ライフサイエンスコーパス: TCRalphabeta

1 T cells that are either TCRgammadelta(+) or TCRalphabeta(+).

2 kg Bi-anti-CD45 or 2.0 to 2.7 mCi/kg Bi-anti-TCRalphabeta.

3 7.9%, P = .023) were significantly higher in TCRalphabeta.

4 er rates of veno-occlusive disease (14.4% vs TCRalphabeta 4.9%, P = .009), acute kidney injury (12.7%

5 HD) was higher after PTCY (15%, 9%-21%) than TCRalphabeta (6%, 2%-9%, P = .007), with no difference i

6 fference in chronic GvHD (PTCY, 11%, 6%-17%; TCRalphabeta, 7%, 3%-11%, P = .173).

7 Single-cell index sorting and TCRalphabeta analyses link expansion of A68/NP(145)(+)CD

8 Paired TCRalphabeta analyses of MAIT cells revealed large clona

9 3-year GvHD-free EFS was 53% (44%-61%) after TCRalphabeta and 41% (32%-50%) after PTCY (P = .080).

10 -free survival (EFS) was 58% (50%-66%) after TCRalphabeta and 57% (48%-66%) after PTCY (P = .804).

11 (95% confidence interval (CI), 71-84) after TCRalphabeta and 66% (57-74) after PTCY (P = .013).

12 he JCI, Poncette et al. used mice with human TCRalphabeta and HLA gene loci to discover CD4+ TCRs of

13 They coexpress TCRalphabeta and natural killer cell markers.

14 ansitions exhibit greater reversibility than TCRalphabeta and ordered force-bond lifetime curves.

15 total IELs-including some but not all of the TCRalphabeta and TCRgammadelta cells-expressed the CD43

16 e are two different clonotypic heterodimers (TCRalphabeta and TCRgammadelta) that define the alphabet

17 CD3(+)TCRalphabeta(+) and CD19(+) cell-depleted haploidentical

18 d numbers of intraepithelial CD8alphabeta(+)/TCRalphabeta(+) and CD8alphaalpha(+)/TCRalphabeta(+) T c

19 hereas IgG2a production is dependent on both TCRalphabeta(+) and TCRgammadelta(+) T cells.

20 all the deficiencies in the CD8alphaalpha(+)TCRalphabeta(+)and CD8alphaalpha(+)TCRgammadelta(+) subs

21 ional (gammadelta and CD4(-) CD8(-) NK1.1(-) TCRalphabeta) and conventional (CD8alphabeta and CD4) T

22 uted between CD4+ T cell receptor-alphabeta (TCRalphabeta)+ and CD4-8-TCRgammadelta+ T cells.

23 the endogenous TRAC and B2M loci to generate TCRalphabeta- and HLA-ABC-deficient T-cells expressing t

24 e rate of engraftment in the absence of anti-TCRalphabeta antibody, 920 cGy TBI were needed for pretr

25 therapy with Bi labeled to anti-CD45 or anti-TCRalphabeta as conditioning for nonmyeloablative HCT mi

26 lls, such CD34+ cells give rise both to CD3- TCRalphabeta+ as well as to dimly staining CD3+ TCRalpha

27 tion of cells (Thy-1(hi)CD16(+)CD44(hi)CD2(-)TCRalphabeta(-)B220(-)M ac-1(-)NK1.1(-)) in the adult mo

28 e CD4(-)CD8(-) double-negative stage and the TCRalphabeta being crucial for positive/negative selecti

29 expression was very low in tumors expressing TCRalphabeta, but its expression level was high and clon

30 entiation of alphabeta lineage cells and the TCRalphabeta can drive differentiation of gammadelta lin

31 The results support the notion that TCRalphabeta can substitute for TCRgammadelta to permit

32 CD3(+)TCRalphabeta(+)/CD19(+) depleted grafts were given in co

33 tment was significantly greater at 80% among TCRalphabeta(+)/CD19(+)-depleted and CB transplants vers

34 Cord transplantation without serotherapy and TCRalphabeta(+)/CD19(+)-depleted grafts produced compara

35 oietic stem cell transplantation (HSCT) with TCRalphabeta+/CD19+ depletion from matched unrelated don

