ライフサイエンスコーパス: TCR

1 TCR expression by T reg cells is continuously required f

2 TCR gene transfer installed BOB1 specificity and reactiv

3 TCR occurred where the elongation complexes were blocked

4 TCR repertoire analysis revealed that CMV tet(low) and t

5 TCR signaling pathways cooperate to activate the inducib

6 TCR-mediated ERK phosphorylation is significantly reduce

7 TCR-transduced HLA-A2(+) T cells efficiently killed HLA-

8 TCR-transduced T cells efficiently lysed primary B-cell

9 The T-cell product includes HA-1 TCR CD4(+) T cells to augment the persistence and functi

10 ent the persistence and function of the HA-1 TCR CD8(+) T cells and includes only memory T cells; nai

11 ety switch to enable elimination of the HA-1 TCR T cells in case of toxicity; and (4) a CD34-CD20 epi

12 ell product and tracking of transferred HA-1 TCR T cells.

13 y mediated by native TCR coexpressed by HA-1 TCR T cells.

14 tural analysis of a prototypical Vbeta8.1(+) TCR-H-2D(b)-GAP5040-48 ternary complex revealed that ger

15 T cells preferentially expressed TRBV4-1(+) TCRs.

16 erapeutic transgene with 4 components: (1) a TCR specific for the hematopoietic-restricted, leukemia-

17 We addressed this problem by developing a TCR-transgenic (Tg) mouse with CD4 T cells that respond

18 ILC2s lack a TCR and respond instead to locally produced cytokines su

19 ging evidence that the binding strength of a TCR for self-peptide presented by MHC (self-pMHC) impact

20 cells, retrovirally transduced with MAGE-A3 TCR plus systemic high-dose IL-2.

21 were observed in lesional vs nonlesional AD, TCR repertoire diversity was similar in lesional and non

22 Two high-affinity TCRs (KD values of approximately 50 and 250 nM) against

23 l responses mediated by shared high-affinity TCRs.

24 is thought to be induced by cytokines after TCR signaling has ceased, although this remains controve

25 n the paradox of specificity in alloreactive TCRs and have implications for their use in immunotherap

26 he existence of highly specific alloreactive TCRs has led to their use as immunotherapeutics that can

27 Splenic CD3(+) alphabeta TCR(+) cells and Foxp3(+) T regulatory cells were presen

28 PR/Cas9 knockout of the endogenous alphabeta TCR resulted in more efficient redirection of CD4(+) and

29 negative T (DNT) cells expressing alphabeta TCR but lacking CD4/CD8 coreceptors play protective as w

30 ss four strains of mice that display altered TCR signal strength in DN cells, which correlates with a

31 r, specific T cell receptor-Vbeta5.(1/2) and TCR-Vbeta11 clonal deletion was detected in host T cells

32 ceptors, T cell receptor (TCR) assembly, and TCR-mediated signaling.

33 lation, retaining proliferative capacity and TCR sensitivity, displaying increased cytotoxic markers

34 cytokine withdrawal induced death (CWID) and TCR restimulation induced cell death (RICD).

35 ion of force application between pre-TCR and TCR mechanosensors, impacting signal initiation.

36 cytoskeleton, suggesting selection for avid TCR microclusters.

37 membrane as a single functional complex, (b) TCR membrane localization and dynamics at the plasma mem

38 BCR/TCR repertoire analysis did not show significant differe

39 ve an accumulation of CD4(+) T cells bearing TCRs using TRAV12-1 (formerly AV2S3).

40 transduction, the NK cell line NK-92 became TCR positive and reacted against pMHC target.

41 port direct evidence for coevolution between TCR and MHC genes, helping to explain how MHC compatibil

42 cretion observed at high Ag density for both TCRs and CARs suggested a role for negative regulators i

43 we further monitored LAT phosphorylation by TCR zeta chain-recruited ZAP-70, which suggests a weakly

44 membrane and in endosomal compartments, (c) TCR signal transduction leading to T cell activation, an

45 ively featureless peptide epitope (canonical TCRs).

46 other TRAV/TRBV combinations (non-canonical TCRs).

47 ransfer of mycobacteria-specific (P25 CD4(+) TCR transgenic) wild-type spleen cells into sanroqueRag1

48 NOD mice expressing the transgenic NY8.3 CD8 TCR.

49 maintaining the conformation of the NKT cell TCR.

