ライフサイエンスコーパス: Siglec

1 ns with sialic acid-binding Ig-type lectins (siglecs).

2 ion of a high affinity ligand for the target Siglec.

3 activation through engagement of inhibitory Siglecs.

4 ulates the inflammatory response by engaging siglecs.

5 taining the selectivity for hCD22 over other Siglecs.

6 of agents to cells expressing CD22 and other Siglecs.

7 s that express glycan ligands for the B cell Siglecs.

8 We also found that the expression of Siglec-1 (a member of sialic acid-binding Ig (I)-like le

9 e functionally null or haploinsufficient for Siglec-1 activity in HIV-1 capture and trans-infection e

10 Mechanistically, Siglec-1 associates with adaptor protein DNAX-activation

11 Siglec-1 depletion decreases TNT length, diminishes HIV-

12 resence of HIV-2/SIVmac Vpx, indicating that Siglec-1 does not counteract restriction factors such as

13 Siglec-1 expression depends on Mtb-induced production of

14 This analysis confirmed increased monocytic Siglec-1 expression in active systemic lupus erythematos

15 Furthermore, Siglec-1 expression was identified in the septal region

16 ctious routes may compensate for the lack of Siglec-1 in fuelling HIV-1 dissemination within infected

17 s with the known in vitro functional role of Siglec-1 in HIV-1 trans-infection.

18 Knockdown of siglec-1 in RAW 264.7 cells resulted in inhibiting the p

19 ltogether, we uncover a deleterious role for Siglec-1 in TB-HIV-1 co-infection and open new avenues t

20 In co-infected non-human primates, Siglec-1 is highly expressed by alveolar macrophages, wh

21 Siglec-1 localizes mainly on microtubule-containing TNT

22 Siglec-1 mediates pre-DC infection of CCR5- and CXCR4-tr

23 Thus, Siglec-1 plays an important role in the development of e

24 Instead, Siglec-1 promotes attachment and fusion of viral particl

25 However, Siglec-1 protein truncation does not have a measurable i

26 crophages, and revealed the up-regulation of Siglec-1 receptor.

27 hat inhibits HIV-1 fusion and infection, but Siglec-1 remains functional and mediates replication-ind

28 ndotoxin tolerant cells and the induction of Siglec-1 suppresses the innate immune response by promot

29 The enhanced TGF-beta1 production by Siglec-1 was significantly attenuated by spleen tyrosine

30 that delivers tumor antigens to human CD169/Siglec-1(+) antigen-presenting cells using gangliosides

31 luding sialic acid-binding Ig-like lectin 1 (Siglec-1), a receptor on monocytes/macrophages, recent a

32 CD169/Siglec-1, an I-type lectin that recognizes gangliosides,

33 , are susceptible to infection by HIV-1 in a Siglec-1-dependent manner.

34 - and blood-borne retroviruses exploit CD169/Siglec-1-mediated capture by subcapsular sinus and margi

35 Altogether, Siglec-1-mediated susceptibility to HIV-1 infection of p

36 bly fibrosing components of CHB, positioning Siglec-1-positive macrophages as integral to the process

37 ve expression of the viral adhesion receptor Siglec-1.

38 Siglec-1/CD169 is a myeloid-cell surface receptor critic

39 r Siglec-10, as well as blockade of the CD24-Siglec-10 interaction using monoclonal antibodies, robus

40 eptor sialic-acid-binding Ig-like lectin 10 (Siglec-10), which is expressed by tumour-associated macr

41 Genetic ablation of either CD24 or Siglec-10, as well as blockade of the CD24-Siglec-10 int

42 ssociated macrophages express high levels of Siglec-10.

43 acid capsule as a molecular mimic to engage Siglec-11 and escape killing.

