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 They coexpress TCRalphabeta and natural killer cell markers.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

65 25(+) T cells demonstrated that inability of TCRalphabeta(+) cells to expand Vdelta2 cells was not re

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

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

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

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

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

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

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

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

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

75 We found that particular TCRalphabeta combinations were selected for recognition

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

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

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

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

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

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

82 cytes due to competitive decrease in surface TCRalphabeta formation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

100 CD8alphaalpha TCRalphabeta(+) intestinal intraepithelial lymphocytes p

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

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

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

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

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

106 SCID mice and TCRalphabeta knockouts sustained a severe but nonlethal

107 TCRalphabeta ligates the membrane-distal antigen-binding

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

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

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

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

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

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

114 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

132 TCRalphabeta signaling is crucial for the maturation of

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

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

135 TCRalphabeta subunits are associated with the CD3 comple

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

168 TCRalphabeta thymocytes differentiate into either CD8alp

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

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

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

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

173 TCRbeta or TCRalphabeta transgenes failed to rescue DNMAML-related

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

175 In TCRalphabeta transgenic mice, in which the transgenic re

176 Antigen binding to TCRalphabeta transmits signals through the plasma membra

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

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

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

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