50 An induced switch of the T reg cell TCR repertoire to a random repertoire also preserved, al

51 Unsupervised clustering and single-cell TCR locus reconstruction identified three cell populatio

52 itiated by adjacent ligand-expressing cells, TCR stimulation is sufficient to induce Notch signaling.

53 In most T cells, TCRs are composed of alphabeta subunits displaying immun

54 nteractions by paratope hotspots) to cluster TCRs with a high probability of sharing specificity owin

55 d safer and more effective than conventional TCR gene transfer.

56 uction leading to T cell activation, and (d) TCR degradation.

57 ve/negative selection threshold by dampening TCR signaling.

58 Four TIL-derived TCRs exhibited strong selection for peptides presented i

59 MV tet(low) and tet(high) CTLs use different TCRs.

60 In this review, we discuss TCR specificity, emphasizing results that have emerged f

61 Regulatory T cells (Tregs) use a distinct TCR repertoire and are more self-reactive compared with

62 r, it remains unknown to what degree diverse TCR-mediated interactions with cognate self-antigens are

63 ded greater thymic output and a more diverse TCR repertoire.

64 How the diverse TCRs interact with a multitude of MHC molecules is unres

65 Despite this potential diversity, TCRs from T cells that recognize the same pMHC epitope o

66 ata support a novel hypothesis by which dual TCR expression can promote autoimmunity by limiting agon

67 on across the TCR complex is involved during TCR triggering, and that the T cell might use its force-

68 molecular evidence for the germline encoded TCR bias for MHC, and for the coreceptor sequestration m

69 oxicity and near-complete lack of endogenous TCR Vbeta expression, consistent with allelic exclusion

70 t is based on the knockout of the endogenous TCR alpha and beta genes, followed by the introduction o

71 h, based on the disruption of the endogenous TCR alpha chain only, followed by the transfer of genes

72 apeutic TCR will compete with the endogenous TCR for the signalling proteins and carries the potentia

73 s, we designed a system where the endogenous TCR-beta is knocked out from the recipient cells using c

74 The molecular mechanism of eukaryotic TCR initiation remains unclear, with several long-standi

75 d Pol II during the initiation of eukaryotic TCR.

76 We found extensive TCR clonotype sharing in Ag-activated cells, especially

77 available tool that can efficiently extract TCR sequence information from short-read scRNA-seq libra

78 he local kinase-phosphatase balance to favor TCR phosphorylation.

79 e we propose a novel and clinically feasible TCR "single editing" (SE) approach, based on the disrupt

80 Neonates with cCMV had fewer TCR excision circles in their blood than non-infected co

81 Despite the lack of focused TCR-peptide binding, the ILA1 T-cell clone was still cro

82 Following TCR-driven stimulation in vitro, CXCR5+ but not CXCR5- C

83 that OX40L/OX40 interaction is critical for TCR-independent selective proliferation of Foxp3(+) Treg

84 Although PKC- is dispensable for TCR-independent Treg proliferation per se, it is essenti

85 However, current methods for TCR inference from scRNA-seq are limited in their sensit

86 inputs may alter the minimal requirement for TCR signaling in CD8 T cells.

87 Here we define the minimal requirements for TCR antigen specificity, through an analysis of TCR sequ

88 ome degree of conserved binding topology for TCR-peptide MHC complexes.

89 lineage scrambling that is disconnected from TCR restriction by MHC.

90 High-throughput sequencing data from TCRs and Igs can provide valuable insights into the adap

91 uction with a pan-cancer-reactive gammadelta TCR used in conjunction with CRISPR/Cas9 knockout of the

92 to identify antigenic ligands of gammadelta TCRs, annexin A2 was identified as the direct ligand of

93 , and gammadelta T cell receptor [gammadelta-TCR]) and cytokines examined (interleukin 2 [IL-2], IL-4

94 e for meromycolate chains in influencing GEM-TCR activity.

95 rations modulate functional responses by GEM-TCRs.

96 d T-cell clonotypes from total blood and gut TCR repertoires in an unbiased manner using immunosequen

97 The HCV1406 TCR was cloned from T cells that expanded when a hepatit

98 he activity of T cells, normal heterodimeric TCRs or synthetic chimeric Ag receptors (CARs).

99 on bone marrow chimeras and show that higher TCR avidity correlates with higher PLZF and reduced T-be

100 To examine how TCR specificity determines iNKT function, we used somati

101 l and physical mechanisms that influence how TCRs bind peptides and MHC proteins.