36 TCRalphabeta+/CD19+ graft depletion effectively prevents

37 absence of HLA-identical siblings, HSCT with TCRalphabeta+/CD19+ graft depletion from MMRDs can be co

38 tients with various PIDs underwent HSCT with TCRalphabeta+/CD19+ graft depletion from MUDs (n = 75) a

39 TCRalphabeta/CD19 cell depletion is a promising graft ma

40 Use of TCRalphabeta/CD19 depletion was associated with a signif

41 demonstrated that, after adoptive transfer, TCRalphabeta(+)CD3(+)CD4(-)CD8(-)NK1.1(-) double-negativ

42 ing grafts, the predominant populations were TcRalphabeta(+)CD3(+)CD8(+) T cells, and CD14(+) monocyt

43 and B lymphocyte expansion, accumulation of TCRalphabeta+ CD3+ B220+ CD4- CD8- lymphocytes in second

44 /CD3-/CD5- (approximately 5-15%), NKR-P1dim-/TCRalphabeta+/CD3+/CD5+ (approximately 1-5%), and NKR-P1

45 he starting material with the majority being TcRalphabeta, CD3 positive T cells, a substantial percen

46 rized by expression of apoptotic markers and TCRalphabeta/CD3, but not CD4, CD8, or NK-associated mar

47 s monovalent and composed of one copy of the TCRalphabeta, CD3deltaepsilon, CD3gammaepsilon and zeta-

48 es caused defects in the formation of stable TCRalphabeta:CD3deltaepsilon:CD3gammaepsilon:zetazeta co

49 determine the structure of a tumor-reactive TCRalphabeta/CD3deltagammaepsilon(2)zeta(2) complex boun

50 1PC, or B-1sec also required the presence of TCRalphabeta CD4 T cells for their development from feta

51 Recently, a novel subset of TCRalphabeta(+) CD4(-) CD8(-) double-negative (DN) T cel

52 nign lymphoproliferation and accumulation of TCRalphabeta(+) CD4(-) CD8(-) double-negative T (DNT) ce

53 elta rearrangements occur normally such that TCRalphabeta(+)CD4(-)CD8(-) cells co-express TCRgammadel

54 Elevated TCRalphabeta(+)CD4(-)CD8(-) double-negative T cells (DNT

55 TCRalphabeta(+)CD4(-)CD8alpha(+)CD8beta(-) intestinal in

56 k CD4+ T cells and have increased numbers of TCRalphabeta+CD4-CD8- T cells, which phenotypically and

57 lized CD4(+) memory T lymphocytes with a CD3/TCRalphabeta/CD4/CD25/CD45RO/CD69 immunophenotype, promo

58 ough aberrant interaction between CD40L+ and TCRalphabeta+CD40+ thymocytes.

59 rder characterized by the expansion of CD8(+)TCRalphabeta(+)CD44(+)CD122(+)Ly-6C(+) T cells that clos

60 phaalpha+ IEL thymic precursors (CD4(-)CD8(-)TCRalphabeta+CD5+) in the absence of TGF-beta.

61 riple C->T deamination-mediated knockouts of TCRalphabeta, CD52, and CD7 have been reported previousl

62 ient characteristics of CD8+ CTLs (large CD8+TCRalphabeta+CD62L-CD11a(hi)perforin+).

63 T-pro are tumor-infiltrating TCRalphabeta(+)CD8(+) cells of reduced cytotoxic potenti

64 wild-type and MHC class I knockout mice, but TCRalphabeta+ CD8(+) cells predominated in the gastric t

65 Conversely, TCRalphabeta((+))CD8alphaalpha((+)) IEL development was

66 o-DP transition, and reduced contribution of TCRalphabeta((+))CD8alphaalpha((+)) IELs to gut epitheli

67 es with altered generation of unconventional TCRalphabeta((+))CD8alphaalpha((+)) IELs.

