ライフサイエンスコーパス: phagocyte

1 ption to promote survival in the mononuclear phagocyte.

2 he true transcriptional reprogramming of the phagocyte.

3 how this is achieved in a model professional phagocyte.

4 ora caninum activated GABAergic signaling in phagocytes.

5 lood and organs are cytotoxic to ~20% of the phagocytes.

6 pression and diminished by gene silencing in phagocytes.

7 cruitment and infection of lung-infiltrating phagocytes.

8 s system before the presence of professional phagocytes.

9 ammasome and causes cytolysis in mononuclear phagocytes.

10 ulating MaR1's key proresolving functions of phagocytes.

11 lymphocytes and tissue-invading inflammatory phagocytes.

12 tein-coupled receptor 6 (LGR6), expressed in phagocytes.

13 immune response and replicating within host phagocytes.

14 re activated during MRP-induced tolerance of phagocytes.

15 pecies (ROS), reminiscent of proinflammatory phagocytes.

16 of cells die and must be swiftly cleared by phagocytes.

17 lls resulted in the regulation of intestinal phagocytes.

18 bacillary replication was controlled in live phagocytes.

19 to facilitate replication within eukaryotic phagocytes.

20 that block sUA or inhibit its recognition by phagocytes.

21 mina, which are then engulfed by blood-borne phagocytes.

22 by enabling their capture and elimination by phagocytes.

23 zed by so-called PS receptors on surveilling phagocytes.

24 and PM18 was killed more readily when inside phagocytes.

25 cAMP that ablates bactericidal capacities of phagocytes.

26 ata, an emerging pathogen, resists attack by phagocytes.

27 orrosion processes and in one cell type, the phagocytes.

28 or dying cells are engulfed and digested by phagocytes.

29 plasticity for a spectrum of differentiated phagocytes.

30 ously the result of the presence of invading phagocytes.

31 setting hampers phagocytosis of IRBC by host phagocytes.

32 disease with a specific focus on mononuclear phagocytes.

33 lude lysis, opsonization, and recruitment of phagocytes.

34 g human pyrin is preferentially expressed in phagocytes.

35 cells and the Dectin-1 signaling pathway in phagocytes.

36 c cells by professional and non-professional phagocytes - a process termed 'efferocytosis' - is essen

37 The engulfment of apoptotic cells by phagocytes, a process referred to as efferocytosis, is e

38 erythrocytes, immature erythroid cells, and phagocytes accounted for the largest increase in splenic

39 f IgG plasma cells, inflammatory mononuclear phagocytes, activated T cells, and stromal cells, which

40 t manipulations affecting IFN-gamma-mediated phagocyte activation are counteracted by effects on IFN-

41 kin, IFN-gamma- or STAT6-mediated changes in phagocyte activation were counteracted by changes in IFN

42 agocytic clearance by resident and recruited phagocytes after myocardial ischemia reperfusion.

43 st1/2 results in increased oxidative injury, phagocyte ageing and death.

44 egative selection is more efficient when the phagocyte also presents the negative selecting peptide.

45 Murine phagocytes also shuttled in vitro.

46 ocytosis, depends on cooperation between the phagocyte and the dying cell.

47 through a mechanism that required monocytic phagocytes and a viral chemokine that recruited macropha

48 etrates the complement receptor 3-expressing phagocytes and ablates their bactericidal capacities by

49 alised PS is prothrombotic and attractive to phagocytes and activated endothelial cells and thus cont

50 inants of GABAergic signaling in parasitized phagocytes and demonstrate a link to calcium responses a

51 fy extravascular tissue-resident mononuclear phagocytes and exclude cells within the vascular lumen.

52 is predominantly synthesized by mononuclear phagocytes and exerts immunoregulatory functional activi

53 7 function, and promote strong activation of phagocytes and immune cells.

54 iated with increased presence of mononuclear phagocytes and in particular with the accumulation of CD

55 tor produced quickly (seconds to minutes) by phagocytes and induces chemotaxis, increases cytokine/ch

56 Yersinia effectors, which are injected into phagocytes and interact with the RhoA-PRK-pyrin axis dur

57 inery in the host-pathogen interplay between phagocytes and invasive coccidian parasites.