44 involving design from the endogenous ligand Siglec-11 and multi-platform characterisation of peptide

45 A computational study of Siglec-11 and Siglec-11-derived peptides offered synergi

46 Here, we studied the inhibitory receptor Siglec-11 that shows uniquely human expression in brain

47 A computational study of Siglec-11 and Siglec-11-derived peptides offered synergistic insight i

48 surfactant protein D, human galectin-8, and Siglec-14, to different NTHi clinical isolates.

49 addition, we generated a new monoclonal anti-Siglec-15 Ab to clarify its expression pattern on immune

50 Genetic ablation or antibody blockade of Siglec-15 amplifies anti-tumor immunity in the TME and i

51 e-scale T cell activity array, we identified Siglec-15 as a critical immune suppressor.

52 Taken together, our results support Siglec-15 as a potential target for normalization cancer

53 Taken together, our findings show a role of Siglec-15 as a regulator of pathologic bone resorption i

54 tential as a target for future therapies, as Siglec-15 blocking Abs are available.

55 eas this Ab demonstrated an almost exclusive Siglec-15 expression on murine osteoclasts and hardly an

56 The role of Siglec-15 in arthritis is still largely unclear.

57 Siglec-15 is a conserved sialic acid-binding Ig-like lec

58 ly expressed on some myeloid cells normally, Siglec-15 is broadly upregulated on human cancer cells a

59 We could show that Siglec-15 is directly involved in pathologic bone erosio

60 To address this, we generated Siglec-15 knockout mice and analyzed them in a mouse art

61 Deficiency of Siglec-15 leads to an impaired osteoclast development, r

62 Thus, Siglec-15 on osteoclasts has a crucial function for bone

63 We demonstrate that Siglec-15 suppresses antigen-specific T cell responses i

64 on on various other immune cell types, human Siglec-15 was more broadly expressed on human myeloid ce

65 bone erosion area and osteoclast numbers in Siglec-15(-/-) mice, whereas the inflammation area and c

66 st, engagement of the activating counterpart Siglec-16 increases elimination of bacteria.

67 mouse Siglec-E with the activating module of Siglec-16.

68 The inhibitory functions of CD22/Siglec-2 and Siglec-G and their contributions to toleran

69 CD33 (Siglec-3) is a transmembrane sialic acid-binding recepto

70 The immunomodulatory receptor Siglec-3/CD33 influences risk for late-onset Alzheimer's

71 e, a third BDCA-2-expressing population, Axl+Siglec-6+ DCs (ASDC), was also found to infiltrate human

72 Siglec 9 on neutrophils and Siglec 7 on NK cells are prominent examples of inhibitor

73 Soluble Siglec-7 (sSiglec-7) levels were measured by ELISA in se

74 sely, therapeutic interventions that inhibit Siglec-7 could have unanticipated consequences and promo

75 Siglec-7 cross-linking inhibited GM-CSF-induced release

76 Finally, Siglec-7 cross-linking on GM-CSF-activated eosinophils i

77 , thereby recruiting the inhibitory receptor Siglec-7 expressed on the NK cell surface which subseque

78 Our data suggest that restoration of human Siglec-7 expression may be a novel therapeutic strategy

79 Over-expression of Siglec-7 in diabetic islets reduced cytokines, prevented

80 Siglec-7 is a human CD33-like siglec, and is localised p

81 Siglec-7 is an inhibitory receptor (IR) expressed on hum

82 Siglec-7 is considered to function as an immunoreceptor

83 Siglec-7 is constitutively expressed on human eosinophil

84 d alphaMe Neu5Ac, the smallest known natural Siglec-7 ligand.

85 he first, high-affinity low molecular weight Siglec-7 ligands to interfere with cancer cell immune ev

86 gnant cells is to camouflage themselves with Siglec-7 ligands, thereby recruiting the inhibitory rece

87 The effect of Siglec-7 on eosinophil viability and degranulation was a

88 Targeting of Siglec-7 on eosinophils might enhance treatment efficacy

89 function, little is known about the role of Siglec-7 on human eosinophils.