102 here is a large amount of information on how TCRs engage with MHC-Ia and MHC-II, our understanding of

103 However, TCRs cloned from an effective and one of two ineffective

104 ll RNA sequencing procedures for identifying TCR clonotypes and transcript phenotypes in individual T

105 by polymerase chain reaction analysis of Ig/TCR gene rearrangements, and patients were assigned to a

106 In TCR-transgenic T cells, c-MPL activation enhances antitu

107 the expression of several genes involved in TCR signaling and cell activation, confirming its role a

108 possible role for an allosteric mechanism in TCR signalling.

109 conclude that UvrD and ppGpp play no role in TCR in E. coli.

110 nce of finely regulated endosomal traffic in TCR signal transduction and T cell activation leading to

111 elopment was favoured in mice with increased TCR signal strength in DN cells.

112 Stiffness also increases TCR-induced immune system, metabolism and cell-cycle-rel

113 or homotropic allostery, in which individual TCRs could positively cooperate and thus enhance the sen

114 sRNA) was required and sufficient to inhibit TCR signaling.

115 Clonotypic analysis of the two iNK TCR types with a single amino acid substitution revealed

116 ructure of, and Ag recognition by, human iNK TCRs.

117 to TCR-mediated stimulation and internalize TCRs mediates detection of ligand density or affinity, c

118 yed proliferation in cells with internalized TCRs.

119 Temporal changes in intratumoral TCR repertoire revealed expansion of T cell clones in th

120 lycolipids by virtue of their semi-invariant TCR, which triggers NKT cell lineage commitment and matu

121 le of being recognized by both the invariant TCR and PRRs and inducing immune responses.

122 y, Vdelta2(+) T cells express semi-invariant TCRs, which are present at birth and shared between indi

123 ggest that the immune system distributes its TCR sequences unevenly, attending to specific foci of re

124 In resting T cells cholesterol keeps TCRs in the resting conformation that otherwise would be

125 tly capture lipid antigens within CD1d-lipid-TCR complexes, while excluding CD1d bound to nonantigeni

126 lectrical conductivity of 94.66 IACS and low TCR of 1,451 10(-6) degrees C(-1) are achieved in the 5

127 f regulatory T (Treg) cells results from low TCR signal strength and low Akt/mTOR signaling.

128 unotherapy and related efforts to manipulate TCR recognition, as well as alloreactivity in general.

129 ter of which is incorporated into the mature TCR in subsequent developmental progression.

130 Mechanistically, TCR stimulation induced rapid sodium influx in Napa(hyh/

131 Expression of this near-monoclonal TCR in a Jurkat cell-transfection system validated fine

132 ential for alloreactivity mediated by native TCR coexpressed by HA-1 TCR T cells.

133 f mixed dimer formation giving rise to a new TCR with unpredictable specificity.

134 The NS3 TCR induced a rapid expression of apoptotic signaling pa

135 of embryonic gene clusters, whereas the NS5A TCR activation induced extended proliferative and metabo

136 s were accompanied by elevated activation of TCR and Toll-like receptor signaling-related proteins.

137 ession program associated with activation of TCR signaling is closely related to specific chromatin l

138 antigen specificity, through an analysis of TCR sequences using a panel of peptide and major histoco

139 nhibitory molecules and other attenuators of TCR signaling, with a focus on their contribution to LIP

140 The contribution of TCR clonotype to inhibitory potency was investigated by

141 and has implications for the development of TCR-based therapeutics.

142 and effectively increases the efficiency of TCR scanning for antigen before the T cell is committed

143 erved residues driving essential elements of TCR recognition.

144 is in mediating proximal signaling events of TCR and CD28 engagement in T cells.

145 we review how the expression and function of TCR complexes are orchestrated by several fine-tuned cel

146 n requires an invariant minimal intensity of TCR signaling that is not modulated by IL-2, thereby res

147 monstrate loss of LAT expression and lack of TCR signaling restoration in LAT-deficient cell lines re

148 (NKCL) did not express significant levels of TCR Vbeta or Vgamma genes.

149 A-seq) can allow simultaneous measurement of TCR sequence and global transcriptional profile from sin

150 nt work on assessment of the preselection of TCR repertoire, molecular evidence for the germline enco

151 rate, exhaustive, and economical recovery of TCR sequences from such populations therefore remains a

152 rotein expression can serve as a reporter of TCR and BCR specific signaling in human PBMCs.

