that the particles that do not induce pro-inflammatory cytokines and high levels of interferons ca

81 s specific antibodies, reduced levels of pro-inflammatory cytokines and innate immune cells.

82 viremia were similar, however, the levels of inflammatory cytokines and MDSC were more pronounced pos

83 ocytes and dendritic cells that produce more inflammatory cytokines both at baseline and following en

84 bserved increased gene expression of the pro-inflammatory cytokines IFN-gamma, TNF-alpha, IL-1beta an

85 caries, dental pulp expresses a range of pro-inflammatory cytokines in response to the infectious cha

86 ole in the elevations in cutaneous and serum inflammatory cytokines induced by epidermal dysfunction.

87 of human MCF-7 breast cancer cells with pro-inflammatory cytokines results in ERalpha-dependent acti

88 sferase levels, apoptotic markers, and human inflammatory cytokines returned to pretreatment levels w

89 riven by growth factors such as VEGF and pro-inflammatory cytokines such as TNF-alpha.

90 lower metabolic activity and release of pro-inflammatory cytokines than CFC tissue, but surprisingly

91 In animal studies, central and blood borne inflammatory cytokines that can be elevated in RA evoke

92 ortantly, strongly reduced the production of inflammatory cytokines upon stimulation with aminobispho

93 acrophages from Cmah(-/-) mice secreted more inflammatory cytokines with LPS stimulation and showed m

94 ed that patients with elevated pro- and anti-inflammatory cytokines would have higher mortality rates

95 e leukocytosis, elevated serum pro- and anti-inflammatory cytokines, and evidence of innate cell acti

96 was implicated as a checkpoint regulator of inflammatory cytokines, as well as an inflammasome activ

97 has been associated with increased levels of inflammatory cytokines, including tumor necrosis factor

98 g functional recovery after SCI by dampening inflammatory cytokines, thus pointing towards a new dire

99 splanchnic nerve (GSN), and elevation of pro-inflammatory cytokines.

100 exhibited significantly increased levels of inflammatory cytokines.

101 were a host of circulating or intra-alveolar inflammatory cytokines.

102 n the increased T-helper 1 cytokine-mediated inflammatory damage in heart.

103 s can enable control of infection or mediate inflammatory damage.

104 xample, cervicitis, endometritis, and pelvic inflammatory disease (PID), including an association wit

105 Chronic pancreatitis (CP) is a fibro-inflammatory disease leading to pain, maldigestion, and

106 Multiple sclerosis is a degenerative inflammatory disease of the CNS characterised by immune-

107 gingival tissue of patients with the chronic inflammatory disease periodontitis (PD).

108 Psoriasis is a chronic inflammatory disease resulting from dysregulated immune

109 A are protective in various animal models of inflammatory disease.

110 shown to protect against the development of inflammatory diseases, such as allergy, asthma, and infl

111 In case of a BAA associated with chronic inflammatory diseases, such as COPD, in patients with he

112 l to inflammation, but also promotes chronic inflammatory diseases.

113 ired for improving the management of chronic inflammatory diseases.

114 erived oxidants contribute to propagation of inflammatory diseases.

115 ukocyte infiltration and are associated with inflammatory disorders involving marked eosinophilia (e.

116 of cathepsin G inhibitors targeting chronic inflammatory disorders.

117 ceptor signaling is a key feature of various inflammatory disorders.

118 nd will be an important asset in future anti-inflammatory drug design.

119 sured the derivatives of the well-known anti-inflammatory drug Piroxicam using THz spectroscopy and e

120 ratory infection (ARI) and nonsteroidal anti-inflammatory drugs (NSAIDs) use could trigger acute myoc

121 ed) shows that colchicine, nonsteroidal anti-inflammatory drugs (NSAIDs), and corticosteroids reduce

122 amming, blockade of these pathways with anti-inflammatory drugs or components of the nucleosome remod

123 ogical inhibitors, such as nonsteroidal anti-inflammatory drugs or small interfering RNAs (siRNAs) ag

124 Nonsteroidal anti-inflammatory drugs use during ARI episodes, especially p

125 mushrooms extracts exert a synergistic anti-inflammatory effect.