68 as unconventional alphabeta T cells, such as TCRalphabeta((+))CD8alphaalpha((+)) intraepithelial lymp

69 igh) DN thymocytes that preferentially yield TCRalphabeta(+) CD8alphaalpha intestinal lymphocytes, we

70 xpression predominantly by mTEC(lo) supports TCRalphabeta(+) CD8alphaalpha intraepithelial lymphocyte

71 The signaling machinery of both TCRalphabeta(+)CD8alphaalpha and TCRgammadelta(+) IEL is

72 subsets with differing abilities to generate TCRalphabeta(+)CD8alphaalpha IEL in vivo.

73 , these data underscore the fact that, while TCRalphabeta(+)CD8alphaalpha IEL resemble TCRgammadelta(

74 The TCRalphabeta(+)CD8alphaalpha IEL subset also has increas

75 Using these methods, TCRalphabeta(+)CD8alphaalpha IEL were compared with thei

76 Interestingly, TCRalphabeta(+)CD8alphaalpha IEL were found to preferent

77 RasGRP1 is critical for agonist selection of TCRalphabeta(+)CD8alphaalpha intraepithelial lymphocyte

78 l roles for Bcl-2 in driving the survival of TCRalphabeta(+)CD8alphaalpha(+) IEL and thymic IELp.

79 homa-related factor (LRF) failed to generate TCRalphabeta(+)CD8alphaalpha(+) IELs and their CD8beta-e

80 t shared by other IEL populations, including TCRalphabeta(+)CD8alphaalpha(+) IELs.

81 The precursors of TCRalphabeta(+)CD8alphaalpha(+) intraepithelial lymphocy

82 We observed defective development of the TCRalphabeta+CD8alphaalpha+ IEL thymic precursors (CD4(-

83 eta signaling induced CD8alpha expression in TCRalphabeta+CD8alphaalpha+ IEL thymic precursors and in

84 ized role for TGF-beta in the development of TCRalphabeta+CD8alphaalpha+ IELs and the expression of C

85 cific deletion of TGF-beta receptor I lacked TCRalphabeta+CD8alphaalpha+ IELs, whereas mice with tran

86 -beta (TGF-beta) controls the development of TCRalphabeta+CD8alphaalpha+ IELs.

87 sion of TGF-beta1 had a larger population of TCRalphabeta+CD8alphaalpha+ IELs.

88 ar mechanisms that direct the development of TCRalphabeta+CD8alphaalpha+ intestinal intraepithelial l

89 n of natural IELs that are TCRgammadelta+ or TCRalphabeta+CD8alphaalpha+ to shape the composition of

90 +)CD8alphaalpha IEL were compared with their TCRalphabeta(+)CD8beta(+) and TCRgammadelta(+) counterpa

91 harbors a large number of T cells, including TCRalphabeta cells that lack expression of CD4 and CD8al

92 The thymic precursors of CD8alphaalpha(+) TCRalphabeta(+) cells (triple-positive for CD4, CD8alpha

93 ative thymocytes led to impaired survival of TCRalphabeta(+) cells and the generation of atypical CD8

94 ration and proliferation of CD8alphaalpha(+) TCRalphabeta(+) cells in VDR KO mice results in fewer fu

95 25(+) T cells demonstrated that inability of TCRalphabeta(+) cells to expand Vdelta2 cells was not re

96 d that the defect in VDR KO CD8alphaalpha(+) TCRalphabeta(+) cells was cell intrinsic.

97 ment likewise induces distinct phenotypes in TCRalphabeta(+) cells.

98 eduction was largely in the CD8alphaalpha(+) TCRalphabeta(+) cells.

99 Ralphabeta(-) to CD2(+)CD16(int/-)CD44(int/-)TCRalphabeta(-) cells, and a later transition to CD4(+)C

100 of CD3+ T-cell receptor (TCR)alphabeta/CD19 (TCRalphabeta) cells or in vivo T-cell depletion using po

101 lthough T cell receptor (TCR)gammadelta+ and TCRalphabeta+ cells are commonly viewed as functionally

102 have previously reported that activated CD8+TCRalphabeta+ cells that express high levels of the beta

103 alphabeta+ as well as to dimly staining CD3+ TCRalphabeta+ cells.