58 ial role in the stabilization of gp91phox in phagocytes and is also a docking site for p47phox during

59 fol sedation reduced populations of effector phagocytes and mature dendritic cells within the kidney

60 nhibiting autophagy during infection of host phagocytes and may provide strategic targets in developi

61 nt results from infection studies with human phagocytes and mice producing pyrin B30.2 FMF variants s

62 at S. aureus toxins drive the death of human phagocytes and mice, whereas the surface adhesin FnbA co

63 the degeneration of spinal cord mononuclear phagocytes and modulates motility of murine microglial p

64 iptional profiling of intestinal mononuclear phagocytes and multidimensional flow cytometry, we found

65 nflammatory monocytes become a chief pool of phagocytes and play a key role in the clearance of highl

66 sis, normalizes lipid deposition in infected phagocytes and reduces numbers of viable intracellular m

67 s accumulated in resident antigen-presenting phagocytes and significantly enhanced the activation of

68 The mutation is present in ~70% of phagocytes and sufficient to result in defective bacteri

69 These data redefine the lineage of intimal phagocytes and suggest that proliferation is insufficien

70 lactic acid bacteria, the oxidative burst of phagocytes and the redox-cycling of secreted small molec

71 s restricted to murine and human mononuclear phagocytes and was induced during monocyte-to-macrophage

72 ATEMENT Microglia are the brain professional phagocytes and, in the adult hippocampal neurogenic nich

73 es bacterial surfaces, recruits professional phagocytes, and causes bacteriolysis.

74 cy compromised the accumulation of MHCII(LO) phagocytes, and this was rescued in Mertk(CR) mice.

75 8(+) cytotoxic T cells in collaboration with phagocytes appears to be a powerful effector mechanism t

76 ng signalling pathway that controls both the phagocyte 'appetite' and its anti-inflammatory response.

77 ls and prevent interaction with SIRPalpha on phagocytes are active against multiple cancer types incl

78 Thus, multiple phagocytes are capable of hyperactivation in response to

79 Given that phagocytes are crucial for controlling P. aeruginosa inf

80 Phagocytes are essential for clearance of CDC-producing

81 at recruited Dock8(-/-)CX3CR1(+) mononuclear phagocytes are exquisitely sensitive to migration-induce

82 Professional phagocytes are highly specialized for engulfing apoptoti

83 Aberrant immune responses including reactive phagocytes are implicated in the etiology of age-related

84 hloride-sensing pathway and chloride flux in phagocytes are key modifiers of the manner in which phag

85 es, collectively termed 'retinal mononuclear phagocytes', are critical determinants of ocular disease

86 esented a reduced activity of mast cells and phagocytes as an effect of the treatment.

87 imple, measurable parameter, persistent prey-phagocyte association, to use for normalization and dose

88 etion of murine CD11b-expressing mononuclear phagocytes at birth led to severe acute hyperoxia-induce

89 enlarged biofilms that provide resistance to phagocyte attacks.

90 M-CSF has myriad effects on mononuclear phagocytes but its role in pneumonia is unknown.

91 is) elicits an anti-inflammatory response by phagocytes, but the mechanisms that underlie this respon

92 not a general property of all leptomeningeal phagocytes, but varies between individual APCs.

93 cytosis and the migration of human and mouse phagocytes by disrupting actin cytoskeletal dynamics via

94 a apoptosis, and then are rapidly removed by phagocytes by the process of efferocytosis that is anti-

95 Recently, it was recognized that phagocytes can achieve a state of hyperactivation, which

96 Like Kupffer cells, bursal TIM4(hi) phagocytes coexpressed many receptors involved in apopto

97 reperfusion injury during kidney transplant, phagocytes coexpressing the F4/80 and CD11c molecules me

98 Human mononuclear phagocytes comprise phenotypically and functionally over

99 During tumor progression, immune system phagocytes continually clear apoptotic cancer cells in a

100 Moreover, the phenotype of UNC93B1-defective phagocytes could be recapitulated by the simultaneous ab

101 t on Nrf2 and led to an improved capacity to phagocyte-damaged neutrophils by efferocytosis.

102 membranes, resolves ER stress, and curtails phagocyte death.

