ライフサイエンスコーパス: TCR

1 TCR analysis revealed a diverse repertoire in SAT of ove

2 TCR repertoire analysis further suggests a role for spec

3 TCR stimulation of T-PLL cells evoked higher-than-normal

4 TCR transfer to T cells of patients enabled killing of a

5 d loses efficiency and accuracy when >10,000 TCRs are analyzed.

6 Here, we describe how a TRAV12-2(+) TCR (termed D462-E4) recognizes an MR1-antigen complex.

7 , the molecular basis of how such TRAV1-2(-) TCRs interact with MR1-antigen complexes remains unclear

8 This cell subset is activated in a TCR-dependent and MHC-unrestricted fashion by so-called

9 Using a TCR-transgenic Nur77-GFP reporter to distinguish "antige

10 LA Trp-167 side-chain conformation abrogated TCR binding, indicating that this indirect binding mecha

11 We detect abundant TCR sequences even after exclusion of methodological con

12 TCR Vgamma9Vdelta2 cells, the most abundant TCR gammadelta cell population in peripheral blood.

13 Additionally, TCR signal strength is able to regulate CD8(+) T cell ef

14 ing ~2x10(8) sequence-diverse peptides, AGA1 TCR specificity was mapped to a central peptide di-motif

15 , HIV-specific, CD8 T cell-derived TCR (AGA1 TCR) using MHC class I yeast display technology.

16 We identified alphabeta TCR sequences that were unique to either tTreg or Tconv

17 In addition, a proportion of alphabeta TCR sequences expressed by tTreg were also found in Tcon

18 the great majority of these shared alphabeta TCR sequences as characteristic of Tconv and not tTreg.

19 throughput approach to profile the alphabeta TCR repertoires of human naive and effector/memory CD4(+

20 Also recognised by the alphabeta-TCR of mucosal associated invariant T cells, MR1 interac

21 well as B cell and T cell receptors (BCR and TCR).

22 libraries, combined with T cell cloning and TCR sequencing, to dissect the human naive and memory CD

23 e regions and allow single cell level Ig and TCR repertoire analysis.

24 uture studies to fully capture rhesus Ig and TCR repertoire diversity and is applicable for improving

25 The diversity of Ig and TCR repertoires is a focal point of immunological studie

26 nnotation and quantification of their Ig and TCR repertoires.

27 the entire variable regions of rhesus Ig and TCR transcripts.

28 Analysis of CD4(+) T-cell subsets and TCR variable beta classes from healthy donors showed pol

29 ted EBV-LMP2-specific T-cell populations and TCRs, which can potentially be used in future TCR gene-t

30 ctivation is modulated by mechanisms such as TCR endocytosis, which is thought to terminate TCR signa

31 e IL-2, IL-4, and IL-7 responses, as well as TCR-mediated activation and proliferation, of CD4+ T cel

32 rried out NMR analysis of a human autoimmune TCR (MS2-3C8) that recognizes a self-peptide from myelin

33 red by cross-recognition of the autoreactive TCR with foreign peptides.

34 g a lifetime are recognized by the available TCR repertoire.

35 provide a safer alternative to high-avidity, TCR-engineered T cells, as IL-12-primed, low-avidity T c

36 The structures of A11 and B12A TCR are nearly identical to those of MHC-restricted TCR,

37 ffective in patients with a diverse baseline TCR repertoire and an associated expansion of singleton

38 position or genetic diversity of HLA and BCR/TCR loci.

39 edge of the genetic diversity at HLA and BCR/TCR loci.

40 short-read RNA-seq-based HLA typing and BCR/TCR repertoire sequencing (AIRR-seq) currently rely on o

41 domain also exhibits a high tendency to bind TCRs.

42 n exhibits a high-affinity motif for binding TCRs, and may form a ternary complex with MHCII.

43 nhibition of Src family kinases (SFK) blocks TCR but not BCR signaling.