90 Siglec-7 surface, but not SIGLEC-7mRNA expression, was c

91 nd inhibition analysis of GD3-binding toward Siglec-7 using synthetic sialoglycoconjugates and a comp

92 Siglec-7 was expressed ex vivo on blood eosinophils from

93 Siglec-7 was expressed on beta-cells and down-regulated

94 Eosinophil expression of Siglec-7 was quantified by flow cytometry and quantitati

95 Siglec-7 was upregulated on purified eosinophils after i

96 ight against cancers, in particular blocking Siglec-7 with low molecular weight compounds.

97 s, we identified a CD11b(+) CD57(-) CD161(+) Siglec-7(+) subpopulation of CD56(dim) CD16(+) NK cells

98 revealed that the CD11b(+) CD57(-) CD161(+) Siglec-7(+) subpopulation of CD56(dim) CD16(+) NK cells

99 d that sialic acid-binding Ig-type lectin-7 (Siglec-7), a glycoimmune checkpoint receptor, selectivel

100 sights into the ligand-binding properties of Siglec-7, we carried out in silico analysis and site-dir

101 es and bind with low micromolar Kd values to Siglec-7.

102 he flexible conformation of the C-C' loop of Siglec-7.

103 Siglec-7 surface, but not SIGLEC-7mRNA expression, was correlated with absolute eo

104 lic acid-binding immunoglobulin-like lectin (Siglec) 8 is selectively expressed on eosinophils, mast

105 lic acid-binding immunoglobulin-like lectin (Siglec)-8 is a cell-surface protein expressed selectivel

106 lic acid-binding immunoglobulin-like lectin (Siglec)-8 is expressed on mast cells and eosinophils, bu

107 e sought to characterize surface and soluble Siglec-8 (sSiglec-8) levels in normal donors (NDs) and e

108 Whereas activation of other IRs, including Siglec-8 and CD300a, has been shown to downregulate eosi

109 re, we report the development of a ligand of Siglec-8 and its closest murine functional orthologue Si

110 donors (EOs) and assess the efficacy of anti-Siglec-8 antibodies in inducing eosinophil cell death in

111 (1) (chimeric 2E2 IgG(1) [c2E2 IgG(1)]) anti-Siglec-8 antibodies was evaluated in vitro by using flow

112 AK002 (lirentelimab) is an anti-Siglec-8 antibody that depletes eosinophils and inhibits

113 The affinity of Siglec-8 binding to purified human airway ligand was det

114 Targeting saporin to Siglec-8 consistently caused extensive cell death in eos

115 and malignant mast cells by exploiting this Siglec-8 endocytic pathway.

116 Siglec-8 endocytosis required actin rearrangement, tyros

117 targeting of an agent to these cells through Siglec-8 endocytosis.

118 red to elicit the unanticipated finding that Siglec-8 engagement promotes rapid beta2-integrin-depend

119 cells and eosinophils, but information about Siglec-8 expression and function in the lung is limited.

120 and flow cytometry were used to characterize Siglec-8 expression in sputum cells from stable asthma.

121 he necessity of various proteins involved in Siglec-8 function for human eosinophils.

122 identify the signaling molecules involved in Siglec-8 function for human eosinophils.

123 These data demonstrate that Siglec-8 functions uniquely as an activating receptor on

124 etic sulfated sialoglycan ligand recognizing Siglec-8 in combination with integrin blocking antibodie

125 Siglec-8 intracellular trafficking was followed by confo

126 Siglec-8 is a CD33 subfamily cell-surface receptor selec

127 Siglec-8 is a human immune-inhibitory receptor that, whe

128 We sought to determine whether Siglec-8 is endocytosed in human eosinophils and maligna

129 Siglec-8 is highly expressed on blood eosinophils from E

130 Siglec-8 is highly expressed on eosinophils and mast cel

131 Gene expression for Siglec-8 is increased in sputum cells in asthma and corr

132 Gene expression for Siglec-8 is inversely and significantly correlated with

133 idase treatment of eosinophils revealed that Siglec-8 is partially masked by sialylated cis ligands.