104 in Valpha14+ T cells, since transduction of TCRalphabeta chains from a high CD1d autoreactive Valpha

105 t single TCRbeta are sufficient to confer on TCRalphabeta chains reactivity toward disease-associated

106 Furthermore, the mutant T cells formed large TCRalphabeta clones and displayed inflammatory and cytot

107 te libraries of natively paired, full-length TCRalphabeta clones, from millions of primary T cells, w

108 lphabeta heterogeneity, underpinned by large TCRalphabeta clonotype expansions of private TCRalphabet

109 We identify related TRAJ24(+) TCRalphabeta clonotypes encoded by identical alpha/beta

110 ptured more than 2.9 million natively paired TCRalphabeta clonotypes from six healthy human donors an

111 The key public-associated TCRalphabeta clonotypes largely persisted across the hum

112 fespan and advocates for boosting persistent TCRalphabeta clonotypes within this key peripheral blood

113 TCRalphabeta clonotype expansions of private TCRalphabeta clonotypes.

114 es on the structural biology of the Fab-like TCRalphabeta clonotypic heterodimer and its unique featu

115 We found that particular TCRalphabeta combinations were selected for recognition

116 ing pre-Talpha/TCRbeta (pre-TCR) and ligated TCRalphabeta complexes, which independently operate the

117 oned and retrovirally transduced into either TCRalphabeta-deficient hybridoma cells or Rag1-/- bone m

118 In the human thymus, a CD10+ PD-1+ TCRalphabeta+ differentiation pathway diverges from the

119 ncy was detected in adults, reflecting lower TCRalphabeta diversity in this group.

120 TCRalphabeta diversity within T(cm) A2/M1(58)(+)CD8(+) T

121 The basis of optimized TCRalphabeta docking geometry on the pMHC linked to TCR

122 cells, and a later transition to CD4(+)CD8(+)TCRalphabeta(+) double-positive T cells that rapidly gen

123 these known subsets, we identify CD4(-)CD8(-)TCRalphabeta(+), double-negative (DN) T cells, in mouse

124 duals, although associated with large clonal TCRalphabeta expansions and increased baseline inflammat

125 variant NKT (iNKT) cells are a population of TCRalphabeta-expressing cells that are unique in several

126 to the B cell lineage as we observed normal TCRalphabeta expression on CD8-expressing splenocytes.

127 cytes due to competitive decrease in surface TCRalphabeta formation.

128 of the TCRgammadelta(+) and CD8alphaalpha(+)TCRalphabeta(+) gut intraepithelial T lymphocytes were a

129 The proliferation rates of the DN TCRalphabeta(+) gut T cells were less in the VDR KO comp

130 one dog conditioned with 1.5 mCi/kg Bi-anti-TCRalphabeta had stable engraftment, whereas two rejecte

131 f these TCRbeta modulate the likelihood of a TCRalphabeta heterodimer productively engaging autoantig

132 tor (TCR) signaling complex is composed of a TCRalphabeta heterodimer that is noncovalently coupled t

133 If public TCR chains modulate a TCRalphabeta heterodimer's likelihood of productively en

134 oning, and, therefore, in docking of diverse TCRalphabeta heterodimers onto variant peptide:class I c

135 Gene transfer of TCRalphabeta heterodimers specific for clonal neoantigen

136 of TCR beta-chains, rather than the combined TCRalphabeta heterodimers that confer specificity.

137 Furthermore, we demonstrated that some TCRalphabeta heterodimers were preferentially expanded f

138 Older adults displayed increased TCRalphabeta heterogeneity, underpinned by large TCRalph

139 ssion and masquerade as double-negative (DN) TCRalphabeta(hi) thymocytes.

140 athway for the generation of CD8alphaalpha(+)TCRalphabeta(+) IEL.

141 Some TCRalphabeta(+)IEL have characteristics in common with c

142 TCRalphabeta+ IEL recruitment may be blocked using the S

143 that myeloid cells are the key mediators of TCRalphabeta+ IEL recruitment to the colon.

144 preferentially give rise to CD8alphaalpha(+)TCRalphabeta(+) IELs, but they required exposure to self

145 d in a decreased percentage of cytotoxic CD8+TCRalphabeta+ IELs expressing intracellular IFN-gamma an

146 the importance of S1P in the recruitment of TCRalphabeta+ IELs to the colon epithelium.