44 Using single-cell and bulk TCR sequencing and structural affinity analyses of cytom

45 onstrate that tumor lymphocytes, assessed by TCR repertoire quantification based on a sequencing meth

46 V-2-specific T cell responses were driven by TCR clusters shared between patients with a characterist

47 rchestrated by signaling events initiated by TCR recognition of peptide Ag in concert with signals fr

48 r rules that underpin antigen recognition by TCRs and have important implications for the development

49 ficient identification of clinical candidate TCRs is complicated by the size and complexity of T cell

50 lished chronic LCMV infection.IMPORTANCE CD8 TCR repertoires responding to chronic viral infections (

51 ment of an exhausted antigen-specific CD8(+) TCR repertoire under checkpoint inhibitor treatment.

52 , by using several strategies of single-cell TCR sequencing in a third cohort, we discovered clonally

53 monstrate that the virus-specific CD8 T cell TCR repertoire is broad and remains stable after acute L

54 ed T cell receptor (TCR)-transgenic T cells (TCR-T cells) are not restricted by cell surface expressi

55 ly determined cryoEM structure of a complete TCR-CD3 complex.

56 due at position 16 is necessary to constrain TCR reactivity for InsB(9-23) by both limiting the devel

57 Together these regulators dampen TCR-proximal signaling and help avoid any subsequent per

58 generation and in vivo monitoring of defined TCR repertoires, we found that the immunodominance of hi

59 When equipped with epitope-defined TCRs or chimeric antigen receptors, these Lckpr-hTCL1Atg

60 a 'public', HIV-specific, CD8 T cell-derived TCR (AGA1 TCR) using MHC class I yeast display technolog

61 crystal structure of two CeD patient-derived TCR in complex with HLA-DQ2.2 and DQ2.2-glut-L1 (PFSEQEQ

62 We determined TCR-peptide-HLA crystal structures and, using a single-c

63 Millions of naive T cells with different TCRs may interact with a peptide-MHC ligand, but very fe

64 There is some evidence that two distinct TCR-defined IL-17-producing gammadelta T cell subsets al

65 T cells of allergic and non allergic donors, TCRs expressing the alpha-chain segment TRAV9-2 or a his

66 ll remodeling by HIV includes downregulating TCR complex components and modulating chemokine receptor

67 the TCR-CD3 complex, for dynamically-driven TCR allostery, and for pMHC-induced structural changes i

68 The molecular rules driving TCR cross-reactivity are poorly understood and, conseque

69 reviously unappreciated contribution of dual TCR cells to the immune repertoire and highlight their p

70 revealing that ~16% of T cells express dual TCRs, notably higher than prior estimates.

71 The D462-E4 TCR footprint on MR1 contrasted that of the TRAV1-2(+) a

72 However, coexpression of endogenous TCR plus CAR led to superior persistence of T cells and

73 KO of the endogenous TCR in T cells strongly ablated alloreactivity in compar

74 was optimized by knocking out the endogenous TCR of primary T cells (DeltaTCR) using CRISPR-Cas9 tech

75 er cell expression and processing, enhancing TCR-T effector function, trafficking, expansion, persist

76 ith severe hyperinflammatory disease exhibit TCR skewing consistent with superantigen activation.

77 embrane, and only around 100 individual Fab':TCR interactions are necessary to stimulate early T cell

78 s review, we examine the molecular basis for TCR activation in light of the recently determined cryoE

79 emonstrated a clear prognosis value both for TCR abundance (HR = 0.39, 95% CI 0.26-0.57, P = 1.3e-06)

80 over, LAT, an essential scaffold protein for TCR signaling, is not required for microcluster formatio

81 Tregs exhibited an increased requirement for TCR engagement for survival.

82 e second harnesses an antibody-based format (TCR-mimic antibodies).