134 Siglec-8 is prominently expressed on the surface of eosi

135 A humanized antibody, AK002, targeting Siglec-8 is undergoing development for treatment of dise

136 ligands and determined the structure of the Siglec-8 lectin domain in complex with its prime glycan

137 mistry, and enzyme treatments confirmed that Siglec-8 ligand on the human airway mucus layer is an is

138 lved by gel electrophoresis and blotted, and Siglec-8 ligands detected.

139 We hypothesized that Siglec-8 ligands in submucosal glands and ducts are norm

140 Siglec-8 ligands were found on postmortem human trachea

141 Internalized Siglec-8 localized to the lysosomal compartment.

142 After cytokine priming, Siglec-8 mAb or glycan ligand binding causes eosinophil

143 l ROS production and apoptosis suggests that Siglec-8 might instead function as an activating recepto

144 T1(S8), is the major high-avidity ligand for Siglec-8 on human airways.

145 Finally, engagement of Siglec-8 on IL-5-primed eosinophils resulted in increase

146 The immunoinhibitory receptor Siglec-8 on the surface of human eosinophils and mast ce

147 g/uptake and selectivity to cells expressing Siglec-8 or -F and, when administered to mice, exhibit i

148 e of targeting liposomes to cells expressing Siglec-8 or -F.

149 structural and mechanistic insights into how Siglec-8 selectively recognizes its glycan target, ratio

150 Our aim was to identify the major Siglec-8 sialoglycan ligand on the mucus layer of human

151 Siglec-8 surface dynamics were examined by flow cytometr

152 requires an understanding of the dynamics of Siglec-8 surface expression.

153 s unrelated to absolute eosinophil counts or Siglec-8 surface expression.

154 as inhibitory receptors, but the ability of Siglec-8 to stimulate eosinophil ROS production and apop

155 ctroscopy to dissect the fine specificity of Siglec-8 toward different sialylated and sulfated carboh

156 Siglec-8 was also shuttled to the surface via a distinct

157 Eosinophil expression of Siglec-8 was assessed by using flow cytometry and quanti

158 Siglec-8 was consistently expressed on eosinophils from

159 mast cells in asthmatic sputum and targeting Siglec-8 with an antibody is a plausible strategy to dec

160 of the OSM(+) cells, 56% +/- 7% were CD16(+)Siglec-8(-), indicating neutrophil lineage.

161 ymal rEos found in nonasthmatic human lungs (Siglec-8+CD62L+IL-3Rlo cells) were phenotypically distin

162 he sputa of eosinophilic asthmatic patients (Siglec-8+CD62LloIL-3Rhi cells), suggesting that our find

163 Human Siglec-8, for instance, has been identified as a therape

164 monstrate whether a toxin can be targeted to Siglec-8-bearing cells to kill these cells.

165 A Siglec-8-ligand with a molecular weight of approximately

166 bition of these kinases completely prevented Siglec-8-mediated eosinophil apoptosis.

167 a Rac GTPase inhibitor) completely inhibited Siglec-8-mediated eosinophil apoptosis.

168 Siglec-8-mediated ROS was generated through reduced nico

169 hibiting protein saporin was conjugated to a Siglec-8-specific antibody to examine the targeting of a

170 tion, and will enable the rational design of Siglec-8-targeted agonists to treat eosinophil- and mast

171 eral blood eosinophils, mast cell lines, and Siglec-8-transduced cells in the presence of inhibitors

172 Maximal endocytosis in Siglec-8-transduced HEK293T cells required an intact imm

173 ed that DMBT1(S8) has picomolar affinity for Siglec-8.

174 Siglec 9 on neutrophils and Siglec 7 on NK cells are pro

175 nistic monoclonal antibodies to human Fas or Siglec-9 affected the viability of mouse neutrophils.