153 f accurate and comprehensive repositories of TCR and Ig alleles.

154 omplexes do not engage in multiple rounds of TCR with successive lesions.

155 outcomes in response to various strengths of TCR signaling.

156 rged from structural and physical studies of TCR binding.

157 The Suppressor of TCR signaling proteins (Sts-1 and Sts-2) are two homolog

158 with MHC-Ia and MHC-II, our understanding of TCR/MHC-Ib interactions is very limited.

159 The composition of TCRs targeting each epitope varied considerably in stabi

160 nsgenic TCR is the preexisting expression of TCRs in the recipient cells.

161 s with the diversified target recognition of TCRs.

162 as the main brake but is likely dependent on TCR signals and CD80/CD86.

163 studied the effect of YFV, DENV, and ZKV on TCR signaling.

164 M sequence diversity is required for optimal TCR signal transduction and subsequent T cell maturation

165 ever, crossing the W131A mutant mice to OTII TCR transgenic mice resulted in increased negative selec

166 ither CD4(+) cells from ROCK2-sufficient OVA TCR transgenic (OT-II) mice or saline i.v. 48 h before c

167 ype representing more than 2% of the overall TCR population.

168 In particular, TCR-Vgamma4(+) chain-expressing CD122(-)IL-23R(-) gammad

169 sequences of peptide targets for pathogenic TCRs of unknown specificity.

170 s triggered by the first few individual pMHC:TCR binding events and effectively increases the efficie

171 By resolving every single pMHC:TCR interaction it is evident that this cooperativity is

172 n peripheral T cells within a few hours post-TCR stimulation and is required for optimal T cell activ

173 e direction of force application between pre-TCR and TCR mechanosensors, impacting signal initiation.

174 ked heterodimer composed of an invariant pre-TCR alpha (pTalpha) subunit and a variable beta subunit,

175 The pre-TCR is a disulfide-linked heterodimer composed of an inv

176 present in all individuals alongside private TCR repertoires specific to each individual.

177 ects, indicating a predominance of "private" TCR specificities.

178 -signalling tail and named the final product TCR-CAR.

179 ressed TCR response at the level of proximal TCR signaling (activation/phosphorylation of PLCgamma, E

180 To determine how TRAF3 promotes proximal TCR signaling, we studied TRAF3-deficient mouse and huma

181 (TCR) usage, with initial evidence of public TCR sequences that are shared by individuals with T1D.

182 ic T cell responses are controlled by public TCRs present in all individuals alongside private TCR re

183 ll clones displayed significantly more rapid TCR signal propagation, more efficient initial lytic gra

184 in their use of the T cell antigen receptor (TCR) alpha-chain variable region (Valpha) and beta-chain

185 raction between the T cell antigen receptor (TCR) expressed by natural killer T cells (NKT cells) and

186 y activation of the T cell antigen receptor (TCR) in a pathway involving calcium and activation of th

187 as recruited to the T cell antigen receptor (TCR) signaling complex, where it reversed inhibitory pho

188 T cell antigen receptor (TCR) signaling in the thymus initiates positive selectio

189 g downstream of the T cell antigen receptor (TCR), but the mechanistic underpinnings of THEMIS functi

190 pon ligation of the T-cell antigen receptor (TCR), the TCR associates with and transactivates CXCR4 v

191 ion mediated by the T cell antigen receptor (TCR).

192 icacy, including suboptimal T-cell receptor (TCR) activation and an immunosuppressive tumor environme

193 tion, complementary DNA for T cell receptor (TCR) alpha- and beta-chains were cloned into a retrovira

194 iated with Notch receptors, T cell receptor (TCR) assembly, and TCR-mediated signaling.

195 lity class II molecules and T-cell receptor (TCR) beta-chain variable domains (Vbetas).

196 fine the role of individual T-cell receptor (TCR) clonotypes in differential antiviral CD8(+) T-cell

197 o express a cancer-specific T-cell receptor (TCR) has shown significant therapeutic potential for bot

198 Signaling through the T-cell receptor (TCR) is critical for T-cell development and function.

199 non-MHC-linked Ir gene in a T cell receptor (TCR) locus that was required for CD8(+) T cell responses

200 rus-specific (HBV-specific) T cell receptor (TCR) may supplement HBV-specific immune responses in chr