103 ad immune dysregulation syndrome, 6 (6.4%) a phagocyte defect, 7 (7.4%) an autoinflammatory disorder,

104 differentiation and survival of mononuclear phagocytes depend on signals from the receptor for macro

105 In studies of hepatic phagocyte depletion in mice, we found that myeloid precu

106 We performed phagocyte depletion to study SerpinB2's role beyond the

107 d-related protein 8/14 [MRP8/14] complex), a phagocyte-derived antimicrobial protein, into the perito

108 nt stages of efferocytosis, and responses of phagocytes during efferocytosis, all of which can alter

109 functions of both lung and liver mononuclear phagocytes during pneumonia, and its absence resulted in

110 unction, hematopoietic response, and myeloid phagocyte dynamics in WT (wild type) C57BL/6 mice with p

111 METH compromises phagocyte effector functions, which might have deleterio

112 Clearance of apoptotic cells (ACs) by phagocytes (efferocytosis) prevents post-apoptotic necro

113 sion to limit neutrophil recruitment as each phagocyte eliminated numerous pathogens.

114 ole for CFH in the inhibition of mononuclear phagocyte elimination from sub-retinal lesions, providin

115 lymph nodes resist and subvert clearance by phagocytes, enabling replication that can seed intense b

116 We conclude that in murine lung, myeloid phagocytes encountering apoptotic cells can deploy alpha

117 Phagocytes engulf pathogens into a membrane bound compar

118 latelets boosts the activity of professional phagocytes, exacerbating inflammatory tissue injury in s

119 Phagocytes express multiple phosphatidylserine (PtdSer)

120 Previous studies using phagocytes from a leukocyte adhesion deficiency type 1 (

121 In single-cell analysis of mononuclear phagocytes from CLM tissues, S-TAM and L-TAM signatures

122 Previous studies have shown that phagocytes from patients with CGD display a defect in au

123 cell clearance develop SLE-like disease, and phagocytes from patients with SLE often display defectiv

124 ation and superoxide anion production, a key phagocyte function.

125 Our collective understanding of old and new phagocyte functions after apoptotic cell phagocytosis de

126 clear how this homeostatic process modulates phagocyte functions in inflammatory diseases.

127 embrane lipase enzyme activity in modulating phagocyte functions.

128 d Ly6C(+) macrophages, suggesting that these phagocytes had phagocytosed those organisms for their er

129 particularly by macrophages and other immune phagocytes, has profound consequences on innate and adap

130 However, myeloid-derived professional phagocytes have not yet colonized the trunk region durin

131 , functions and therapeutic effects of these phagocytes have, however, been difficult to study.

132 immunity," who is credited with discovering phagocytes in 1882.

133 pathways that trigger hyporesponsiveness of phagocytes in clinically relevant diseases are only bare

134 Anopheles gambiae, demonstrating the role of phagocytes in complement recognition and prophenoloxidas

135 ed recruitment and activation of mononuclear phagocytes in MARCO(-/-) mice was linked to diminished e

136 n our understanding of the roles of mosquito phagocytes in mosquito vector competence and demonstrate

137 veral of the genes and pathways modulated in phagocytes in response to apoptotic cells have been link

138 rum of functions executed by tissue-resident phagocytes in response to homeostatic apoptosis, therefo

139 Microglia are the primary phagocytes in the brain and have been well-documented as

140 Microglial cells are phagocytes in the central nervous system (CNS) that beco

141 etween autoreactive Th cells and mononuclear phagocytes in the CNS drives initiation and maintenance

142 nthetic ligand XBD173 prevents reactivity of phagocytes in the laser-induced mouse model of neovascul

143 cells, inhibited accumulation of mononuclear phagocytes in the outer retina, and protected photorecep

144 opsonization on Y. pestis interactions with phagocytes in vitro and in vivo Opsonization of Y. pesti

145 lows characterization of retinal mononuclear phagocytes in vivo and in situ.

146 lation is best characterized in professional phagocytes, in particular macrophages, where LAP has ins

147 nity derive from characteristics inherent to phagocytes, including chemotaxis toward and engulfment o

148 o promote the destruction of cancer cells by phagocytes, including macrophages and neutrophils.

149 Innate immunity, mediated by mononuclear phagocytes, including monocytes and macrophages, is a fi

150 d type, although accumulation of mononuclear phagocytes increased in postischemic Ackr2(-/-) kidneys.

151 gram transcript, is expressed by mononuclear phagocytes infiltrating primary melanoma and is induced

152 In SIRSs, phagocytes initially develop a hyperinflammatory respons

153 ecifically resulting in specific cell corpse/phagocyte interactions (phagocytic synapses) that imping

154 tes are key modifiers of the manner in which phagocytes interpret the engulfed apoptotic corpse.

155 ctively, resulting in a strong influx of the phagocytes into the peritoneal cavity.