176 arthritis was studied with both (68)Ga-DOTA-Siglec-9 and (18)F-FDG PET/CT to determine the ability o

177 Binding of MUC1-ST to Siglec-9 did not activate the phosphatases SHP-1 or SHP-

178 ogical ligands, whereas the related receptor Siglec-9 does not.

179 Siglec-9 is a sialic-acid-binding lectin expressed predo

180 elets also express high levels of inhibitory Siglec-9 on their surface, and that GBS can engage this

181 Most importantly, however, (68)Ga-DOTA-Siglec-9 was comparable to (18)F-FDG in detecting arthri

182 (68)Ga-DOTA-Siglec-9 was rapidly cleared from the blood circulation,

183 lusion: Intravenous injection of (68)Ga-DOTA-Siglec-9 was safe and biodistribution was favorable for

184 Results: (68)Ga-DOTA-Siglec-9 was well tolerated by all subjects.

185 The effective radiation dose of (68)Ga-DOTA-Siglec-9 was within the same range as the effective radi

186 Injection of 150 MBq of (68)Ga-DOTA-Siglec-9 would expose a subject to 3.3 mSv.

187 ic acid-binding immunoglubulinlike lectin 9 (Siglec-9) is a ligand of vascular adhesion protein 1.

188 ecific MUC1 glycoform, through engagement of Siglec-9, 'educated' myeloid cells to release factors as

189 A (68)Ga-labeled peptide of Siglec-9, (68)Ga-DOTA-Siglec-9, holds promise as a novel

190 oprotein on erythrocytes, engaged neutrophil Siglec-9, a sialic acid-recognizing receptor known to da

191 )Ga-labeled peptide of Siglec-9, (68)Ga-DOTA-Siglec-9, holds promise as a novel PET tracer for imagin

192 ossible repeated clinical use of (68)Ga-DOTA-Siglec-9, such as in trials to elucidate the treatment e

193 Notably, Siglec-9, the functionally equivalent human paralog of S

194 trophils via agonistic antibodies to Fas and Siglec-9.

195 ctivating pathway that follows engagement of Siglec-9.

196 us injection of 162 +/- 4 MBq of (68)Ga-DOTA-Siglec-9.

197 iquely human interactions of a pathogen with Siglecs and support the long-standing hypothesis that ac

198 m sialic acids may interact with endometrial Siglecs and that these interactions facilitate sperm sur

199 Siglec-7 is a human CD33-like siglec, and is localised predominantly on human natural

200 nally, treatment of humanized mice with anti-Siglec antibody led to robust depletion of IL-5-induced

201 c acid-recognizing Ig superfamily lectins or Siglecs are a family of cell surface proteins largely ex

202 CD33-related Siglecs are a family of proteins widely expressed on inn

203 Moreover, we examined whether Siglecs are expressed on human and mouse endometria, whi

204 CD33-related-Siglecs are immune receptors that recognize self-associa

205 The majority of Siglecs are inhibitory receptors expressed in immune cel

206 e that also expresses Siglec ligands, B cell Siglecs are recruited to the immunological synapse, resu

207 Sialic acid-binding Ig-type lectins (Siglecs) are cell surface receptors found on immune cell

208 ic-acid-binding immunoglobulin-like-lectins (siglecs) are expressed in human pancreatic islets in a c

209 ic acid-binding immunoglobulin-type lectins (Siglecs) are expressed on the majority of white blood ce

210 Removal of Siglec-E causes the development of exaggerated signs of

211 -1 recruitment between dimeric and monomeric Siglec-E expressed on HEK293A cells.

212 t-resident macrophages express Siglec-E, and Siglec-E expression decreases on islet-resident macropha

213 Thus, we further investigated the impact of Siglec-E homodimerization.

214 lpha-2,8-disialic acids that are ligands for Siglec-E in vivo.

215 We show that Siglec-E is required for Escherichia coli-induced endocy

216 Although all antibodies detected Siglec-E on transfected human HEK-293T cells, only two r

217 Elimination of murine inhibitory Siglec-E partially reversed platelet suppression in resp

218 ition to form a disulfide bridge between two Siglec-E polypeptides.