83 gene knockout mice lacking either functional TCRs or MHC class II molecules on B cells, the liposomal

84 CRs, which can potentially be used in future TCR gene-therapy to treat EBV-associated latency type II

85 In summary, we show how dynamic gammadelta TCR repertoires develop directly after birth and present

86 rget cells, via a membrane-linked gammadelta TCR recognizing intact non-MHC proteins on the opposing

87 Evidence of the gammadelta TCR/ligand recognition modalities that respective human

88 ells, MR1 interacts with specific gammadelta-TCRs using strikingly diverse binding modes, suggesting

89 The signaling mechanism connecting graded TCR signaling to the generation of varying amounts of IR

90 In the discovery dataset, higher TCR abundance was associated with better prognosis (haza

91 es and to IL6, and showed evidence of higher TCR-transmitted signals, which are also characteristics

92 r the LAIR-1-induced inhibition of the human TCR signal transduction.

93 ty profiles for three newly identified human TCRs specific for the cancer testis Ag NY-ESO-1(157-165)

94 Humanized TCR/HLA-transgenic allergy mice were treated in vivo wit

95 TCR-T therapies, such as selection of ideal TCRs targeting validated epitopes with well-characterize

96 e solved the structure of a newly identified TCR in complex with a clinically relevant peptide derive

97 e were enriched in cells bearing type B IELp TCR usage.

98 nt fraction (27-53% and 42-49%) of rhesus Ig/TCR diversity.

99 ma9Vdelta2(+) T cells underwent an immediate TCR-driven polyclonal proliferation within the first 4 w

100 In addition, we reveal a bias in TCR recombination and selection, which is attributed to

101 duals, indicating a shared Ag-driven bias in TCR usage.

102 y is associated with a selective increase in TCR sensitivity to self-peptide MHC in vivo and an enhan

103 is of structurally driven polyspecificity in TCRs, which is not possible with existing tools.

104 no structural information of MHC-independent TCRs is available, and their structural recognition of n

105 whereby the strength of self-peptide-induced TCR signal lead to the up-regulation of CD5, which subse

106 ch contains a collagen-like domain) inhibits TCR signaling by decreasing the phosphorylation of key c

107 osphorylates the TCR/CD3 complex to initiate TCR signaling.

108 ceptor T cells, but additionally integrating TCR signaling with parallel signals from other surface i

109 Interestingly, TCR stimulation in the presence of IL-2 upregulates intr

110 Here we show that, upon internalization, TCR continues to signal from a set of specialized endoso

111 urthermore, both the generation of invariant TCRs and the intrathymic acquisition of effector functio

112 In contrast, more limited TCR repertoire mixing was observed in two women with les

113 We define the basis by which the MAIT TCR can differentially recognize AMLs, thereby providing

114 associated with epithelial cells, NKT, MAIT, TCR-gammadelta, Monocytes, and CD8 + T-cells that are re

115 inflammation, and suggest that manipulating TCR signal strength along with Ag affinity, may be used

116 Mapping TCR clones to common viral epitopes (CMV, EBV, and influ

117 Preselecting CD29-expressing MART1 TCR-engineered T cells potentiated the killing of target

118 Mechanistically, TCR ligation leads to clathrin-mediated internalization

119 s with agonistic CD3 and CD28 Abs, mimicking TCR and costimulatory signals, coordinately induces 4-1B

120 aried the level of Ag expression to modulate TCR signaling, we found that low Ag concentrations promo

121 of the Nck1/CD3e interaction for modulating TCR activity in autoimmune and inflammatory diseases.

122 Using a mouse TCR transgenic CD4(+) T cell, BthetaOM, that is specific

123 Increased Ki67 expression, narrowed TCR V-beta repertoire usage and diluted T-cell receptor

124 L1-treated mice showed an even more narrowed TCR repertoire, with reduced TCR diversity compared to t

125 on via affinity-enhanced versions of natural TCRs (e.g., immune-mobilizing monoclonal T cell receptor

126 ets (i.e., B, CD3 + T, CD4 + T, CD8 + T, NK, TCR-gammadelta, Mucosal associated invariant (MAIT), and

127 atures for the efficient deployment of novel TCR-T therapies, such as selection of ideal TCRs targeti

128 eserve an effector program in the absence of TCR signaling.