156 the efferocytic receptor MerTK on recipient phagocytes is a critical mediator for transplantation to

157 Reactive oxygen species (ROS) production in phagocytes is a major defense mechanism against pathogen

158 disposal of apoptotic bodies by professional phagocytes is crucial to effective inflammation resoluti

159 disposal of apoptotic bodies by professional phagocytes is impaired by a limited understanding of the

160 nt, homeostasis, and function of mononuclear phagocytes is the colony stimulating factor-1 receptor (

161 CCR2(+) monocytes, generation of TipDC, and phagocyte killing of yeast.

162 Macrophages are professional phagocytes known to play a vital role in controlling Myc

163 ion of pattern recognition receptors on host phagocytes known to recognize C. neoformans Altogether,

164 As professional phagocytes, macrophages are susceptible to endolysosomal

165 With human and mouse phagocytes, MaR1 (0.01-10 nM) enhanced phagocytosis, eff

166 Moreover, phagocytes may contain so called "passenger" transcripts

167 Dust exposure significantly reduced phagocyte-mediated bacterial killing, and exposure to hi

168 cessive activation of T cells and associated phagocyte-mediated damage.

169 utrophils and mucosal surfaces and a role in phagocyte-mediated host defense.

170 hesis that M-CSF is required for mononuclear phagocyte-mediated host defenses during bacterial pneumo

171 TLR ligands induce sustained augmentation of phagocyte metabolism and antimicrobial function.

172 ut whether uptake of apoptotic cells by lung phagocytes might dampen house dust mite (HDM)-induced lu

173 contains specialized subsets of mononuclear phagocytes (MNPs) and T cells, but whether these have de

174 Mononuclear phagocytes (MNPs) are a highly heterogeneous group of ce

175 s that localize monocyte-derived mononuclear phagocytes (MNPs) to the medulla.

176 a chance event, and involves alterations of phagocyte mobility, intercellular tethering, and phagoso

177 Phagocytes mobilize interferon-inducible responses upon

178 genic subretinal accumulation of mononuclear phagocytes (MP) that characterize AMD and showed acceler

179 e function of renal interstitial mononuclear phagocytes (MPCs) remains unclear, however.

180 Mononuclear phagocytes (MPs) including monocytes, macrophages and de

181 Proinflammatory mononuclear phagocytes (MPs) play a crucial role in the progression

182 ween effector CD4(+) T cells and mononuclear phagocytes (MPs).

183 e uptake of infected necrotic cells by other phagocytes, Mtb growth therein, and sustained infection.

184 For efficient efferocytosis, phagocytes must be able to internalize multiple ACs.

185 NCF1, encoding the p47(phox) subunit of the phagocyte NADPH oxidase (NOX2), as the putative underlyi

186 Phagocyte NADPH oxidase but not myeloperoxidase was requ

187 e of the gp91phox-p22phox heterodimer of the phagocyte NADPH oxidase in human cells and that EROS mut

188 The phagocyte NADPH oxidase is composed of cytosolic compone

189 The phagocyte NADPH oxidase is responsible for the neutrophi

190 Superoxide anion production by the phagocyte NADPH oxidase plays a crucial role in host def

191 Phagocyte NADPH oxidase produces superoxide anions, a pr

192 which GAS generates an anoxic niche to evade phagocyte NADPH oxidase-mediated clearance.

193 These results indicate that phagocyte NADPH oxidase-mediated GAS killing is compromi

194 hat ROS production was dependent on the NOX2 phagocyte NADPH oxidase.

195 nodeficiency marked by a defect in NOX2, the phagocyte NADPH oxidase.

196 hat it is essential for host defense via the phagocyte NAPDH oxidase.

197 Macrophages are professional phagocytes necessary for liver inflammation, fibrosis, a

198 stitial THP positively regulates mononuclear phagocyte number, plasticity, and phagocytic activity.

199 flammatory NF-kappaB-dependent activation in phagocytes occurs rapidly after myelin injury.

200 Various phagocytes of mammals and invertebrates produce ETs, how

201 by the IL-1 receptor antagonist anakinra in phagocytes of patients with CGD.

202 They are the professional phagocytes of the brain and help orchestrate the immunol

203 bility of handling these dead cells falls on phagocytes of the immune system, which surveil their sur

204 ganglia, corresponding to accumulated lipid phagocytes on histology and typical for late-stage necro

205 l abnormalities, and are rapidly captured by phagocytes or processed by the hepatobiliary system.

