ライフサイエンスコーパス: cell recognition

1 tially enhance our understanding of CD4(+) T cell recognition.

2 , without altering peptide conformation or T cell recognition.

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

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

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

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

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

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

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

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

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

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

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

14 epitope where this modification abolished T cell recognition.

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

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

17 ent in HERV transcription without altering T cell recognition.

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

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

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

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

22 ting fundamental differences in gammadelta T cell recognition.

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

24 les to the immunological synapse upon target cell recognition.

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

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

27 polarized membrane structures involved in T cell recognition.

28 are directionally released following target cell recognition.

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

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

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

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

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

34 resented peptides contribute critically to T-cell recognition.

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

36 tial method to exogenously control events in cell recognition.

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

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

39 ophisticated strategies to circumvent immune cell recognition.

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

41 intraepitope sequence variability has upon T-cell recognition.

42 to differences in peptide presentation and T cell recognition.

43 A1 (BTN2A1) as essential to Vgamma9Vdelta2 T cell recognition.

44 periplasm of inhibitor cells prior to target-cell recognition.

45 e carrier protein were critical for helper T cell recognition.

46 pressed many receptors involved in apoptotic cell recognition.

47 FN-gamma production in the context of target cell recognition.

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

49 biquitin-binding receptor NBR1, precluding T cell recognition.

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

51 ie many biological phenomena, including cell-cell recognition.

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

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

54 igation, with the potential to broaden ML NK cell recognition against a variety of NK cell-resistant

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

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

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

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

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

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

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

62 mplexes (MHC) play a critical role in immune cell recognition and can trigger an antitumor immune res

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

64 Selective cell recognition and capture has recently attracted sign

65 hat tumor cell PIK3CA-AKT signaling limits T cell recognition and clearance of pancreatic cancer cell

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

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

68 nd computational methods for understanding T cell recognition and discuss the potential for improved

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

70 s often have extended fibers to mediate host cell recognition and entry, serving as promising targets

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

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

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

74 In this study, we have characterized the T cell recognition and immune responses in mice to two nat

75 Host cell recognition and internalization are mediated by tox

76 ycoprotein spike complex (GPC) mediates host cell recognition and is an important determinant of cros

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

78 urally presented on AML blasts and enables T cell recognition and killing of AML.

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

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

81 T cell recognition and MHC I surface expression under infl

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

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

84 uces ligand density on tumor cells for CAR T-cell recognition and releases a soluble BCMA (sBCMA) fra

85 Our results show that ancient mechanisms of cell recognition and selection are active in humans and

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

87 , 5, and 7 of Ad5 may be involved in Kupffer cell recognition and subsequent destruction.

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

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

90 een learnt about the mechanisms of apoptotic cell recognition and uptake, several key areas remain in

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

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

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

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

95 more neo-antigens, increasing chances for T cell recognition, and clinically correlates with better

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

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

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

99 sed individuals, suggesting cross-reactive T cell recognition between circulating "common cold" coron

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

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

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

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

104 y rendering them less vulnerable to CD8(+) T-cell recognition but at increased risk of NKG2A(+) NK ce

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

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

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

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

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

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

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

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

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

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

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

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

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

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

119 processes, including non-self-cell and self-cell recognition, cell signaling, cellular structure mai

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

121 ered a diverse library of multireceptor cell-cell recognition circuits by using synthetic Notch recep

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

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

124 e evasion can involve abrogation of leukemia cell recognition due to loss of HLA genes, immunosuppres

125 steine-rich peptides, implying roles in cell-cell recognition during double fertilization.

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

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

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

129 l processes, from protein quality control to cell recognition, energy storage, and cell wall formatio

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

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

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

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

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

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

136 The results provide new insights into the cell recognition function of Pcdh-gammaC4 in neurons and

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

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

139 Artificially controlled cell recognition has potentially far-reaching applicatio

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

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

142 PPE (Pro-Pro-Glu) proteins are targets for T-cell recognition in Mtb.

143 The principal of cell recognition in this sensor is based on applying an

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

145 ) has evolved elaborate ways to evade immune cell recognition, including downregulation of classical

146 in understanding the molecular basis of cell-cell recognition, including unique phenomena associated

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

162 suggest Kirrel3 functions as a synaptogenic, cell-recognition molecule, and this function is attenuat

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

164 Cell recognition molecules are key regulators of neural

165 by cell-type-specific programs with diverse cell recognition molecules expressed in different combin

166 Neuroplastin cell recognition molecules have been implicated in synap

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

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

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

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

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

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

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

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

175 The importance of antiviral CD8(+) T cell recognition of alternative reading frame (ARF)-deri

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

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 Killing depends on T cell recognition of antigens presented by class I major

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

184 ass the therapeutic requirement for CD8(+) T cell recognition of cancer cells and may provide a gener

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

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

187 trate the need to evaluate MHC binding and T cell recognition of Cys-containing peptides under condit

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

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

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

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

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

193 Here, we evaluate the potential for T cell recognition of HERV elements in myeloid malignancie

194 Our study thus uncovers T cell recognition of HERVs in myeloid malignancies, there

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

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

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

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

199 and that they can impact species-specific T-cell recognition of HSV.

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

201 ntly understood to focus on deflecting CD8 T cell recognition of infected cells by disrupting antigen

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

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

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

205 efficiently cross-presented whereas direct T cell recognition of leukemia cells intensifies exhaustio

206 T-cell recognition of ligands is polyspecific.

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

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

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

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

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

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

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

214 T cell recognition of minor histocompatibility Ags (MiHA)

215 T cell recognition of minor histocompatibility antigens (m

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

217 t- versus-host disease (GVHD) due to human T-cell recognition of murine major histocompatibility comp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

234 T cell recognition of specific antigens mediates protectio

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

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

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

238 chanisms play a crucial role in subsequent T-cell recognition of target cells and the specificity of

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

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

241 5 transgenic and NOD mice, we investigated T-cell recognition of the HIP2.5 epitope, which is a fusio

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

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

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

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

246 luded by self-N-glycan shielding, limiting B cell recognition of the underlying polypeptide surface.

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

248 To determine if T cell recognition of these ECM components played a role i

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

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

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

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

253 bone marrow of MM patients to inhibit CAR T-cell recognition of tumor cells, and potentially limit e

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

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

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

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

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

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

260 Unlike mucosal-associated invariant T cells, recognition of target cells by the TCR was indepe

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

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

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

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

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

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

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

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

269 of RIG-I on tumor antigen presentation and T cell recognition proposes innate immunoreceptor targetin

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

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

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

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

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

275 of such HLA variation on natural killer (NK) cell recognition remains unclear.

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

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

278 irectly affect and complicate the subsequent cell recognition step.

279 Synapse formation is comprised of target cell recognition, synapse assembly, and synapse maintena

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

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

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

283 o viral evasion of natural killer cells or T cell recognition, the evasion of antibody-mediated effec

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

285 idal invasive disease in Africa, escape MAIT cell recognition through overexpression of ribB This bac

286 and can be enriched with functions including cell recognition, tissue penetration, and imaging.

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

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

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

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

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

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

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

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

295 hor positions often significantly enhanced T cell recognition, whereas substitutions at non-MHC ancho

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

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

298 e cell surface in order to evade cytotoxic-T-cell recognition, while leaving HLA-C and HLA-E molecule

299 reate a simple mathematical model coupling T-cell recognition with an evolving cancer population that

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