147 TCRgammadelta+NKG2A+ IELs, IL-15-stimulated TCRalphabeta+ IELs, and HLA-E+ enterocytes resulted in a

148 ith its ligand, HLA-E, on enterocytes and/or TCRalphabeta+ IELs.

149 igh TCRalpha transcription and expression of TCRalphabeta in mouse and human T lymphocytes, requiring

150 NK1.1(+) TCRalphabeta(int) CD1-restricted T (NKT) cells are a uni

151 at one of these populations, CD8alphaalpha(+)TCRalphabeta(+) intestinal intraepithelial lymphocytes (

152 CD8alphaalpha TCRalphabeta(+) intestinal intraepithelial lymphocytes p

153 In the gut, the Thy-1(+)TCRalphabeta(+) intraepithelial lymphocyte (IEL) compart

154 or CD4 and CD8alphabeta double-negative (DN) TCRalphabeta(+) intraepithelial T cells, although numero

155 ompatibility complex (MHC) restriction of DN TCRalphabeta(+) intraepithelial T cells.

156 sed in TCRalphabeta transgenic mice when the TCRalphabeta is expressed early in T cell development.

157 alphabeta T lineage commitment when only the TCRalphabeta is expressed.

158 The TCRalphabeta-Jurkat libraries enabled repeated screening

159 SCID mice and TCRalphabeta knockouts sustained a severe but nonlethal

160 TCRalphabeta ligates the membrane-distal antigen-binding

161 The generation of the TCRalphabeta lineage of T cells occurs in the thymus thr

162 With regard to TCRalphabeta lineage T cells, exclusion at the tcr-b, bu

163 at commitment of thymic precursors to the DN TCRalphabeta(+) lineage is imprinted by their TCR specif

164 evelop into unconventional TCRgammadelta and TCRalphabeta lymphocytes in a process of extrathymic lym

165 an increase in the ratio of CD8(+) to CD4(+)TCRalphabeta lymphocytes.

166 The anti-TCRalphabeta mAb 15.9D5 was selected for in vivo studies

167 injections of Bi linked to anti-CD45 or anti-TCRalphabeta mAb followed by marrow grafts from DLA-iden

168 ur dogs were treated with 0.13 to 0.46 mg/kg TCRalphabeta mAb labeled with 3.7 to 5.6 mCi/kg (137-207

169 ing a gamma-emitting indium-111-labeled anti-TCRalphabeta mAb showed uptake primarily in blood, marro

170 Unlike TCRalphabeta-mediated, MHC-restricted Ag recognition but

171 beta constant (TRBC) knockout, thus avoiding TCRalphabeta mispairing and maximizing TCR expression an

172 anti-CD45 or anti-T-cell receptor alphabeta (TCRalphabeta) monoclonal antibodies (mAb), together with

173 ARS-CoV-2-specific T cell memory with common TCRalphabeta motifs in unvaccinated seroconverted childr

174 and 2019 from an HLA-mismatched donor using TCRalphabeta (n = 167) or PTCY (n = 139).

175 pression and chemotactic responses of murine TCRalphabeta NKT cells were examined to define their hom

176 We find that precursor thymocytes expressing TCRalphabeta not only mature in the alphabeta pathway as

177 e choices: T rather than B lymphocytes, then TCRalphabeta or TCRgammadelta, CD4 or CD8, and Th1 or Th

178 l described a structural basis for preferred TCRalphabeta pairing that determined exquisite specifici

179 er of antigen receptor heterodimers, such as TCRalphabeta pairs, expressed in the population are unde

180 um of nearly identical crystal structures of TCRalphabeta-pMHC agonist and antagonist complexes.

181 ct surface comparable in size to that of the TCRalphabeta-pMHC but potentially with a rather distinct

182 HC interaction directly analogous to that of TCRalphabeta-pMHC.

183 d a higher frequency of the CD8alphaalpha(+) TCRalphabeta(+) precursors (double-negative [DN] TCRalph

184 that in vivo administration of a mAb against TCRalphabeta prevented rejection of allogeneic marrow gr

185 ocyte CD8alpha(+)TCRgammadelta(+)/CD8alpha(+)TCRalphabeta(+) ratio.

