ライフサイエンスコーパス: cell recognition

1 and TNF and IFNgamma production upon target-cell recognition.

2 endosomal degradation, in order to evade NK cell recognition.

3 lated viral peptides, resulting in altered T cell recognition.

4 ion of tumor cells to human Vgamma9Vdelta2-T cell recognition.

5 that the latter is involved with p23 in host cell recognition.

6 ricted manner, and peptide is required for T cell recognition.

7 uences of such force-induced unbinding for T cell recognition.

8 d or select for mutant viruses that escape T cell recognition.

9 T cell receptor ligand CD1d, abrogating iNKT cell recognition.

10 esting a potential CMV evasion to KIR2DL3 NK cell recognition.

11 CD8, which functions as coreceptor for tumor-cell recognition.

12 les to the immunological synapse upon target cell recognition.

13 esentation as a critical factor for CD4(+) T-cell recognition.

14 ant role in inflammation, immunity, and self-cell recognition.

15 polarized membrane structures involved in T cell recognition.

16 are directionally released following target cell recognition.

17 n, however, does not always correlate with T-cell recognition.

18 in early-stage biofilm development and host cell recognition.

19 nts a major molecular hurdle necessary for T-cell recognition.

20 that did not facilitate strong escape from T cell recognition.

21 e primarily for the peptide specificity of T-cell recognition.

22 resented peptides contribute critically to T-cell recognition.

23 Ls that select viral variants which escape T-cell recognition.

24 tial method to exogenously control events in cell recognition.

25 CTL escape, and a mutation at P8 enhanced T-cell recognition.

26 resent phosphopeptides for specific CD4(+) T cell recognition.

27 minish class I HLA binding, or (iii) alter T-cell recognition.

28 intraepitope sequence variability has upon T-cell recognition.

29 dered Ad-infected cells more sensitive to NK cell recognition.

30 ts to select aptamers (designed DNA/RNA) for cell recognition.

31 rypanosomes are predicted sites for T- and B-cell recognition.

32 cted cells vulnerable to natural killer (NK) cell recognition.

33 inding strengths of these aptamers in cancer cell recognition.

34 g to speculation that Dscam proteins mediate cell recognition.

35 cleus, inconsistent with a role in apoptotic cell recognition.

36 ed by surface receptors, which direct target cell recognition.

37 that may be the targets of intraepithelial T-cell recognition.

38 mechanism by which M. tuberculosis evades T cell recognition.

39 acent residues, abrogating TCR binding and T-cell recognition.

40 s to retain high DQ2 affinity but abrogate T cell recognition.

41 , without altering peptide conformation or T cell recognition.

42 ized neighboring melanoma cells for CD4(+) T cell recognition.

43 act as a signal for the host to activate NK-cell recognition.

44 ts MHC class II molecules to impair CD4(+) T cell recognition.

45 during infection resulting in a defect in T cell recognition.

46 mited repertoire of antigenic peptides for T-cell recognition.

47 an allograft that does not prompt innate NK cell recognition.

48 ional protection against CD8(+) and CD4(+) T cell recognition.

49 ndin type 1 repeats, implying a role in host cell recognition.

50 Ag-dependent manner, thereby modulating MAIT cell recognition.

51 e the binding landscape for metal-specific T cell recognition, alanine screens were performed on a se

52 ddition to their appropriate genotypes, cell-cell recognition also requires compatible phenotypes, wh

53 c modification of the pig, and xenogeneic NK cell recognition and activation may be inhibited by the

54 ent sensitizes tumor cells to natural killer cell recognition and activation.

55 tures on cell surfaces are critical for cell-cell recognition and adhesion and in host-pathogen inter

56 To fuse, myoblasts undergo cell-cell recognition and adhesion and merger of membranes be

57 is an intricate process that is initiated by cell recognition and adhesion, and culminates in cell me

58 tion and somatic mutation requirements for B-cell recognition and affinity maturation.