126 between preadmission use of drugs with anti-inflammatory effects and risk of new-onset depression an

127 und that MR-409 exerted antioxidant and anti-inflammatory effects in retinas of the treated rats, as

128 igated the potential antidepressant and anti-inflammatory effects of BHB on rats exposed to acute and

129 kingly, cGAMP exerts cell-type-specific anti-inflammatory effects on macrophages, hepatocytes, and ad

130 ch to enhance their antinociceptive and anti-inflammatory effects, as well as to protect the nervous

131 fatty acids (PUFAs) provide beneficial anti-inflammatory effects, in part through their conversion t

132 e, which may be attributable in part to anti-inflammatory effects.

133 hanolamine mediate an array of pro- and anti-inflammatory effects.

134 that ETO-curcumin may provide superior anti-inflammatory efficacy compared to standard curcumin.

135 index (DAI) dose-dependently, while the anti-inflammatory efficacy of standard curcumin remained cons

136 nd the expression of M2 marker Arginase 1 in inflammatory-elicited macrophages.

137 temcomitans Ltx with respect to clinical and inflammatory findings in individuals with or without per

138 Hidradenitis suppurativa (HS) is a recurrent inflammatory follicular disease that commonly affects th

139 malabarica as natural antioxidative and anti-inflammatory functional food ingredients was demonstrate

140 umor necrosis factor alpha (TNFalpha) to pro-inflammatory gene expression in the nucleus.

141 uating lipopolysaccharide- (LPS) induced pro-inflammatory gene expression in THP-1 macrophages.

142 lular drivers of global reprogramming of the inflammatory gene networks in the innate immune cells ar

143 /80(+)) phenotype, reduced the expression of inflammatory genes (TNF-alpha, IFN-gamma, IL-1beta, IL-6

144 ZT2 increased the expression of several pro-inflammatory genes within the spleen; this was not evide

145 FD markedly induced expression of immune and inflammatory genes, which was not attenuated by Ex.

146 nes and elevated expression of catabolic and inflammatory genes.

147 etected at GR transrepression sites near pro-inflammatory genes.

148 nant model of GR-mediated transrepression of inflammatory genes.

149 ch as chronic small vessel disease and other inflammatory, granulomatous, infective, metabolic, and g

150 t inhibits the maturation of Th17 cells into inflammatory IFN-gamma-coproducing effector cells.

151 eal cavity, decreased the production of anti-inflammatory IL-10, and stimulated the secretion of IL-6

152 NFalpha and IL-1beta) and increased the anti-inflammatory (IL-10 and IL-4) cytokine levels.

153 Thus, NMUR1 signalling promotes inflammatory ILC2 responses, highlighting the importance

154 ncreased expression of genes associated with inflammatory, innate and adaptive immune responses.

155 o bovine cartilage explants, suppressing pro-inflammatory interleukin-6 (IL-6) expression after inter

156 Young women with AMI had higher inflammatory levels compared with young men.

157 dipose tissue and lymph nodes and display an inflammatory-like phenotype atypical of adipose resident

158 te development and/or progression of chronic inflammatory lung diseases including asthma, chronic obs

159 r numbers of granulocytes, plasmablasts, and inflammatory Ly6C(hi) CCR2(+) monocytes, as well as incr

160 rine systemic infection, LipA suppresses pro-inflammatory macrophage activation, rendering these cell

161 functions differ in proinflammatory and anti-inflammatory macrophages, we compared the macropinocytic

162 the macropinocytic activity of pro- and anti-inflammatory macrophages.