186 mice expressing a rearranged transgenic (Tg) TCRalphabeta receptor.

187 el subset of nonintestinal CD8alphaalpha+CD4-TCRalphabeta+ regulatory T cells (CD8alphaalpha Tregs) t

188 s and tissues that rivalled, remarkably, the TCRalphabeta repertoire diversity of virus-specific CD8(

189 f predominantly naive phenotypes and diverse TCRalphabeta repertoires.

190 tivity evokes the developmental selection of TCRalphabeta(+) repertoires.

191 ll RNA and T cell receptor sequencing (scRNA+TCRalphabeta-Seq) combined with other multiomics profili

192 ell RNA and T cell receptor profiling (scRNA+TCRalphabeta-seq), we show that irrespective of STAT3 mu

193 ting over 4,600 in-frame single-cell-derived TCRalphabeta sequence pairs from 110 subjects.

194 TCRs, TCR-repertoire, and single-cell RNA + TCRalphabeta-sequencing data) from 515 patients with pri

195 TCRalphabeta signaling is crucial for the maturation of

196 Suboptimal TCRalphabeta signatures in older adults led to less prol

197 s is almost completely arrested at the CD2(+)TCRalphabeta(-) stage by the presence of mature T cells

198 is surprisingly intact, whereas the Thy-1(-)TCRalphabeta(+) subset is almost completely absent.

199 TCRalphabeta subunits are associated with the CD3 comple

200 double-positive (DP) stage and up-regulated TCRalphabeta surface expression in the absence of cell p

201 ure molecular signatures similar to those of TCRalphabeta T cells from peripheral blood.

202 of a population of non-malignant CD4(-)CD8(-)TCRalphabeta T cells that interact with CXCL16 expressin

203 ymic recipients generated conventional naive TCRalphabeta T cells with a broad Vbeta repertoire and i

204 Infiltrating CD8alpha(+) cells were TCRalphabeta T cells with a nonconventional phenotype th

205 alphabeta(+) T cells form a third lineage of TCRalphabeta T lymphocytes expressing a variable TCR rep

206 e T (DNT) cells are a unique subset of CD3 + TCRalphabeta + T lymphocytes that lack CD4, CD8, or NK1.

207 cluding double negative CD4(-)CD8alphabeta(-)TCRalphabeta(+) T (DNT) cells, in the intraepithelial co

208 ent can promote a relatively normal Thy-1(+) TCRalphabeta(+) T cell pool from the limited population

209 very was comparable to previous reports with TCRalphabeta(+) T cell-depleted and CD19(+) B cell-deple

210 bone marrow that generates CD4(+) and CD8(+) TCRalphabeta(+) T cells after tissue culture for 48 hr i

211 ptococcus pneumoniae was dependent on CD4(+) TCRalphabeta(+) T cells and B7-dependent costimulation t

212 Qa-1 pathway for priming of CD8alphaalpha(+)TCRalphabeta(+) T cells and have implications for a DC-b

213 CD8alphaalpha(+)TCRalphabeta(+) T cells are a special subset of innate-l

214 The new insights indicate that DN TCRalphabeta(+) T cells form a third lineage of TCRalpha

215 innate-like, unconventional CD8alphaalpha(+)TCRalphabeta(+) T cells in naive mice and in human perip

216 xpansion of double-negative (DN) CD4(-)CD8(-)TCRalphabeta(+) T cells in SRW-treated DQ6/CD4(null) mic

217 There are fewer total numbers of TCRalphabeta(+) T cells in the gut of VDR knockout (KO)

218 with apoptotic T cells prime CD8alphaalpha(+)TCRalphabeta(+) T cells in vivo, which in turn provides

219 nfiltration of activated CD4+ and CD8alpha(+)TCRalphabeta(+) T cells into the lamina propria and is a

220 a-1 pathway and presented to CD8alphaalpha(+)TCRalphabeta(+) T cells is not understood.

221 sed in such Cre(+) RAG2(fl/fl) mice, and the TCRalphabeta(+) T cells that develop are limited in thei

222 Low proliferation of DN TCRalphabeta(+) T cells was a result of the very low exp

223 functional CD8alphabeta(+), CD4(-), CD3(+), TCRalphabeta(+) T cells with a diverse TCR repertoire.