206 emented with lipA ROS derived from the NADPH phagocyte oxidase complex and RNS derived from the induc

207 ctive oxygen species (ROS) produced by NADPH phagocyte oxidase isoform (NOX2) are critical for the el

208 N-formyl peptide receptors (FPRs) serve as phagocyte pattern-recognition receptors that play a cruc

209 (M)beta(2), CD11b/CD18, or Mac-1) of myeloid phagocytes, penetrates their plasma membrane, and delive

210 pid accumulation and induced an inflammatory phagocyte phenotype.

211 Monocytes are circulating mononuclear phagocytes, poised to extravasate to sites of inflammati

212 (LC) are thought to be the only mononuclear phagocyte population in the epidermis where they detect

213 his study, we further define the mononuclear phagocyte populations that are present in the neonatal l

214 We identified four mononuclear phagocyte populations, of which two were transcriptional

215 se is largely informed from analysis of bulk phagocyte populations; however, this precludes the resol

216 ew focuses on new discoveries related to how phagocytes process the metabolic cargo they receive duri

217 a define a distinct role for TSPO in retinal phagocyte reactivity and highlight the protein as a drug

218 as then used to remove phosphatidylserine, a phagocyte recognition marker, from the outer leaflet of

219 ograft neutrophil sequestration, mononuclear phagocyte recruitment, and T cell activation, all of whi

220 ndent, impair pathogen clearance, antagonize phagocyte recruitment, diminish phagocytosis and decreas

221 ith suppressed antibacterial defenses, i.e., phagocyte recruitment, IgA secretion, and Muc5b expressi

222 d previously suppressed responses, including phagocyte recruitment, IgA secretion, and mucous cell me

223 addition, a large population of mononuclear phagocytes resident in the kidney can modulate these res

224 The phagocyte respiratory burst is crucial for innate immuni

225 Nbeal2-deficient neutrophils had an enhanced phagocyte respiratory burst relative to Nbeal2-expressin

226 ate and identify a specialized population of phagocytes responsible for anemia and thrombocytopenia a

227 g time, they were primarily considered to be phagocytes responsible for removing debris during CNS de

228 tion of human and murine myeloid mononuclear phagocytes revealed the presence of a conserved and tigh

229 an extensive population of renal mononuclear phagocytes (RMPs), with substantial phenotypic and funct

230 s review, we outline the mechanisms by which phagocytes sense apoptotic cell death and discuss how ph

231 nked to impaired phagocytosis by specialized phagocytes: Sertoli cells and the retinal pigmented epit

232 Thymic phagocytes serve to remove dead thymocytes, but whether

233 e, we find that different immune mononuclear phagocytes share a conserved steady-state program during

234 /molecular model Dictyostelium and mammalian phagocytes share mechanistic pathways for chemotaxis and

235 Pharmacological inhibition or phagocyte-specific deficiency of Scd1 accelerated remyel

236 of inflammation is executed through distinct phagocyte-specific mechanisms.

237 In contrast to other cardiac phagocyte subsets, resident cardiac MHCII(LO)CCR2(-) (ma

238 Our previous data suggest that mononuclear phagocytes such as CD11c(+) conventional dendritic cells

239 killing by macrophages, as well as by other phagocytes such as neutrophils or monocytes.

240 d to a lesser extent by other 'professional' phagocytes (such as monocytes and dendritic cells) and '

241 Non-microglial mononuclear phagocytes, such as CNS-associated macrophages and circu

242 and dendritic cells) and 'non-professional' phagocytes, such as epithelial cells.

243 n cell shape are perhaps best exemplified by phagocytes, such as neutrophils.

244 e latter previously shown to be required for phagocyte survival.

245 The mononuclear phagocyte system (MPS) is a family of cells including pr

246 The mononuclear phagocyte system (MPS) is defined as a cell lineage in w

247 were primarily deposited in the mononuclear phagocyte system (MPS) such as the liver and spleen.

248 The mononuclear phagocyte system (MPS, e.g., liver, spleen) is often tre

249 on, and survival of cells of the mononuclear phagocyte system (MPS; progenitors, monocytes, macrophag

250 mes and silicon particles in the mononuclear phagocyte system and improved tumoritropic and organotro

251 tor GFP transgene throughout the mononuclear phagocyte system), quantitative analysis of Iba1-stained

252 ation, minimize clearance by the mononuclear phagocyte system, and limit uptake in healthy tissue.