163 tivation and NET formation may contribute to inflammatory manifestations observed in patients with AT

164 ted by the decrease in the expression of pro-inflammatory markers and by the induction of a pro-regen

165 b/SND1 mice exhibited a relative increase in inflammatory markers and spheroid-generating tumor-initi

166 est as growing literature indicates that pro-inflammatory markers can directly modulate affective beh

167 ion was used to analyze the relation between inflammatory markers measured on 1) ICU admission and da

168 ssociation of DNA methylation with levels of inflammatory markers using cis-methylation quantitative

169 lation (GMD), urinary nitric oxide (NO), and inflammatory markers were measured before and after FBX

170 Secondary outcomes included inflammatory markers.

171 trated increased skin expression of the anti-inflammatory mediator arginase-1 (P = 0.005), and a sust

172 ationic Protein and histamine, two important inflammatory mediators previously described in the perio

173 This triggers production of innate inflammatory mediators that stimulate the production of

174 ed similar responses in clinical parameters, inflammatory mediators, and proportions of individual mi

175 e unexpectedly primed to respond robustly to inflammatory mediators.

176 < 0.001-0.001) were increased in response to inflammatory mediators.

177 uately controlled with over-the-counter anti-inflammatory medications.

178 t is essential in shaping the protumorigenic inflammatory microenvironment in colon cancer.

179 hrough extracellular matrix and form lasting inflammatory microstructures.

180 Combined, these results suggest that the inflammatory milieu found in Crohn's disease could lead

181 t SP110b plays a crucial role in shaping the inflammatory milieu that supports host protection during

182 Our results suggest that in these inflammatory models, acute administration of peripherall

183 synaptic function, increased permeability to inflammatory molecules, disrupted glutamate homoeostasis

184 oid cells, and upregulated expression of the inflammatory molecules, IL-1beta and S100A9, by the myel

185 n myeloid cells and promoting the release of inflammatory molecules, including IL-1beta.

186 ere accompanied by increased accumulation of inflammatory monocyte macrophages and neutrophils in the

187 in the lungs of male mice, and depletion of inflammatory monocyte macrophages partially protected th

188 lomyelitis (EAE) impairs the accumulation of inflammatory monocyte-derived cells (MCs) in the CNS, le

189 Depletion of CCR2(+) inflammatory monocytes and pharmacologic blockade of IL-

190 We identified both inflammatory monocytes and tissue-resident macrophages a

191 concomitant with pancreatic infiltration of inflammatory monocytes that triggered immunopathology.

192 described in mice and humans: the classical inflammatory monocytes, which are rapidly mobilized upon

193 investigated the imaging characteristics of inflammatory NTZ-PML lesions and PML-IRIS to determine d

194 biliary atresia (BA), a disease resulting in inflammatory obstruction of the extrahepatic biliary tra

195 um channel NaV 1.7 is required for acute and inflammatory pain in mice and humans but its significanc

196 ete Freund's adjuvant, a model of peripheral inflammatory pain.

197 Clinical, functional, and inflammatory parameters were assessed at baseline and at

198 d damaged sites and plays prominent roles in inflammatory pathologies and cancer.

199 nduce the Nrf2 phase II antioxidant and anti-inflammatory pathway at micromolar concentrations, showi

200 via an endogenous cerebral cholinergic anti-inflammatory pathway.

201 Transcriptomic analysis revealed broad inflammatory pathways associated with uric acid priming,

202 flammatory regulators and activation of anti-inflammatory pathways in FCRx samples.

203 Consistent with an inhibitory influence of inflammatory pathways on cardiac reprogramming, blockade

204 properties in nanomedicine to down-regulate inflammatory pathways or to be employed as diagnostic to

205 Multiple inflammatory pathways showed stronger enrichment in AD t

206 signalling pathways as well as activation of inflammatory pathways.

207 tions supports the role of a specific immune/inflammatory patient profile in the improved response to

208 the pretreatment clinical and intracerebral inflammatory phenotype and 9-month survival of 764 adult

209 able asthma and relate composition to airway inflammatory phenotype and other phenotypic characterist

210 In diabetes, macrophages display a prolonged inflammatory phenotype in late wound healing.

211 rough which developmental environments shape inflammatory phenotypes across the life course.