59 microneme complex, which contributes to host cell recognition and attachment via the action of TgMIC1

60 he generation of mutant viruses that evade T cell recognition and cannot be avoided by simply increas

61 Selective cell recognition and capture has recently attracted sign

62 ermeable molecules, cell-cell communication, cell recognition and cell adhesion are mediated by membr

63 ous CTL-mediated lysis, independent of tumor cell recognition and CTL reactivity.

64 ncreasingly recognized as important to tumor cell recognition and destruction, as well as to protecti

65 lymphocytes with diverse patterns of target-cell recognition and effector function.

66 to its neck region that participate in host cell recognition and entry.

67 oproteins, Gn and Gc, which orchestrate host cell recognition and entry.

68 assembly has shown high potential for cancer cell recognition and for in vivo drug delivery applicati

69 Host cell recognition and internalization are mediated by tox

70 contrary to previous reports, CD4(+)CD28(-) cell recognition and killing can be specific and discrim

71 To study T cell recognition and killing mechanisms, we generated a

72 marrow dendritic cells (DCs) that impairs T-cell recognition and killing of myeloma cells.

73 ly rendering them vulnerable to gammadelta T cell recognition and lysis.

74 T cell recognition and MHC I surface expression under infl

75 E3/19K has a dual function: inhibition of T-cell recognition and NK cell activation.

76 ivity of WGA-Fc effectively modulates fungal cell recognition and promotes the elimination of fungal

77 P6 facilitate influenza virus escape from T-cell recognition and provide a model for the number, nat

78 tural differences among the PIMs impact host cell recognition and response and are predicted to influ

79 SI is an important model system for cell-to-cell recognition and signaling and could be potentially

80 underlying reasons for the complexity in NK cell recognition and signaling are proposed.

81 , 5, and 7 of Ad5 may be involved in Kupffer cell recognition and subsequent destruction.

82 derlying immunity to pathogens that resist T cell recognition and the extracellular cues governing pl

83 ould control the orientation of the particle-cell recognition and thereby the initiation of T cell ac

84 ires "escape mutations" that reduce CD8(+) T cell recognition and viral control.

85 cellular functions, e.g. tumor and apoptotic cell recognition and wound healing, but the mechanism of

86 R contact residue significantly diminishes T cell recognition and, in contrast to the original sequen

87 at at least some LITRs have a role in target cell recognition and/or cytotoxicity.

88 these mutations resulted in a loss of CD4+ T-cell recognition, and (iii) subsequent to viral resurgen

89 ciated with host receptors required for host cell recognition, and calcineurin function distinguishes

90 ells to AgAbs led to antigen presentation, T-cell recognition, and target cell killing.

91 ecause the target epitopes for CD4 and CD8 T-cell recognition are "unlinked" on different cells (reci

92 phasize the merits of including functional T cell recognition assays to gain a more complete picture

93 host cells and play important roles in host cell recognition, attachment and penetration.

94 ved cell adhesion proteins are implicated in cell recognition between synaptic partners, but how thes

95 ereas chlorine dioxide and heat inhibit host-cell recognition/binding.

96 lls in a manner that may decrease HLA- tumor cell recognition but allows for improved NK cell-mediate

97 only implicates the citrulline residue in T cell recognition but also highlights the potential value

98 ith its hydrophilic head group exposed for T-cell recognition, but CD1b structures show scaffold lipi

99 tercalated disc; it is known to mediate cell-cell recognition, but its natural function is poorly und

100 partially dependent on NKG2D-mediated tumor cell recognition, but surprisingly was still effective i

101 ls to various stress situations led to tumor cell recognition by a Vgamma8Vdelta3 TCR.

102 Tumor cells frequently escape from CD8+ T cell recognition by abrogating MHC-I antigen presentatio

103 gets of the bacillus, as defined by strong T-cell recognition by both mice and humans infected with M

104 roautophagy targeting could improve melanoma cell recognition by CD4(+) T cells and should be explore

105 and significantly affected the efficiency of cell recognition by CD8(+) T cells.

106 of evidence indicate that the lack of SCCHN cell recognition by CTL reflects defects in targeted TA

107 ed immunotherapy of SCCHN by restoring SCCHN cell recognition by CTL.

108 e initial communities is coaggregation (cell-cell recognition by genetically distinct bacteria).