224 lphabeta(+) precursors (double-negative [DN] TCRalphabeta(+) T cells) in the gut.

225 beta(+)/TCRalphabeta(+) and CD8alphaalpha(+)/TCRalphabeta(+) T cells, and reduced numbers of lamina p

226 Moreover, purified primary human TCRalphabeta(+) T cells, CD4(+), or CD8(+) T cells also

227 results in fewer functional CD8alphaalpha(+) TCRalphabeta(+) T cells, which likely explains the incre

228 the context of Qa-1 to prime CD8alphaalpha(+)TCRalphabeta(+) T cells.

229 characteristics in common with conventional TCRalphabeta(+)T cells whereas others share an unconvent

230 alphabeta T cell receptor (TCRalphabeta) T cells modified to express chimeric antig

231 s, including TCRgammadelta+ T cells and some TCRalphabeta+ T cell subsets (including Th1, Tfh, and Tr

232 CD8alphaalpha+CD4-TCRalphabeta+ T cells are a special lineage of T cells f

233 , the resident allogeneic bone marrow CD8(+) TCRalphabeta+ T cells had the unique capacity to elimina

234 he CD8(+)T-cell antigen receptor-alphabeta+ (TCRalphabeta+) T cells within the marrow transplants med

235 105 patients (93 T-cell receptor alphabeta [TCRalphabeta] T-LGL and 12 TCRgammadelta T-LGL).

236 val and proliferation and is NK1.1(+) CD3(-) TCRalphabeta(-) TCRdeltagamma(-) CD4(-) CD8(-) CD19(-) C

237 were produced, all of which were CD4(+)CD8(-)TCRalphabeta(+)TCRgammadelta(-).

238 y response is equivalent in WT, T-deficient (TCRalphabeta(-/-), TCRgammadelta(-/-)), and Toll-like re

239 ree other widely used MHC class I-restricted TCRalphabeta Tg mouse strains and compared it with that

240 In all three TCRalphabeta Tg strains, as in control mice, thymocyte n

241 ells express private expanded and unexpanded TCRalphabeta that are absent or unexpanded in unaffected

242 e T cell antigen receptor alphabeta subtype (TCRalphabeta) that 'preferentially' migrated to the inte

243 T+ CD11c+ IEL and LPL expressed a phenotype, TCRalphabeta+ Thy-1+ CD8+ similar to that expressed on r

244 TCRalphabeta thymocytes differentiate into either CD8alp

245 Consequently, while nearly all developing TCRalphabeta thymocytes express a single TCRbeta protein

246 The agonist-selected TCRalphabeta(+) thymocytes are CD4 and CD8 double-negati

247 oting that the key features stabilizing this TCRalphabeta TM interface also appear with high evolutio

248 geneic barriers, most notably, by disrupting TCRalphabeta to prevent graft-versus-host disease, and m

249 n early transition from CD2(-)CD16(+)CD44(hi)TCRalphabeta(-) to CD2(+)CD16(int/-)CD44(int/-)TCRalphab

250 o demonstrate that a functionally rearranged TCRalphabeta transgene is sufficient to restore thymocyt

251 TCRbeta or TCRalphabeta transgenes failed to rescue DNMAML-related

252 adelta gene rearrangements are suppressed in TCRalphabeta transgenic mice when the TCRalphabeta is ex

253 In TCRalphabeta transgenic mice, in which the transgenic re

254 highly conserved T cell receptor alphabeta (TCRalphabeta) transmembrane (TM) interface forms a rigid

255 Antigen binding to TCRalphabeta transmits signals through the plasma membra

256 on a newly described subset, CD8alphaalpha(+)TCRalphabeta(+) Tregs, which in mice recognize a T-cell

257 nd clones representing a novel population of TCRalphabeta+ Tregs that control activated Vbeta8.2+ CD4

258 a TRuC) and fully restored by exchanging the TCRalphabeta variable domains for those of the CAR (also

259 onversely, a dominant public TRAV27/TRBV19(+)TCRalphabeta was selected in HLA-A*0201(+)donors respond

260 on surface versus the upright orientation of TCRalphabeta would alter the direction of force applicat