ライフサイエンスコーパス: phagocyte

1 e to phagocytosis and killing by a secondary phagocyte.

2 tory cell death (pyroptosis) of the infected phagocyte.

3 ption to promote survival in the mononuclear phagocyte.

4 or dying cells are engulfed and digested by phagocytes.

5 ectly coating bacteria to promote killing by phagocytes.

6 le from the phagocytic route in professional phagocytes.

7 tween teleost CD4(+) T cells and mononuclear phagocytes.

8 te a permissive niche for its replication in phagocytes.

9 reactive oxygen species (ROS) production by phagocytes.

10 the inhibition of autophagy in infected host phagocytes.

11 pus nephritis, suggesting a direct effect on phagocytes.

12 tes engulfment and destruction of targets by phagocytes.

13 ion of Nod1-dependent signals to circulating phagocytes.

14 e their being functionally interdependent in phagocytes.

15 duction in classic activation of mononuclear phagocytes.

16 hasone accelerated the repopulation of liver phagocytes.

17 ofessional, non-professional and specialized phagocytes.

18 B) and ASC-mediated inflammasome assembly in phagocytes.

19 elial cells and can transform the cells into phagocytes.

20 e the most prevalent cytoplasmic proteins in phagocytes.

21 fection despite increased numbers of splenic phagocytes.

22 less infiltration of pathogenic mononuclear phagocytes.

23 ng a pathway similar to that of professional phagocytes.

24 r microbes through activation of mononuclear phagocytes.

25 rial colony forming units and recruitment of phagocytes.

26 bacillary replication was controlled in live phagocytes.

27 that block sUA or inhibit its recognition by phagocytes.

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

29 by enabling their capture and elimination by phagocytes.

30 and PM18 was killed more readily when inside phagocytes.

31 cAMP that ablates bactericidal capacities of phagocytes.

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

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

34 lls resulted in the regulation of intestinal phagocytes.

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

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

37 as the simultaneous depletion of mononuclear phagocytes abolished the virus control.

38 However, how phagocytes acquire chloride from their residing environm

39 d differentiation of monocytes and prevented phagocyte activation and ROS production.

40 vascular grafts by reducing host mononuclear phagocyte activation.

41 g on the bacterial genotype and the state of phagocyte activation.

42 ring the spreading phase, demonstrating that phagocytes actively constrict during late-stage phagocyt

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

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

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

46 aired Cu and/or Zn detoxification systems in phagocytes and animal models of infection has been repor

47 in receptors drive contact formation between phagocytes and antibody-coated solid particles, signalin

48 acellular parasite that infects professional phagocytes and causes visceral leishmaniasis (VL).

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

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

51 blish how to identify human lung mononuclear phagocytes and how they function in normal conditions, s

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

53 Perforin-2 is expressed constitutively in phagocytes and inducibly in parenchymal, tissue-forming

54 pe of particles engulfed by non-professional phagocytes and influence their inflammatory response.

55 f biological activities of fish Il10 on both phagocytes and lymphocytes showing functional conservati

56 we investigated the effects of carp Il10 on phagocytes and lymphocytes.

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

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

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

60 n, and methods to measure chloride levels in phagocytes and their phagosomes.

61 otic cells to enhance ABCA1 within engulfing phagocytes and with functional consequences in vivo.

62 e levels, promoting extracellular killing by phagocytes, and generating a granulomatous response.

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

64 Mononuclear phagocytes are a heterogeneous family that occupy all ti

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

66 e we show that colonic CX3CR1(+) mononuclear phagocytes are critical inducers of the innate response

67 the notion that tissue and blood mononuclear phagocytes are equivalent systems.