201 Defects in T cell receptor (TCR) repertoire are proposed to predispose to autoimmuni

202 T-cell receptor (TCR) repertoires directed to some immunodominant gluten

203 Diversity of T cell receptor (TCR) repertoires, generated by somatic DNA rearrangement

204 By analyzing T-cell receptor (TCR) sequence repertoires taken from the blood and thymu

205 Strong T cell receptor (TCR) signaling largely induces cell death during thymocy

206 Here we examined how T cell receptor (TCR) signals establish and arbitrate Bcl6-Blimp-1 counte

207 T-cell receptor (TCR) triggering and subsequent T-cell activation are ess

208 oire of target antigens and T cell receptor (TCR) usage, with initial evidence of public TCR sequence

209 onses to SEB can occur in a T cell receptor (TCR) Vbeta-specific manner but are largely contributed b

210 ice expressing a transgenic T cell receptor (TCR) with specificity for ovalbumin (OVA) on CD4(+)-T ce

211 nse to signals engaging the T cell receptor (TCR), express high levels of the immunosuppressive cytok

212 n, leading to a decrease in T cell receptor (TCR)-dependent intracellular Ca(2+) response.

213 y linking antigen receptor (T cell receptor, TCR) signals to downstream pathways.

214 ls activated through their T cell receptors (TCR) by protein antigens orchestrate immune responses.

215 ns recognized by alphabeta T-cell receptors (TCRs) drive the activation of invariant natural killer T

216 meric antigen receptors or T-cell receptors (TCRs) has demonstrated clinical efficacy.

217 x (MHC) class I-restricted T-cell receptors (TCRs) or chimeric antigen receptors to genetically modif

218 selection, T cells bearing T cell receptors (TCRs) with high affinity for self-antigen are eliminated

219 Remarkably, TCR stimulation in the presence of monensin phenocopied

220 Eukaryotic transcription-coupled repair (TCR) is an important and well-conserved sub-pathway of n

221 hown that this transcription-coupled repair (TCR) is mediated by the Mfd translocase.

222 selection and inhibitory receptors restrain TCR signaling to enforce both central and peripheral tol

223 lass II-restricted, HLA-DPB1*0401-restricted TCR that recognized the cancer germline antigen, MAGE-A3

224 o promote function of the class I-restricted TCR in CD4(+) T cells; (3) an inducible caspase 9 safety

225 ilar to the sensitivity of T cell signaling, TCR-pMHC interactions with Kds of </=15 microM were need

226 Overall, single TCR gene editing represents a clinically feasible approa

227 We have fused a soluble TCR construct to a CAR-signalling tail and named the fin

228 pth characterization of ten epitope-specific TCR repertoires of CD8(+) T cells from mice and humans,

229 4(+) T(Pam3) cells encoding the OVA-specific TCR OT2, when transferred into mice bearing established

230 We demonstrated with chicken OVA-specific TCR-transgenic mice that the same tolerizing protocol (C

231 llowed by the introduction of tumor-specific TCR genes, and that proved safer and more effective than

232 nsfer of genes encoding for a tumor-specific TCR.

233 However, approximately 40% of GIL-specific TCRs express a wide variety of other TRAV/TRBV combinati

234 Most GIL-specific TCRs utilize alpha/beta chain pairs encoded by the TRAV2

235 astic leukemia blasts compared with standard TCR transfer.

236 induce expression of FOXP3 after suboptimal TCR stimulation.

237 ecific repertoire was largely devoid of such TCRs.

238 It is implicated as suppressed TCR-signaling cascades, reduced alterations in activatio

239 ls from CCI patients exhibited no suppressed TCR response at the level of proximal TCR signaling (act

240 ng that Themis might be important to sustain TCR signals during these key developmental processes.

241 We conclude that TCR/ITK signalling through the Ras/IRF4 pathway is requi

242 In addition, we demonstrate that TCR-CAR redirection was not restricted to T cells.

243 Our results suggest that TCR transfer combined with genome editing could lead to

244 Moreover, the observation that TCRs assemble into nanoclusters might allow for homotrop

245 The TCR repertoire of Gag293-specific CD4(+) T cells proved

246 ave shown that force transduction across the TCR complex is involved during TCR triggering, and that

247 nalysis of the lipid antigens trapped at the TCR-CD1d interface.

248 comprehensive interface exchange between the TCR alpha/beta constant domain pair and the IgG1 CH3 hom

249 1d is distinct from interactions between the TCR and major histocompatibility complex (MHC).