212 ferent from that seen in patients with other inflammatory phenotypes, particularly eosinophilic asthm

213 the associations between changes in dietary inflammatory potential and risk of colorectal cancer (CR

214 d with breakfast skipping also increased the inflammatory potential of peripheral blood cells after l

215 s than curcumin alone, highlighting the anti-inflammatory potential of turmeric.

216 During the inflammatory process in periodontal disease, chemokines

217 vels of CCL-2 and IL-8 and contribute to the inflammatory process promoting the recruitment of other

218 only recently have the importance of sterile inflammatory processes in this effect been revealed.

219 , afferent cVN activation amplifies systemic inflammatory processes, leading to activation of the hyp

220 vascular wall is a critical event in chronic inflammatory processes, such as atherosclerosis, but the

221 enotypes that involve distinct T cell-driven inflammatory processes.

222 ected Unc93b1(-/-) mice had a very different inflammatory profile from infected Il1r1(-/-) and Pycard

223 An association between chronic inflammatory prostate and periodontal diseases has been

224 nses, and constitute a valuable pool of anti-inflammatory proteins for potential future therapeutic a

225 , interleukin-13, interleukin-17, macrophage inflammatory proteins-1alpha, and macrophage inflammator

226 inflammatory proteins-1alpha, and macrophage inflammatory proteins-1beta) when CD73 was lacking.

227 Surgery launches a systemic inflammatory reaction that reaches the brain and associa

228 edium chain fatty acids can activate the pro-inflammatory receptor GPR84 but so also can molecules re

229 The patients were unable to orchestrate an inflammatory response against LPS and expressed three fa

230 umans, which is characterized by exacerbated inflammatory response and extensive lung pathology.

231 the diversity and spatiotemporal role of the inflammatory response and its interactions with resident

232 uimod induces a monomorphic and self-limited inflammatory response in healthy subjects, as well as pa

233 We conclude that the inflammatory response mechanism is not active in mouse e

234 entiation can trigger the development of the inflammatory response mechanism, as indicated by the tra

235 h in vitro and in vivo, resulted in a higher inflammatory response of the encountering macrophages, m

236 quick SOFA (qSOFA), and removed the systemic inflammatory response syndrome (SIRS) criteria from the

237 primary outcome was a composite of systemic inflammatory response syndrome and dysfunction of at lea

238 Systemic Inflammatory Response Syndrome and quick Sequential Orga

239 expression is precisely regulated during the inflammatory response to control infection and limit the

240 sponsible for allergic sensitization and the inflammatory response, while IgE binding to CD23 is invo

241 x, inducing local pancreatic fibrosis and an inflammatory response.

242 esult in a potent and sometimes pathological inflammatory response.

243 lar glucose metabolism as well as the innate inflammatory response.

244 y but success is likely to be limited by the inflammatory response.

245 produces a known toxin nor induces a robust inflammatory response.

246 sis is difficult due to the ongoing systemic inflammatory response.

247 nd a subsequent type I interferon-associated inflammatory response.

248 nfection induced metabolic dysregulation and inflammatory responses and affected the immune cell cont

249 sized that IL-15(-/-) mice will have reduced inflammatory responses during the development of allergi

250 athway, an effect that may be exacerbated by inflammatory responses in immunocompetent hosts.

251 EBOV replication coinciding with systematic inflammatory responses in otherwise asymptomatic rhesus

252 e results highlight critical roles of innate/inflammatory responses in SIVmac239 infection.

253 s and HAI titers with reduced viral load and inflammatory responses in the cVLP group.