68 Professional phagocytes are highly specialized for engulfing apoptoti

69 Mononuclear phagocytes are often present in AMD lesions, but the pro

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

71 portunity to avoid entrapment in mononuclear phagocytes (as a part of the host immune system), and at

72 o document the diversity of lung mononuclear phagocytes at steady-state, we performed bronchoscopies

73 genes that were differentially expressed by phagocytes bearing apoptotic IECs overlapped with suscep

74 Many phagocyte behaviors, including vascular rolling and adhe

75 , IL-22, or both, which activate mononuclear phagocytes but also recruit neutrophils and induce epith

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

77 ured by their overlap with other mononuclear phagocytes, but new mouse models have allowed for the se

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

79 function due to the substitution of original phagocytes by bone marrow-derived surrogates were also e

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

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

82 At least in principle, mononuclear phagocytes can be enlisted to clear Abeta/beta-amyloid f

83 ANCA-activated phagocytes cause vasculitis and necrotizing crescentic G

84 cascade hypothesis" and bringing mononuclear phagocytes center stage in the treatment of Alzheimer's

85 pitulated activation of the myeloid cell and phagocyte chemotactic genes and pathways, which we initi

86 Phagocytes clear dying cells within an organism to preve

87 ons, RvD2 limited PMN infiltration, enhanced phagocyte clearance of bacteria, and accelerated resolut

88 ed to assess the role of mucosal mononuclear phagocytes, consisting of monocytes, macrophages, and de

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

90 Activated human phagocytes converted 17-hydro(peroxy)-4Z,7Z,10Z,13Z,15E,

91 ll killing and to survive temporarily within phagocytes correlated with persistence in the periphery

92 Impairment of this critical mononuclear phagocyte crosstalk results in the generation of IFNgamm

93 y molecule because of its ability to promote phagocyte cytotoxic functions and enhance the function o

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

95 E. coli from copper toxicity and redox-based phagocyte defenses distinguishes it from other E. coli s

96 oxidative killing and mobilization of other phagocyte defenses.

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

98 elated formin G (ForG) from the professional phagocyte Dictyostelium discoideum localizes to endocyti

99 tion of neutrophils overwhelmed Pce-mediated phagocyte disruption.

100 essary for the expansion of lung mononuclear phagocytes during infection but did not affect the numbe

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

102 romotes early M2 skewing of lung mononuclear phagocytes during the innate phase, but not the adaptive

103 This specialty of fetal phagocytes effectively retains the memory of antigens in

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

105 totoxic and, in collaboration with activated phagocytes, eliminate chimeric partners during the "take

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

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

108 G2c antibodies and FcgammaR(+) CD11b(+) cell phagocytes, especially neutrophils, which are sufficient

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

110 Phagocytes express multiple phosphatidylserine (PtdSer)

111 When released from activated or necrotic phagocytes, extracellular MRP8/MRP14 promote inflammatio

112 al studies and analysis of human mononuclear phagocytes from blood and small tissue resections around

113 acquired and analyzed pulmonary mononuclear phagocytes from fully intact nondiseased human lungs (in

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

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

116 homeostasis requires continuous turnover of phagocytes from the bloodstream, yet whether environment

117 but the extent to which altered mononuclear phagocyte function contributes to this defect is unclear

118 he mechanisms by which many bacteria disrupt phagocyte function remain unclear.

119 s infections in patients with neutropenia or phagocyte functional defects, such as chronic granulomat

120 Rapid enhancement of phagocyte functionality is a hallmark of neutrophil prim

121 sequential manner with rapid enhancement of phagocyte functionality, followed by CD54 and dectin-2 m

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

123 in these subjects and its role in regulating phagocyte functions.

124 The diversity of mononuclear phagocytes has made it difficult to ascribe cellular fun

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

126 cates that these proinflammatory mononuclear phagocytes have a central role in orchestrating local al

127 howed it was expressed mainly on the myeloid phagocytes in human blood.

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

129 Phenotypic descriptions of the mononuclear phagocytes in nondiseased lungs provide a precedent for

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

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

132 py and shed light on the importance of fetal phagocytes in shaping the developing immune system and i

133 Microglia, the primary phagocytes in the brain, are positively correlated with

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

135 imary immune effector cells and professional phagocytes in the central nervous system, remains conten

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

137 To test whether microglia are efficient phagocytes in the diseased brain as well, we confronted

138 l and antimicrobial functions of mononuclear phagocytes in the lungs and liver.

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

140 bsets within a well-characterized network of phagocytes in the small intestinal lamina propria.