129 nforced TCL1A enhanced phospho-activation of TCR kinases, second-messenger generation, and JAK/STAT o

130 vaccination, also induced the activation of TCR Vdelta1 and Vdelta1(-)Vdelta2(-) gammadelta T cells.

131 , our approach allows a combined analysis of TCR repertoires and other T cell transcription profiles

132 For example, batch annotation of TCR repertoire sequencing samples allows for annotating

133 mportant implications for the development of TCR-based therapies.

134 n naive animals, Nod2 operates downstream of TCR ligation to suppress activation of memory CD4(+) T c

135 ffector cytokine R production independent of TCR Ag affinity.

136 indings give insights into the initiation of TCR signaling, suggesting that changes in coreceptor-Lck

137 tinctive feature stems from the mechanism of TCR activation, which is thought to involve steric phosp

138 findings imply a simple phenotypic model of TCR signaling in which multiple T cell responses share a

139 tures, probably reflecting distinct modes of TCR fitting to MHC-II variants.

140 ta identify Trib1 as a negative regulator of TCR signaling and downstream function, and reveal a link

141 The role of TCR in tTreg selection remains incompletely understood.

142 Clonality and skewing of TCR repertoires were associated with interferon type I a

143 hat is shared, regardless of the strength of TCR stimulation.

144 Crystal structures of TCR-HLA-C complexes revealed that TCR9a to 9c recognized

145 guishing features of these cells in terms of TCR signaling, use of coreceptor and costimulatory molec

146 The increased yield of TCR specificity identification methods and the overall i

147 successful case of ACT included oligoclonal TCRs of high affinity recognizing distinct conformations

148 Their actions depend on TCR recognition of peptide-MHC molecules; yet the degree

149 uring T-cell development and is dependent on TCR signaling.

150 ls exist, the majority of studies focused on TCR Vgamma9Vdelta2 cells, the most abundant TCR gammadel

151 id searches in bulk immunome data for BCR or TCR sequences based on their CDR3 sequence or V3J clonot

152 t delivers in vitro-transcribed (IVT) CAR or TCR mRNA for transiently reprograming of circulating T c

153 In OT-II CD4(+) anti-OVA TCR transgenic mice sensitized to ovalbumin antigen, B c

154 suppress their ability to polarize naive OVA-TCR transgenic CD4(+) T cells into IFN-gamma-secreting c

155 ined for their ability to polarize naive OVA-TCR transgenic CD4(+) T cells.

156 ns of germline-encoded regions of particular TCR Vgamma regions with specific BTN/BTNL family members

157 ion via protein kinase C suggests persistent TCR stimulation as a potential contributing factor in Ga

158 libraries used to probe diverse, polyclonal TCR repertoires in various settings.

159 help prioritize the vast array of potential TCR-T optimizations for future clinical products.

160 deletion of Bcl6 from thymocytes reduced pre-TCR-induced differentiation to DP cells, disrupted expan

161 Here, we show that pre-TCR signalling leads to increased expression of the tran

162 ow that in DN thymocytes WNK1 transduces pre-TCR signals via OXSR1 and STK39 kinases, and the SLC12A2

163 Distinct predominant TCR clones were detected in cervical and TLSB specimens

164 down-regulates kinases involved in proximal TCR activation.

165 d screening and panning for antigen-reactive TCRs using peptide major histocompatibility complex bind

166 We found that, upon T cell antigen receptor (TCR) stimulation, T cells upregulated the IL-23 receptor

167 dies suggest that a T cell antigen receptor (TCR)-dependent mechanism may be responsible for the earl

168 T cell receptor (TCR) activation is modulated by mechanisms such as TCR e

169 ually all T-PLL expressed a T-cell receptor (TCR) and/or CD28-coreceptor without overrepresentation o

170 on of T cells expresses two T cell receptor (TCR) clonotypes, though the extent and functional signif

171 ty, and mutation of the key T-cell receptor (TCR) contact residue within the epitope prevents diabete

172 mixed lymphocyte reaction, T-cell receptor (TCR) deep sequencing, tetramer-guided naive CD4 T-cell p

173 n the thymus when their new T cell receptor (TCR) engages and signals in response to self-peptides.