109 of abundant peptide presentation for target cell recognition by immunodominant CTL was tested by sma

110 caspase activation within minutes of target cell recognition by murine cytotoxic lymphocytes.

111 We propose a concept for target cell recognition by NK cells beyond "missing self" and "

112 irment was not related to a defect in target cell recognition by NK cells but to the degradation of N

113 o downregulation of ULBP2, diminishing tumor cell recognition by NK cells.

114 late in the lytic cycle and impairs CD8(+) T cell recognition by targeting cell surface MHC class I m

115 al (cis) associations and regulation of cell-cell recognition by trans interaction with ganglioside b

116 R1-Ag tetramers that specifically stain MAIT cells, recognition by the MAIT TCR, and our emerging und

117 ot alter other surface molecules involved in cell recognition (calreticulin, CD31, or CD47).

118 position 5 (P5) within the epitope reduced T-cell recognition, changes at P4 or P6 enabled CTL escape

119 Peptide immunization and T cell recognition data generated from 90 peptides indicat

120 spective on investigating human gammadelta T-cell recognition, demonstrating that diversification at

121 As a novel cell-cell recognition determinant it contributes to the avail

122 verse families of cell-surface molecules for cell recognition during circuit assembly.

123 carbon and nitrogen sources and ligands for cell recognition during host colonization.

124 The requirement for MHC-restricted T cell recognition during thymic selection and peripheral

125 Whereas most models of T-cell recognition emphasize TCR discrimination of differi

126 This diversity is essential for cell recognition events required for wiring the brain.

127 bohydrates (the glycocalyx), fundamental for cell-recognition events.

128 heir susceptibility to EBV-specific CD8(+) T cell recognition falls dramatically, concomitant with a

129 T cell recognition foot-print and pMHC-I structural analys

130 individual proteins are the unit of B cell-T cell recognition for a large virus.

131 atment, HCMV evasins cooperatively impared T cell recognition for several different MHC I allotypes.

132 KpOmpA is involved in cell-cell recognition, for adhesion and immune response mecha

133 llotypes, single evasins largely abolished T cell recognition; for others, a concerted action of evas

134 ting that translocation accelerated infected cell recognition from after to before HLA-I downregulati

135 Cell-cell recognition guides the assembly of the vertebrate b

136 r those tumors express antigens capable of T-cell recognition has not been explored.

137 Artificially controlled cell recognition has potentially far-reaching applicatio

138 The molecular details of the toxin-cell recognition have been elusive.

139 The earliest molecular events in T-cell recognition have not yet been fully described, and

140 with cell transformation serves as a mode of cell recognition in innate immunity.

141 tion profiling for the characterization of T-cell recognition in various diseases, including in small

142 ells, modulation of Akt was linked to target cell recognition, independently of phagocytosis, whereas

143 l micronemes are central components for host cell recognition, invasion, egress, and virulence.

144 Although the specificity of T cell recognition is determined by the interaction of T c

145 ative cells demonstrates that differential T-cell recognition is due to a single nucleotide polymorph

146 Functional cognate T cell recognition is mediated via the interaction of a T

147 dom model of recognition and suggests that T-cell recognition is MHC biased.

148 genic for the H-2 locus indicates that CD4 T-cell recognition is necessary for autoantibody productio

149 cessed antigens become available for naive B cell recognition is not clear.

150 n atlas-guided voxel classification process: cell recognition is realized by smoothly deforming the a

151 In a model in which T cell recognition is restricted to a single foreign antig

152 One very striking feature of T-cell recognition is the formation of an immunological sy

153 sponses, which limits the diversity of CD4 T cell recognition, is generally attributed to intracellul

154 Traditionally, cross-reactive T-cell recognition, known as molecular mimicry, as well as

155 oprotein (MojV-G) indicates a differing host-cell recognition mechanism.

156 le from dead cells, the phage selectivity in cell recognition minimizes false-negative and false-posi

157 ate that four adhesion molecules of the Irre cell recognition module (IRM) family play a redundant ro

158 potentially encodes 19,008 ectodomains of a cell recognition molecule of the immunoglobulin (Ig) sup

159 on of Clec9a, a CD103(+) DC-specific damaged cell-recognition molecule.