219 We hypothesized that engaging Siglec-E through ST8Sia6-generated ligands may inhibit t

220 by replacing the inhibitory domain of mouse Siglec-E with the activating module of Siglec-16.

221 s, and only two antibodies recognized native Siglec-E within spleen lysates.

222 Islet-resident macrophages express Siglec-E, and Siglec-E expression decreases on islet-res

223 cation has complex effects on recognition by Siglec-E, in relationship to the underlying structures.

224 the functionally equivalent human paralog of Siglec-E, occurs as a monomer.

225 ta relating to the structure and function of Siglec-E, the major CD33-related Siglec expressed on mou

226 rat monoclonal antibodies specific to mouse Siglec-E, with no cross-reactivity to Siglec-F.

227 Siglec-E-deficient dendritic cells infected with E. coli

228 result of the inability to internalize TLR4, Siglec-E-deficient dendritic cells were also defective f

229 itic cells from wild-type mice, but not from Siglec-E-deficient mice, after E. coli infection.

230 Moreover, whereas all antibodies recognized Siglec-E-Fc on immunoblots, binding was dependent on int

231 features that Sia-antigen imposed on DCs are Siglec-E-mediated and maintained under inflammatory cond

232 Siglec-E16 enhanced proinflammatory cytokine expression

233 Notably, Siglec-engaging antigenic liposomes formulated with an h

234 function of Siglec-E, the major CD33-related Siglec expressed on mouse neutrophils, monocytes, macrop

235 ic acid-binding, immunoglobulin-like lectin (Siglec) F is a glycan-binding protein selectively expres

236 and its closest murine functional orthologue Siglec-F that is capable of targeting liposomes to cells

237 anulocytes to be SSC(high) CD11b(+) CD125(+) Siglec-F(+) (where SSC(high) indicates a high side scatt

238 stered to mice, exhibit in vivo targeting to Siglec-F(+) eosinophils.

239 ransition from a Siglec-F(med) CD11c(-) to a Siglec-F(high) CD11c(low) phenotype in lung tissue was a

240 Gradual transition from a Siglec-F(med) CD11c(-) to a Siglec-F(high) CD11c(low) ph

241 sinophils peaked during P10-14 and exhibited Siglec-F(med/high)CD11c(-/low) phenotypes, similar to al

242 1b(+) DC lineage, including CD101, TREM1 and Siglec-F, and shows that the absence of CD103(+)CD11b(+)

243 d in TNC significantly induced expression of Siglec-F, CD11c, eosinophil peroxidase, and other marker

244 mouse Siglec-E, with no cross-reactivity to Siglec-F.

245 trol lung eosinophilia through engagement of Siglec-F.

246 sive and direct interactions between TLR and Siglec families of pattern recognition receptors.

247 ctates tight specificity distinct from other Siglec family members and any other endogenous glycan re

248 The Siglec family of cell surface receptors have emerged as

249 Ig-like lectin (Siglec)-G are members of the Siglec family of inhibitory coreceptors expressed on B c

250 CD22, a member of Siglec family of sialic acid binding proteins, has restr

251 In this review we describe the Siglec family, its roles in regulation of immune cell si

252 One of these is CD22, a member of the Siglec family.

253 CD22, a sialic acid-binding Ig-type lectin (Siglec) family member, is an inhibitory coreceptor of th

254 binding assays between sperm and recombinant Siglec-Fc chimeric proteins to measure interactions.

255 were defined as IL-5-dependent peribronchial Siglec-FhiCD62L-CD101hi cells with a segmented nucleus.

256 monary rEos are IL-5-independent parenchymal Siglec-FintCD62L+CD101lo cells with a ring-shaped nucleu

257 disease processes, and approaches to target Siglecs for treatment of human disease.

258 ses predicted that only some human and mouse Siglecs form disulfide-linked dimers.