174 and activation depend upon T cell receptor (TCR) interactions with a wide variety of antigenic pepti

175 ty is governed primarily by T cell receptor (TCR) recognition of peptide-human leukocyte antigen (pHL

176 but the involved alphabeta T cell receptor (TCR) repertoire has not been comprehensively analyzed.

177 nce on the antigen-specific T cell receptor (TCR) repertoire is unknown.

178 nation of immunophenotypic, T cell receptor (TCR) repertoire, functional, and transcriptomic data.

179 act on the exhausted CD8(+) T cell receptor (TCR) repertoire.

180 The diversity of T-cell receptor (TCR) repertoires is achieved by a combination of two int

181 Activation of the T cell receptor (TCR) results in binding of the adapter protein Nck (nonc

182 l increase in the number of T-cell receptor (TCR) sequences and their cognate antigens.

183 onal profiling coupled with T cell receptor (TCR) sequencing reveal lineage connections in T cell pop

184 Pre-T-cell receptor (TCR) signal transduction is required for developing thym

185 hat antigen recognition and T cell receptor (TCR) signaling depend on forces applied by the T cell ac

186 NA sequencing revealed that T cell receptor (TCR) signalling was enhanced in these cells.

187 T cell receptor (TCR) transductants and BTN3-deficient human 293T cells r

188 strength downstream of the T cell receptor (TCR) within activated thymocytes and peripheral T cells.

189 , similar to the endogenous T cell receptor (TCR), antigen engagement triggers the formation of CAR m

190 le receptors, including the T-cell receptor (TCR), co-receptors, and cytokine receptors.

191 isrupts Qa-1 binding to the T cell receptor (TCR)-CD8 complex and impairs the CD8 Treg response.

192 opulation that respond in a T cell receptor (TCR)-dependent manner to phosphoantigens which are gener

193 barcoded templates into the T cell receptor (TCR)-locus revealed gene constructs that enhanced fitnes

194 Adoptively transferred T cell receptor (TCR)-transgenic T cells (TCR-T cells) are not restricted

195 by the TRAV1-2(+) alphabeta T cell receptor (TCR).

196 d protein-1 (MR1) via their T cell receptor (TCR).

197 chains that constitute the T cell receptor (TCR).

198 ng, we established that the T cell receptor (TCR):CD3 complex is required for USSN-induced T cell act

199 The diverse repertoire of T-cell receptors (TCR) plays a key role in the adaptive immune response to

200 athogenic superantigens to T cell receptors (TCRs) and/or major histocompatibility complex class II (

201 T-cell receptors (TCRs) are immune proteins that primarily target peptide

202 o express antigen-specific T cell receptors (TCRs) are potent therapies for viral infections and canc

203 complex (pMHC) ligand for T cell receptors (TCRs) is inactive from solution yet capable of activatin

204 Four T cell receptors (TCRs) made up the TIL infusion and recognized two KRAS-G

205 expressing MCPyV-specific T cell receptors (TCRs) show increased cytokine production, migration towa

206 H, an algorithm to cluster T-cell receptors (TCRs) that recognize the same epitope and to predict the

207 The binding of T cell receptors (TCRs) to their target peptide MHC (pMHC) ligands initial

208 BFB-MYH11 epitope-specific T cell receptors (TCRs) transduced into CD8+ T cells conferred antileukemi

209 tudying the composition of T cell receptors (TCRs) using next-generation sequencing (NGS) in neonates

210 uch like MHC molecules and T cell receptors (TCRs).