250 In the resting conformation, the TCR is not phosphorylated and is inactive.

251 e potential role of Tregs in controlling the TCR repertoire breadth to a non-self-antigen, a TCRbeta

252 We developed the TCR gene editing technology that is based on the knockou

253 and unique, sexually dimorphic motifs in the TCR hypervariable regions in the SjS(S) mice.

254 sidering the ability of CD31 to modulate the TCR's activation threshold via the recruitment of tyrosi

255 aptor signaling molecule that is part of the TCR complex and essential for T-cell development, as dem

256 se processes, the binding specificity of the TCR is a key component.

257 detects selection for proper folding of the TCR receptor protein.

258 ection influences the self-reactivity of the TCR repertoire during ontogeny.

259 An expansion of the TCR repertoire was observed for nine Vbeta subtypes, whe

260 We find that the strength of the TCR signal results in differential Akt enzymatic activit

261 3 helix at the membrane-proximal face of the TCR, a region implicated in interactions with the CD3 co

262 duction in activating phosphorylation of the TCR-associated kinase Lck.

263 urther analyses showed that recycling of the TCR-CD3 complex was impaired, leading to increased lysos

264 e that MHC restriction can be imposed on the TCR repertoire during thymic development, and it has bee

265 ell activation because it phosphorylates the TCR complex and the Zap70 kinase.

266 on of the T-cell antigen receptor (TCR), the TCR associates with and transactivates CXCR4 via phospho

267 We found that the TCR-signal-induced transcription factor Irf4 is essentia

268 face of MHC-bound peptides accessible to the TCR contains sufficient structural information to enable

269 Hence, an introduced therapeutic TCR will compete with the endogenous TCR for the signall

270 This TCR-mediated feedback is a global effect on the intercel

271 and Ad5 maximized antitumor efficacy through TCR avidity enhancement, it produced no autoimmunity, re

272 matic mutations that recover CD247, and thus TCR expression, in a newly identified CD247-deficient pa

273 Three of the TIL TCRs were specific for non-mutated self-antigens, two of

274 s is a consequence of factors in addition to TCR sequence that modulate functionality and contribute

275 In addition to TCR signaling, costimulatory pathways are involved in T

276 udy, we hypothesized that MP cells, naive to TCR stimulation, constitute a transient population that

277 al is acquired in the human thymus, prior to TCR signaling, but rather than describing end-stage diff

278 l populations in their ability to respond to TCR-mediated stimulation and internalize TCRs mediates d

279 l up-regulation of miR-34c-5p in response to TCR stimulation in naive CD4 T cells.

280 ve previously shown that the resulting tonic TCR signaling also influences their fate upon activation

281 sue of transducing T cells with a transgenic TCR is the preexisting expression of TCRs in the recipie

282 airing between the endogenous and transgenic TCRs, may harbor autoreactive specificities.

283 atop HLA-E when compared with the TRBV14(+) TCR-HLA-E ternary complex.

284 We report the structures of a TRBV9(+) TCR in complex with the HLA-E molecule presenting the tw

285 Our data revealed that the TRBV9(+) TCR adopts a different docking mode and molecular footpr

286 After a primary transfer, the donor Treg TCR repertoire was substantially narrowed, yet the recip

287 Of Bim and Nur77, two TCR-induced proteins with proapoptotic function, Bim has

288 gammadelta T cells and their activation upon TCR-mediated or cytokine-mediated stimulation.

289 rane cholesterol and sphingomyelin, and upon TCR triggering they exhibit altered morphology and polar

290 ression in human primary CD4(+) T cells upon TCR stimulation, inhibiting NF-kappaB signaling via its

291 ammadelta T cells expressing Vgamma2 Vdelta2 TCRs.

292 ified as the direct ligand of Vgamma8Vdelta3 TCR, and was found to be expressed on tumor cells upon t

293 inds the same residues on the Vgamma9Vdelta2 TCR as the Vgamma9Vdelta2 T cell Ag-presenting transmemb

294 EGFR expression on Th2 cells was TCR-signaling dependent, and therefore, our data reveal

295 h during thymocyte development, whereas weak TCR signals induce positive selection.

296 A major pathway that was compromised, when TCR signaling was suboptimal, was linked to ribosome bio

297 1% of the total proteins expressed, whereas TCRs have the advantage of targeting any peptide resulti

298 ATOs initiated with TCR-engineered HSPCs produced T cells with antigen-speci

299 nserved public sequences were central within TCR sequence-similarity networks.

300 compatibility and bias can be encoded within TCRs.