253 nocytes are key effectors of the mononuclear phagocyte system, playing critical roles in regulating t

254 sident macrophages that form the mononuclear phagocyte system.

255 y increased renal infiltrates of mononuclear phagocytes, T cells, Ly6C(high) inflammatory macrophages

256 Macrophages are professional phagocytes that are essential for host defense and tissu

257 Microglia are the principal phagocytes that clear cell debris in the central nervous

258 D11b(+)F4/80(hi)CD64(+)CX3CR1(+) mononuclear phagocytes that contribute to maintaining high levels of

259 umans and mice host a network of mononuclear phagocytes that differ in their ontogeny, surface marker

260 In overview, TIM4 is associated with phagocytes that eliminate apoptotic cells in the chick.

261 We show that specialized phagocytes that internalize red blood cells develop in T

262 Neutrophils are phagocytes that kill large pathogens by releasing neutro

263 Macrophages are the professional phagocytes that protect the host from infection or injur

264 division of labor among the tissue resident phagocytes that sample them.

265 Macrophages are phagocytes that serve as a first line of defense against

266 In SLC12A2-deficient phagocytes, the canonical anti-inflammatory program was

267 ymal macrophages of the CNS; as professional phagocytes they are important for maintenance of the bra

268 As the dominant circulating phagocyte, they are rapidly recruited from the bloodstre

269 lia are more than mere bystanders or amyloid phagocytes; they can act as governors of neuronal functi

270 We use reference human phagocyte THP-1 cells with different prey and opsonizati

271 to battle the immune response by destroying phagocytes through targeted lysis.

272 uding the activation of resident mononuclear phagocytes, tissue infiltration by non-resident inflamma

273 rey (MOP) ratio needed to elicit half of the phagocytes to associate persistently (MOP(50)) is determ

274 Exposure of mononuclear phagocytes to beta-glucan, a naturally occurring polysac

275 xclusively in the lamina propria mononuclear phagocytes to directly enhance IL-1beta but not IL-18 se

276 such as S. pyogenes will enable professional phagocytes to eliminate the pathogen.

277 STAT6 KO impaired the capacity of phagocytes to engulf red blood cells in the ICH brain an

278 The inflammatory responsiveness of phagocytes to exogenous and endogenous stimuli is tightl

279 n in vivo and in vitro generated mononuclear phagocytes to facilitate their full potential in the cli

280 These cells are swiftly removed by phagocytes to minimize inflammation and limit expansion

281 ved hepcidin acted on ferroportin-expressing phagocytes to promote local iron sequestration, which re

282 echanisms for dendritic cells and some other phagocytes to sample and present antigens from the extra

283 d their activation promotes the migration of phagocytes to sites of infection.

284 Impaired ability of arterial phagocytes to uptake apoptotic cells (efferocytosis) pro

285 that myelin uptake temporarily skewed these phagocytes toward a disease-resolving phenotype, while s

286 Following S. aureus-loaded phagocyte translocation from the mucosal surface, S. aur

287 vate the inflammasome in colonic mononuclear phagocytes, triggering inflammation.

288 Phagocytes use their actomyosin cytoskeleton to migrate

289 anisms of intracellular pathogen carriage by phagocytes, we show S. pyogenes remain extracellular dur

290 using transgenic zebrafish with fluorescent phagocytes, we showed that a mutation of an established

291 Recruited lung mononuclear phagocytes were abundant in CF and were separated into t

292 Renal mononuclear phagocytes were studied 24 and 72 hours after 30 minutes

293 cant increase in apoptotic corpse uptake per phagocyte, whereas the loss of SLC12A4 inhibited corpse

294 d downstream hyperactivation of inflammatory phagocytes, which are capable of host tissue damage.

295 so-called don't eat me molecules on inflamed phagocytes, which reduces their capacity for programmed

296 sequential engagement of Fc-receptors on the phagocyte with antibodies on the target surface, leading

297 Depletion of monocytic phagocytes with clodronate completely prevented MCMV fro

298 , (2) a proinflammatory state of mononuclear phagocytes with increased IL-1beta and TNF-alpha content

299 nd toxicity of reactive species generated in phagocytes, with a focus on the response of macrophages

300 ions between neutrophils and tissue-resident phagocytes within the influenza-infected mouse airway.