211 y clonotypically expressed T-cell receptors (TCRs).

212 n more narrowed TCR repertoire, with reduced TCR diversity compared to that of persistently infected

213 Unlike conventional T cells, which require TCR ligation, iNKT cells can also be stimulated independ

214 The temperature coefficient of resistivity (TCR) and pressure sensitivity (eta(P)) are 0.038 degrees

215 d expression of NKG2D and DAP12 and restored TCR signaling in senescent-like CD27(-)CD28(-)CD8(+) T c

216 nearly identical to those of MHC-restricted TCR, including the conformations of CDR1 and 2.

217 he beta chains of two MHC class I-restricted TCRs, thereby revealing a common allosteric pathway amon

218 We integrate RNA-seq, DNA sequencing, TCR-seq and SNP array data across multiple regions of li

219 ession is required to maintain the signature TCR.Vgamma7(+) IEL phenotype, including specific respons

220 Similar TCRs were identified in EBV(RPP)-specific CD8(+) T cell

221 ity to that triggered by T reg cell-specific TCR deficiency.

222 with a significantly reduced NP396-specific TCR repertoire diversity: Shannon indices of 4 in immuni

223 eptor without overrepresentation of specific TCR clonotypes.

224 egments were present among the CD1b-specific TCRs, but chain swap experiments demonstrated that CD1b

225 cells modified to express EBV-LMP2-specific TCRs showed IFNgamma secretion and cytotoxicity towards

226 ith HLA-A*01:01-restricted EBV-LMP2-specific TCRs was optimized by knocking out the endogenous TCR of

227 Next-generation sequencing of NP396-specific TCRs showed that exhaustion corresponds with a significa

228 s well as structures of three tumor-specific TCRs bound to p53R175H-HLA-A2.

229 We present TCRBuilder, a multi-state TCR structure prediction tool.

230 t express upstream Vbeta peptides in surface TCRs and carry Trbv31-DJbeta2 rearrangements.

231 such as chronic viral infections, sustained TCR signaling can result in T cell exhaustion mediated i

232 R endocytosis, which is thought to terminate TCR signalling.

233 We have recently discovered that TCR-induced calcineurin activates DAPK1, which interacts

234 Second, we find that TCR CD3e can provide a switch by modulating its residenc

235 We also show that TCR chain usage is non-random, suggesting common antigen

236 We show that TCR is initiated by RNAPIIo-bound CSB, which recruits CS

237 These findings suggest that TCR signal strength and Ag affinity independently contri

238 These data suggest that TCR-induced signalling results in a coordinated activati

239 The TCR repertoire was analyzed by next-generation sequencin

240 Although the TCR-dependent and -independent activation of iNKT cells

241 Here, we analyze the TCR repertoire of single HIV-infected cells harboring tr

242 ss signaling pathways downstream of both the TCR and the Dectin-1 receptor.

243 bolic kinase, mTORC1, stimulated by both the TCR signal and growth factors, and this function of Peli

244 signaling cascade resembled that used by the TCR, except that unexpectedly, Th1 cells employed the IT

245 When compared to uninfected cells, the TCR repertoire of reservoir cells is heavily biased: exp

246 and TLRs are completely dispensable for the TCR activation pathway when a strong agonist is used.

247 aling models that have been proposed for the TCR.

248 activated T cells-pathway signaling from the TCR complex.

249 Nur77 integrates signals emanating from the TCR to control thymic iNKT cell tolerance induction, ter

250 y transmembrane adaptor protein LAT from the TCR.

251 force-induced conformational changes in the TCR-CD3 complex, for dynamically-driven TCR allostery, a

252 dels for the generation and selection of the TCR beta chain (TRB) from sequenced repertoires of 651 i

253 ere, we define the assembly mechanism of the TCR complex in human isogenic knockout cells.

254 essing BCR or B cells expressing part of the TCR complex.