141 The numbers of activated microglia and phagocytes in TREM2 KO mice were decreased compared with

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

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

144 ed gene expression signatures unique to each phagocyte, including macrophage-specific lipid metabolis

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

146 d removal of apoptotic cells by professional phagocytes, including dendritic cells and macrophages, p

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

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

149 Strikingly, the density of mononuclear phagocytes increased upon descending the airways.

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

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

152 Live images of beta cell-phagocyte interactions documented the intimacy of the me

153 To date, the majority of work on S. aureus-phagocyte interactions has focused on neutrophils and, t

154 After selective depletion of liver phagocytes, intravascular myeloid precursors began to di

155 We revealed that a phagocyte is able to internalize particles via a chemoat

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

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

158 e capacity for intracellular survival within phagocytes is likely a critical factor facilitating the

159 to or defective attainment of this anion by phagocytes is linked to innate immune defects.

160 s by both professional and semi-professional phagocytes is required for resolution of organ damage an

161 a process of clearance of apoptotic cells by phagocytes, is essential for successful resolution of in

162 phenotypic analysis of pulmonary mononuclear phagocytes isolated from whole nondiseased human lungs a

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

164 Ultimately, this secondary phagocyte kills the bacteria.

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

166 causes a maturational arrest in mononuclear phagocyte lineage cells and severe secondary pulmonary a

167 of CSF1R-expressing cells of the mononuclear phagocyte lineage that constitute the tumor mass in dt-G

168 fate-mapping studies, three main mononuclear phagocyte lineages have been defined, namely, macrophage

169 yet whether environmental signals influence phagocyte longevity in the absence of inflammation remai

170 As professional phagocytes, macrophages are susceptible to endolysosomal

171 We propose that mammalian phagocytes may also use this mechanism to engulf and ing

172 ance of dying cells by activated neighboring phagocytes may precipitate the transition to heart failu

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

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

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

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

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

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

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

180 Phagocytes mobilize interferon-inducible responses upon

181 sociation with subretinal CD14(+)mononuclear phagocyte (MP) infiltration that is also reported in RP.

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

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

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

185 tion and chronic accumulation of mononuclear phagocytes (MPs).

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

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

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

189 ANCA-induced phagocyte NADPH oxidase (Phox) may contribute by generat

190 urprisingly has now extended well beyond the phagocyte NADPH oxidase - an industrial strength produce

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

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

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

194 tion of reactive oxygen species (ROS) by the phagocyte nicotinamide adenine dinucleotide (NADPH) oxid

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

196 engulfment of apoptotic neutrophils by human phagocytes occurs, how heterogeneity of phagocyte popula

197 Various phagocytes of mammals and invertebrates produce ETs, how

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

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

200 Microglia are the primary phagocytes of the central nervous system.

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

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

203 more, once Mtb is ingested into professional phagocytes, other host molecules are engaged to report o

204 one treatment of gp91(phox-/-) mice enhanced phagocyte oxidant production and host defense.

205 , a murine model of human CGD, would enhance phagocyte oxidant production and killing of Staphylococc

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

207 The phagocyte oxidative burst, mediated by Nox2 NADPH oxidas

208 Different mononuclear phagocytes, particularly dendritic cells, were labeled b

209 aled unique insights into various aspects of phagocyte physiology.

210 r findings provide evidence that mononuclear phagocytes play a key role in clearance of the ospC muta

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

212 significantly upregulated by the mononuclear phagocyte population concomitant with an increased recru

213 Our findings suggest that the mononuclear phagocyte population is directly involved in the product

214 2016) identify a tissue-resident mononuclear phagocyte population that promotes weight gain and gluco

215 w cytometry was used to identify mononuclear phagocyte populations among cells labeled by each route

216 d defines a competitive relationship between phagocyte populations for tumour loading during metastat

217 uman phagocytes occurs, how heterogeneity of phagocyte populations influences efferocytosis signaling

218 ngs-'myelinosomes'-, which are surrounded by phagocyte processes and promoted in their formation by a

219 th molecules during the respiratory burst of phagocytes provided an excellent opportunity.

220 a conserved, phosphatidylserine-recognizing phagocyte receptor.

221 ral role for IL-33 in regulating mononuclear phagocyte recruitment to the photoreceptor layer and pos

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

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

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

225 of IGF-1 to its receptor on non-professional phagocytes redirected their phagocytosis, such that upta

226 d their location, as well as the dynamics of phagocyte repopulation after full depletion.