254 a demonstrate MyD88 signaling mediates early inflammatory responses in the joint but also contributes

255 ndant in atherosclerotic plaques and promote inflammatory responses via the complement system and inf

256 B lymphocytes in the presence of detectable inflammatory responses, suggesting the involvement of co

257 ata demonstrate that BCD inhibits CC-induced inflammatory responses, which may be explained by BCD-me

258 s and ubiquitination events that orchestrate inflammatory responses, with an emphasis on the NLRP3 in

259 gering a switch from proinflammatory to anti-inflammatory responses.

260 or and a central regulator of cell death and inflammatory responses.

261 ent example of how ubiquitin signals control inflammatory responses.

262 f dendritic cell maturation and promotion of inflammatory responses.

263 and an important mediator of autoimmune and inflammatory responses.

264 ar glucose metabolism can influence cellular inflammatory responses.Several metabolic factors affect

265 Several diseases, including inflammatory rheumatic and autoimmune diseases, infectio

266 tly involved in the pathogenesis of systemic inflammatory rheumatoid arthritis (RA) and AD.

267 and NF-kappaB pathways account for the anti-inflammatory role of MCL after PGN stimulation.

268 nism involves the suppression of CD36-driven inflammatory signaling and derepression of liver X recep

269 By understanding these inflammatory signaling processes, new approaches for qui

270 E2-conjugating enzyme, leading to prolonged inflammatory signaling.

271 anation for BCAP-mediated down-regulation of inflammatory signaling.

272 olic fatty liver disease (NAFLD) by altering inflammatory signalling in RSF.

273 ifs (RHIM) play a key role in cell death and inflammatory signalling(1-3).

274 ociated with inflammation, but the source of inflammatory signals and the mechanisms by which these s

275 Tumors contain hostile inflammatory signals generated by aberrant proliferation

276 who had undergone bilateral FESS for chronic inflammatory sinonasal disease 3-5 years prior to the st

277 ation contributes to macrophage retention at inflammatory sites during atherogenesis.

278 arge diagnosis and 647 patients with primary inflammatory skin condition admission diagnosis were sel

279 A total of 413 patients with a primary inflammatory skin condition discharge diagnosis and 647

280 Psoriasis, a chronic inflammatory skin disease associated with increased susc

281 fector cells involved in the pathogenesis of inflammatory skin diseases including chronic urticaria w

282 pe NaV 1.7 is required for sensing acute and inflammatory somatic pain in mice and humans but its sig

283 rosclerosis, but the control of the vascular inflammatory state is still largely unclear.

284 n exposure to IL-1alpha polarize to a highly inflammatory state that enables them to stimulate the re

285 oaches for quieting chronic or inappropriate inflammatory states may be revealed and this could serve

286 CD11b activity and the chronically increased inflammatory status in patients.

287 roteins and lipids in human fibroblasts upon inflammatory stimulation and subsequent treatment with d

288 lar code that defines endogenous proteins as inflammatory stimuli by marking them for recognition by

289 ted re-entry into dormancy after exposure to inflammatory stress stimuli.

290 ptococcosis-associated immune reconstitution inflammatory syndrome (C-IRIS), upon initiation of antir

291 y (PML) and full-blown immune reconstitution inflammatory syndrome (PML-IRIS).

292 patients at risk of TB immune reconstitution inflammatory syndrome (TB-IRIS), in Cape Town, South Afr

293 a novel immune checkpoint role in inhibiting inflammatory T cell responses.

294 ls influenced the extent of induction of the inflammatory T cell subset in vitro that mainly drives l

295 patients are associated with persistent pro-inflammatory T-helper (TH)2 and TH17 responses.

296 reduced most significantly, whereas the anti-inflammatory Th2 subset (CCR3(+)) was increased after DM

297 tion in patients who did not respond to anti-inflammatory therapies.

298 Therapeutically, anti-inflammatory therapy, meibomian gland heating and expres

299 The Canakinumab Anti-Inflammatory Thrombosis Outcomes Study (CANTOS) used com

300 erlying vascular inflammation and associated inflammatory vascular diseases are not well defined.