259 Modulators of Siglec function are likely to be developed and investiga

260 Many Siglecs function as inhibitory receptors on innate and a

261 Most CD33-related Siglecs function as inhibitory receptors, but the abilit

262 -surface proteins, including BTLA, IRF4, and Siglec G.

263 CD22 and sialic acid-binding Ig-like lectin (Siglec)-G are members of the Siglec family of inhibitory

264 he inhibitory functions of CD22/Siglec-2 and Siglec-G and their contributions to tolerance and autoim

265 to be associated with autoimmunity, loss of Siglec-G does not result in autoimmune disease in BALB/c

266 all cells display sialic acids, and CD22 and Siglec-G have distinct, yet overlapping, specificities f

267 In this study, we analyzed the role of Siglec-G in induction and maintenance of B cell toleranc

268 These results indicate that Siglec-G is important to maintain tolerance in B cells a

269 ouse RBCs are essentially devoid of CD22 and Siglec-G ligands.

270 We find that aging Siglec-G-deficient and Siglec-G x FcgammaRIIb double-deficient mice develop an

271 ss of the inhibitory receptor FcgammaRIIb in Siglec-G(-/-) mice does not result in exacerbation of di

272 We find that aging Siglec-G-deficient and Siglec-G x FcgammaRIIb double-def

273 Siglec-G-deficient mice, which have increased numbers of

274 the type I IFN, IFN-alpha, in vitro and that Siglec-H knockout (KO) mice produce more IFN-alpha after

275 In contrast, uninfected aging Siglec-H KO mice developed a mild form of systemic autoi

276 several weeks after a single mCMV infection, Siglec-H KO mice developed a severe form of systemic lup

277 autoimmune disease after virus infection in Siglec-H KO mice was accompanied by a type I IFN signatu

278 These results show that Siglec-H normally serves as a modulator of type I IFN re

279 retion of type I IFN of pDCs is modulated by Siglec-H, a DAP12-associated receptor on pDCs.

280 In this study, we show that Siglec-H-deficient pDCs produce more of the type I IFN,

281 Immunomodulation by Siglecs has been extensively studied, but relationships

282 Siglecs have been best studied in the tumor context in a

283 A promising strategy to target Siglecs involves the use of liposomal nanoparticles with

284 These results demonstrate that the lack of Siglec ligands on the surface of murine RBCs permits B c

285 ate Ag on a cell surface that also expresses Siglec ligands, B cell Siglecs are recruited to the immu

286 nanoparticles with a multivalent display of Siglec ligands.

287 ic acid-binding immunoglobulin-like lectins (Siglec)-like domains of streptococcal serine-rich repeat

288 tein than is observed in structures of other Siglec-like adhesins.

289 l responses to erythrocyte Ags and show that Siglec-mediated B cell tolerance is restricted to cell t

290 Sialylated LOS also engages inhibitory Siglecs on host leukocytes, dampening innate immunity.

291 o However, we observed expression of several Siglecs on the endometrium and that these receptors inte

292 ic acid-binding immunoglobulin-like lectins (Siglecs) play a pivotal role in regulating many immune r

293 human microglia, including TLR, Fcgamma and SIGLEC receptors, as well as TAL1 and IFI16, regulators

294 Since mice do not have paired Siglec receptors, we generated a model by replacing the

295 hibitory sialic acid-binding Ig-like lectin (Siglec) receptors, and enhanced binding to the NK-activa

296 CD169 is a Siglec that may function as an adhesion molecule and a f

297 K cells are prominent examples of inhibitory Siglecs that can potentially dampen anti-tumor immunity.

298 lic acid-binding immunoglobulin-like lectin (Siglec) that is highly expressed on B-cells and B cell l

299 tory Sia-recognizing Ig superfamily lectins (Siglecs) to block neutrophil and macrophage activation.

300 Of note, CD33 is the only Siglec with a peroxisome-targeting sequence, and this mo