255 ugh the regions between CDR2 and CDR3 of the TCR gamma chain and modulated by the affinity of the CDR

256 -fate decision, but a critical aspect of the TCR has been overlooked: tonic TCR signaling.

257 The function of the TCR proteins CSB, CSA and UVSSA and the manner in which

258 Here we investigated the evolution of the TCR repertoire and its affinity during the course of inf

259 Analysis of the TCR repertoire in adult COVID-19 patients demonstrates t

260 estinal mucus helps limit the shaping of the TCR repertoire of developing thymocytes by intestinal lu

261 uces local changes in the flexibility of the TCR zeta-chain, this naturally leads to rate enhancement

262 to clathrin-mediated internalization of the TCR-CD3zeta complex, while maintaining CD3zeta signallin

263 tyrosine kinase) to the CD3e subunit of the TCR.

264 notably distinct from the structures of the TCR:HLA-DQ2.5:gliadin epitope complexes.

265 ent and activation, as it phosphorylates the TCR/CD3 complex to initiate TCR signaling.

266 BP performed equally well or better than the TCR.

267 Together, we demonstrate that the TCR repertoire contracts over time and is almost exclusi

268 study CD4(+) T cell exhaustion, we used the TCR-transgenic B6 TEa cells that recognize a major trans

269 The TCRs employ structurally distinct strategies that are hi

270 The improved stability and folding of the TCRs reduces glycosylation, perhaps through conformation

271 mune sentinels at barrier surfaces and their TCR-independent functions, we put forth the need to clas

272 an also be stimulated independently of their TCR.

273 mmadelta T cells may therefore utilize their TCR like a cell-surface Fab repertoire, somewhat analogo

274 Therapeutic TCRs exhibited high affinities, ranging from nanomolar t

275 These TCR/CD3 bispecifics can redirect T cells to kill tumor c

276 The third TCR engaged a flipped peptide conformation, leading to t

277 is study, we dissected the response of three TCR gammadelta cell subsets and mucosal-associated invar

278 king pMHC or using multivalent antibodies to TCR.

279 lerates the rate of the cellular response to TCR stimulation, controlling the time to onset of Irf4 g

280 d expression of CD69 and CD25 in response to TCR stimulus.

281 aspect of the TCR has been overlooked: tonic TCR signaling.

282 y compartment by negatively regulating tonic TCR triggering in response to weak agonists.

283 s lacking SLAMF6 and expressing a transgenic TCR for gp100-melanoma antigen.

284 trasted that of the TRAV1-2(+) and TRAV36(+) TCRs' docking topologies on MR1.

285 r alpha (TRA) and T cell receptor beta (TRB) TCR chains.

286 ent antibodies, monovalent Fab'-DNA triggers TCRs only when physically coupled to the membrane, and o

287 We show that the unique TCR reactivity to the overlapping peptides is present in

288 mon allosteric pathway among three unrelated TCRs.

289 Using TCR alpha and beta repertoire sequencing for T-cell subs

290 esentation: Vbeta8 TCR congenic and Valpha14 TCR transgenic NC mice.

291 els of iNKT cell over-representation: Vbeta8 TCR congenic and Valpha14 TCR transgenic NC mice.

292 3 chimeras showed that alpaca Vgamma9Vdelta2 TCRs recognize PAg in the context of human and alpaca BT

293 In contrast, IFN-gamma response via TCR and plasma IgG specific for Bp were still intact.

294 impact initiation of signal transduction via TCR.

295 CD154 expression was TCR-mediated since single clones could be specifically r

296 X-024 reduces T cell proliferation upon weak TCR stimulation but does not significantly affect phosph

297 sequently, it is unclear the extent to which TCRs targeting the same Ag recognize the same off-target

298 ly ablated alloreactivity in comparison with TCR-expressing T cells.

299 The same association was observed with TCR abundance (HR = 0.41, 95% CI 0.18-0.93, P = 0.03 and

300 AIT cells during infection, in parallel with TCR repertoire alterations.