160 Cell recognition molecules are key regulators of neural

161 Neuroplastin cell recognition molecules have been implicated in synap

162 f-avoidance is mediated by a large family of cell recognition molecules of the immunoglobulin superfa

163 sophila Dscam1 gene encodes a vast number of cell recognition molecules through alternative splicing.

164 Here, we sought to identify candidate cell recognition molecules underlying this specificity.

165 of this interaction than those of other cell-cell recognition molecules will require CD4 mutants with

166 ce in Drosophila da sensory neurons requires cell-recognition molecules encoded by the Dscam locus.

167 s by increasing the mRNA level of one of the cell-recognition molecules, CED-7.

168 We find that innate apoptotic cell recognition occurs in a strikingly species-independ

169 autoimmunity that incorporates both T and B cell recognition of a myelin autoantigen.

170 ng infection and subsequent cross-reactive T-cell recognition of a similar self antigen provokes an i

171 imeric antigen receptors (CARs) direct tumor cell recognition of adoptively transferred T cells.

172 ll surface can modulate the sensitivity of T cell recognition of agonist peptide.

173 ment of lung injury induced by CD8+ effector cell recognition of alveolar Ag in vivo in the absence o

174 leukocyte antigen (HLA)-DR4 molecule, and T cell recognition of an epitope of Borrelia burgdorferi o

175 omyces dermatitidis confers protection via T cell recognition of an unknown but conserved antigen.

176 T-cell recognition of antigen aberrantly expressed on bile

177 Here we review recent advances in CD8(+) T cell recognition of antigen in lymphoid as well as in no

178 The perspective that naive B-cell recognition of antigen in the absence of T-cell hel

179 T cell recognition of antigen is a physical process that r

180 timulatory endogenous peptides can enhance T cell recognition of antigen, but MHCI- and MHCII-restric

181 T cell recognition of antigen-presenting cells depends on

182 e exploited this phenomenon to develop the T-cell recognition of APCs by protein transfer (TRAP) assa

183 If this advantage depends upon CD8 T-cell recognition of B57-restricted epitopes, mother-to-c

184 n-induced autoimmunity, is associated with T cell recognition of Borrelia burgdorferi outer surface p

185 usly unknown skin immune response based on T cell recognition of CD1a proteins and lipid neoantigen g

186 Tolerance required host natural killer T-cell recognition of CD1d on donor marrow cells.

187 orrelated with those to AdHu26, suggesting T-cell recognition of conserved epitopes.

188 To address this issue, we explored CD8+ T-cell recognition of epitopes derived from two other rela

189 Whereas T-cell recognition of foreign peptides is essential for pr

190 Adaptive immunity is initiated by T cell recognition of foreign peptides presented on dendri

191 findings help to clarify the mechanism of T-cell recognition of gp100 during melanoma responses and

192 designed to enhance MHC binding and hence T cell recognition of gp100 in HLA-DR4(+) melanoma patient

193 To address the structural basis for T cell recognition of H1 and H5, overlapping synthetic pep

194 ere we examined antigenic presentation and T-cell recognition of HA-1, a prototypic autosomal mHag de

195 R-TCR gene therapy, we analyzed transgenic T-cell recognition of hematopoietic stem cells (HSCs) and

196 Despite the ubiquitous nature of histones, T cell recognition of histone H4 peptide was specifically

197 rminants that can profoundly influence CD4 T cell recognition of HIV-1 gp120.

198 e process of membrane fusion, and blocking T-cell recognition of HLA class II-peptide complexes throu

199 It thus seems unlikely that classic T cell recognition of HLA-B27 is of primary importance in

200 ted, there was a specific defect in CD8(+) T cell recognition of HLA-E/Hsp60sp, which was associated

201 ology of GVHD is complex and involves immune cell recognition of host Ags as foreign.

202 mouse model that HLA-DRB1*04:02-restricted T cell recognition of human Dsg3 epitopes leads to the ind

203 specific patterns of interference with CD8 T cell recognition of infected cells.