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

228 The phagocyte respiratory burst is crucial for innate immuni

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

230 ough similar proportions of Live-P and Die-P phagocytes responded to exogenous stimuli, Die-P phagocy

231 Evasion of the host phagocyte response is critical for successful infection.

232 Macrophage gene expression determines phagocyte responses and effector functions.

233 or the central nervous system (CNS), and the phagocytes responsible for routine non-inflammatory clea

234 ws for enhanced degradation and detection by phagocytes, resulting in robust IL-1beta production.

235 phenotype and function of renal mononuclear phagocytes (rMPs) expressing key markers of both Msmall

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

237 Eukaryotic phagocytes search and destroy invading microorganisms vi

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

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

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

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

242 ocytes responded to exogenous stimuli, Die-P phagocytes showed marked deficits in all parameters meas

243 nscriptomic profiling of mucosal mononuclear phagocytes sorted after 1 week of continued allergen cha

244 function of podosomes are increased via the phagocyte-specific kinase Hck and Wiskott-Aldrich syndro

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

246 wnregulation of the inflammatory response of phagocytes, stimulation of proliferation of subsets of m

247 te gene function within specific mononuclear phagocyte sub-populations.

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

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

250 sis, followed by apoptotic cell clearance by phagocytes such as macrophages.

251 s (such as macrophages) and non-professional phagocytes (such as epithelial cells) clear billions of

252 Professional phagocytes (such as macrophages) and non-professional ph

253 Phagocytes, such as neutrophils and macrophages, engulf

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

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

256 ymer structure in modulating the mononuclear phagocyte system (MPS) accumulation of polyion complexes

257 The mononuclear phagocyte system (MPS) comprises monocytes, macrophages

258 effectively avoid uptake by the mononuclear phagocyte system (MPS) in vivo with a long blood circula

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

260 development and function of the mononuclear phagocyte system (MPS).

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

262 immunobiology, with cells of the mononuclear phagocyte system being critical in mediating efferocytos

263 The pulmonary mononuclear phagocyte system is a critical host defense mechanism co

264 The mononuclear phagocyte system is a heterogeneous group of leukocytes

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

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

267 The mononuclear phagocyte system, derived from the bone marrow progenito

268 sident macrophages that form the mononuclear phagocyte system.

269 bacteria and apoptotic cells and are better phagocytes than bone marrow-derived macrophages.

270 a Dictyostelium discoideum is a professional phagocyte that chases bacteria through chemotaxis and en

271 emoattractive stimulant(s) of macrophages, a phagocyte that they are able to survive within and event

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

273 tebrate epidermal cells as broad-specificity phagocytes that likely contribute to neural repair and w

274 morphologic characterization of mononuclear phagocytes that potentially access inhaled antigens in h

275 The diverse array of phagocytes that reside within different tissues, combine

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

277 sequence resulted from macrophage-like fetal phagocytes that took up OVA and differentiated toward de

278 and gamma-hemolysin CB (HlgCB) target human phagocytes through interaction with the complement recep

279 delivery of bacteria and immune complexes to phagocytes, through a process known as immune adherence,

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

281 changes in beta2 integrins that allow these phagocytes to effectively accomplish their mission in th

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

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

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

285 ally any cell type ranging from professional phagocytes to mucosal epithelial cells.

286 tion that lens cells themselves could act as phagocytes to remove toxic apoptotic debris.

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

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

289 research has focused on the uptake of ACs by phagocytes, tolerogenic signals exposed by the ACs are m

290 d aminoglycoside neomycin alone, accelerated phagocyte turnover and increased the rates of their spon

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

292 Five pulmonary mononuclear phagocytes were observed, including macrophages, monocyt

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

294 Sorted mononuclear phagocytes were subjected to RNA extraction and gene exp

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

296 ed chemokines that facilitate recruitment of phagocytes, which can eliminate extracellular protozoa (

297 acellular survival niche within professional phagocytes, which ultimately facilitates dissemination.

298 In vitro, cyhv3Il10 deactivates phagocytes with a prominent effect on macrophages, while

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

300 everal prototypical inhibitory activities on phagocytes with mammalian IL-10, including deactivation