204 ng vacuole, its presence is crucial for iNKT cell recognition of infected macrophages.

205 lterations in HA glycosylation may affect NK cell recognition of influenza virus-infected cells in ad

206 Natural killer (NK) cell recognition of influenza virus-infected cells invol

207 er, intravital imaging suggests that early B-cell recognition of large foreign antigens may be transi

208 T-cell recognition of ligands is polyspecific.

209 Here, we review recent data on NK cell recognition of melanoma at various stages of the di

210 o MHC class II molecules for direct CD4(+) T cell recognition of melanoma cells.

211 B cell recognition of membrane-bound antigens leads to the

212 nderstanding of the evolution of alphabeta T-cell recognition of MHC and MHC-like ligands.

213 NK cell recognition of MHC class I proteins is important de

214 Antiviral CD8(+) T cell recognition of MHC class I-peptide complexes on the

215 CD4(+) T cell recognition of MHC:peptide complexes in the context

216 B-cell recognition of microbial antigens may be limited by

217 T cell recognition of minor histocompatibility Ags (MiHA)

218 T cell recognition of minor histocompatibility antigens (m

219 T reactions are induced primarily by donor T-cell recognition of minor histocompatibility antigens (m

220 nsplantation is believed to be mediated by T-cell recognition of minor histocompatibility antigens on

221 The glycans do not affect CD4 T cell recognition of more distant epitopes and are not es

222 In this study, we investigate the basis of T cell recognition of myelin that governs the progression

223 Data on CD4 T cell recognition of N448 mutants combined with proteolys

224 Hence, N-glycans can determine CD4 T cell recognition of nearby gp120 epitopes by regulating

225 ctivity has been correlated with activated T-cell recognition of neoantigens, which are tumour-specif

226 different elements that may impair CD8(+) T cell recognition of neoantigens.

227 Our findings suggest that efficient CD4(+) T-cell recognition of neurotropic JCV variants is crucial

228 rmationally flexible, potentially reducing B-cell recognition of neutralizing antibody epitopes.

229 T cell recognition of peptide-MHC is highly specific and i

230 T cell recognition of peptide/allogeneic MHC complexes is

231 e immune responses have been attributed to T-cell recognition of peptides derived from the coupled ca

232 T-cell recognition of pMHC and the adhesion ligand interce

233 compatibility complex class II binding and T-cell recognition of polymorphic sequences were evaluated

234 We assessed T cell recognition of potential hepatitis C virus (HCV) va

235 p40(phox) in skewing epitope selection and T cell recognition of self Ag.

236 T-cell recognition of self and foreign peptide antigens pr

237 CD4(+) T cell recognition of self-GPI peptide/MHC class II comple

238 that reveal barriers preventing peripheral T cell recognition of self-peptide-MHC complexes, as well

239 When analyzing T-cell recognition of shared melanoma antigens before and

240 This suggests that gammadelta T cell recognition of T22 utilizes the conserved ligand-pr

241 gated alloantibody produced through naive Th cell recognition of target alloantigen but, crucially, b

242 when help was provided conventionally, by Th cell recognition of target alloantigen.

243 Thus, T cell recognition of the 70-kDa autoantigen by HLA-DR4-tr

244 that fetal intervention enhances maternal T cell recognition of the fetus and that T cell activation

245 rocess also may lead to increased maternal T cell recognition of the foreign conceptus and subsequent

246 ng presentation of viral Ags and cytotoxic T cell recognition of the infected cell.

247 Natural killer (NK) cell recognition of the nonclassical human leukocyte ant

248 wever, little is known about the nature of T cell recognition of the polysaccharide-MHCII complex or

249 to make protoxin expression dependent upon T-cell recognition of the prostate-specific membrane antig

250 phenotype analysis, allowing the study of T cell recognition of these cells.

251 elta (CDR3delta) loop mediating gammadelta T cell recognition of this molecule.

252 ived peptide ligands is essential for CD8+ T-cell recognition of Toxoplasma gondii infected cells.

253 ation of stress-ligands leads to impaired NK cell recognition of transformed cells.

254 However, T-cell recognition of tumor cells could be inhibited by tr

255 EphA2 monoclonal antibodies are coapplied, T-cell recognition of tumor cells is further increased ove

256 In this study, we have analyzed the NK cell recognition of tumor target cells derived from the

257 ent failures were correlated with impaired T-cell recognition of tumor targets.

258 -LPD, with failures ascribable to impaired T-cell recognition of tumor-associated viral antigens or t

259 tral tenet of cancer immunoediting is that T-cell recognition of tumour antigens drives the immunolog

260 afforded by the CLDC adjuvant required CD8 T-cell recognition of viral peptides presented by classica

261 In an effective immune response, CD8+ T cell recognition of virally derived Ag, bound to MHC cla

262 CD8(+) T cell recognition of virus-infected cells is characterist

263 by continual processing of graft parenchymal cells; recognition of donor haemopoietic fraction was no

264 d Ca(2+) mobilization (p = 0.016) and target cell recognition (p < 0.0001), with the latter independe

265 r role in key biological events such as cell-cell recognition, pathogenesis inflammation, and host pa

266 us and henipavirus parasitization of cell-to-cell recognition pathways for systemic virus disseminati

267 a unique example of pathogen mimicry of host-cell recognition pathways that drive virus capture and d

268 erent enough to mediate highly specific cell-cell recognition phenomena.

269 nder nonhematopoietic cells susceptible to T cell recognition, prevention of such circumstances favor

270 the speed of protein complexation during the cell recognition process.

271 The host cell recognition protein of the Escherichia coli bacteri

272 esion molecule (Dscam) genes encode neuronal cell recognition proteins of the immunoglobulin superfam

273 es probably affect T-cell and natural killer cell recognition, providing a sound basis for the joint

274 educed microglial surveillance and apoptotic cell recognition receptor expression and was not directl

275 However, upon target-cell recognition receptor surface levels were maintained

276 ures of ectodomain fragments comprising cell-cell recognition regions of mouse gamma-Pcdhs gammaA1, g

277 How viruses evade natural killer T cell recognition remains unclear.

278 CD8+ T-cell activation, delivery, and target cell recognition should yield greater clinical benefit.

279 udy characterized immune-dominant IgE- and T-cell-recognition sites of Phl p 5.

280 irectly affect and complicate the subsequent cell recognition step.

281 concerning the origins and evolution of cell-cell recognition systems involved in discrimination betw

282 Degenerate T-cell recognition that included T-cell responses to borre

283 Upon target cell recognition, the conformational state of LFA-1 chan

284 Thus, the sites of helper T-cell recognition, the dominant epitopes, are targets for

285 During target cell recognition, these cells receive both activating an

286 homophilic binding between cells, conferring cell recognition through a poorly understood mechanism.

287 efficiently blocks antigen-specific CD8(+) T cell recognition through HLA-A-, HLA-B-, and HLA-C-restr

288 c design aimed at focusing both B cell and T cell recognition to a single short glycan displayed at t

289 is currently unknown how DNGR-1 couples dead cell recognition to cross-priming.

290 residues of antigenic epitopes that weaken T cell recognition to the point that the immune system is

291 ts and will thus restrict antigen-specific T-cell recognition to the same population.

292 rs, a resurgence in discoveries underlying T-cell recognition, tumor immune evasion, and T-cell memor

293 culin (CRT), a protein involved in apoptotic cell recognition, was found to be a new PR3 partner coex

294 Comparing virus evolution with T-cell recognition, we demonstrated that: (i) resurgence w

295 lecules present phosphopeptides for CD4(+) T-cell recognition, we determined the crystal structure of

296 itutions that result in escape from CD8(+) T cell recognition were not observed, premature stop codon

297 NK cell effector capacity and during target cell recognition, where the engagement of inhibitory rec

298 ion program in NK cells that promotes target cell recognition while limiting cytokine-driven activati

299 has been implicated downstream of apoptotic cell recognition while Toll-like receptors are the proto

300 site of HLA-DP2, played a dominant role in T cell recognition with no contribution from the HLA-DP2 a