ライフサイエンスコーパス: CFSE

1 CFSE dilution analyses revealed that hypercholesterolemi

2 CFSE labeling demonstrated that TGF-beta1 inhibited entr

3 CFSE proliferation and CD154 expression flow cytometry-b

4 CFSE staining in combination with T-cell- and B-cell-spe

5 CFSE staining of purified human tonsillar B cells demons

6 CFSE(+) Th1 cells colocalized with injected tumor cells

7 CFSE(lo) CD4(+) T cells contained only 0.3-10.7% of tetr

8 CFSE-based flow-cytometric assays will be useful in eval

9 CFSE-labeled C57BL/6 (H-2(b)) spleen and lymph node cell

10 CFSE-labeled PBMCs were stimulated with CMV, tetanus tox

11 CFSE-labeled T cells were cocultured with GR1(+) CD11b(+

12 CFSE-labeled wild-type and IFN-gamma-deficient Tc1 cells

13 CFSE-labeling demonstrated that these T cells were able

14 CFSE-labeling studies showed extensive NK cell prolifera

15 CFSE-positive DCs (CD11c(+), CD11b(+), and low-to-interm

16 mice; however, significantly more (P <.003) CFSE-positive (CFSE(+)) NK cells were found in control m

17 In addition, a CFSE-based approach was tested and found to be sufficien

18 MDSCs to inhibit T cells was evaluated by a CFSE-based T-cell proliferation assay.

19 ll division was also found to be normal in a CFSE dilution assay.

20 whereas uninfected cells consisted of only a CFSE-low population.

21 Through a CFSE-based assay for quantitatively monitoring in vitro

22 , CD45RB, CD62L, CD69, caspase-3 activation, CFSE dilution, size, number of cells recovered, and cyto

23 d MLR proliferation and recruited additional CFSE-labeled autologous Tregs compared with addition of

24 esulting from failed BMT, because almost all CFSE-labeled donor cells were killed at 0.5 and 3 h in s

25 feration of T cells was assessed by BrdU and CFSE labeling.

26 ith this observation, Bromodeoxyuridine- and CFSE-labeling studies reveal a shorter in vivo life span

27 liferation activity; 34.2% of the cells) and CFSE-low (indicating high proliferation activity; 62.5%

28 ies with BrdU (5-bromo-2'-deoxyuridine)- and CFSE [5-(and 6)-carboxyfluorescein diacetate succinimidy

29 The present study using immunoscope and CFSE-labeling analysis demonstrates that the expansion o

30 Activation occurred, as CFSE-associated fluorescence was reduced 2-fold with eac

31 For functional assays, CFSE-stained CD4+ T cells were coincubated with differen

32 azol-2-yl)-2,5-diphenyltetrazolium bromide), CFSE (carboxy fluorescein succinimidyl ester) dilution,

33 llergen-stimulated proliferation assessed by CFSE dilution is less sophisticated and widely applicabl

34 the IS and cell proliferation as assessed by CFSE labeling and [(3)H]thymidine incorporation were sup

35 CD4 T cell proliferation was assessed by CFSE staining, and the expression of GRAIL in splenocyte

36 sured by ELISA, T-cell responses assessed by CFSE-based proliferation assays and ELISA, and basophil

37 re CD8(+)alphabetaTCR(+), as demonstrated by CFSE staining.

38 tion and effector functions were detected by CFSE dilution and intracellular staining, respectively.

39 tion induced by alloantigen as determined by CFSE staining and flow cytometry.

40 B-cell proliferation was measured by CFSE staining.

41 Tracking post-REP TIL proliferation by CFSE dilution, as well as sorting for CD8(+)CD28(+) and

42 cells did become activated, as reflected by CFSE dilution and CD44 up-regulation.

43 try into subsequent cell divisions (shown by CFSE staining), although NOD cells showed greater number

44 reatly reduced numbers of alloreacting CD3(+)CFSE(lo) cells, activation Ag-expressing CD4(hi) and CD8

45 slow to respond to allergen (CD19(hi) CD3(-) CFSE(mid) ).

46 cells that divided rapidly (CD19(mid) CD3(-) CFSE(lo) ) showed higher CD27 (P = 0.008) and lower CD19

47 nd Tbet was analyzed in sorted CD3(+) CD4(+) CFSE(low) cells proliferating upon stimulation of PBMC w

48 o detected in Dau c 1-reactive CD3(+) CD4(+) CFSE(low) cells.

49 Absolute numbers of CD4(+)/CFSE(lo)/interferon (IFN)- gamma (+), CD8(+)/CFSE(lo)/IF

50 y allostimulation were identified as CD8(+), CFSE(low) cells and were categorized as CTL by the expre

51 ), CD8(+)/CFSE(lo)/granzyme A(+), and CD8(+)/CFSE(lo)/CD107a(+) T cells present after in vitro stimul

52 (+), CD8(+)/CFSE(lo)/IFN- gamma (+), CD8(+)/CFSE(lo)/granzyme A(+), and CD8(+)/CFSE(lo)/CD107a(+) T

53 CFSE(lo)/interferon (IFN)- gamma (+), CD8(+)/CFSE(lo)/IFN- gamma (+), CD8(+)/CFSE(lo)/granzyme A(+),

54 Vaccinia-specific CD8(+)/CFSE(lo)/IFN- gamma (+) and granzyme A(+) T cell respons

55 As for IM, the most primitive cells (CFSE(max)) persisted and accumulated over 72 hours with

56 IL-4/CD40 ligand trimer-stimulated B cells, CFSE studies revealed that the Bryo-mediated inhibition

57 ersus 41.0% +/- 8.3% of monocytes containing CFSE-labeled parasites; P < 0.001) and the magnitude of

58 These frequencies were validated by counting CFSE(low), tetramer-positive T cells after in vitro expa

59 cells were labeled with the fluorescent dye CFSE and were stimulated with specific peptide Ag.

60 using the dilution of the intracellular dye CFSE as an indicator of CD8(+) T cell alloactivation and

61 receptor excision circles (TRECs) or the dye CFSE, and clonal expansion has been documented by record

62 combination of tetramer, IFN-gamma-ELISPOT, CFSE proliferation, CD107a/b cytotoxic degranulation, an

63 tes with the crystal field splitting energy (CFSE) Delta evoked by the coordination ligands.

64 boxyfluorescein diacetate succinimide ester (CFSE) proliferation assays followed by CTL-associated cy

65 n and carboxyfluorescein succinimidyl ester (CFSE) dilution experiments.

66 with carboxyfluorescein succinimidyl ester (CFSE) fluorescent dye.

67 nto 2 carboxyfluorescein succinimidyl ester (CFSE) groups, CFSE-high (indicating low proliferation ac

68 l dye carboxyfluorescein succinimidyl ester (CFSE) in 3- to 4-day mixed leukocyte reaction co-culture

69 xy-fluorescein diacetate succinimidyl ester (CFSE) labeled CD4CD25FOXP3 cells by flow cytometry were

70 with carboxy fluorescein succinimidyl ester (CFSE) labeled T cells.

71 oxyfluorescein diacetate succinimidyl ester (CFSE) labeling of the cells, followed by counting of cel

72 xy-fluorescein diacetate succinimidyl ester (CFSE) staining and ELISA analysis of IFN-gamma.

73 oxyfluoresccin diacetate succinimidyl ester (CFSE) staining.

74 oxyfluorescein diacetate succinimidyl ester (CFSE) to track cell division and cultured in low or high

75 xyfluorescein diacetate, succinimidyl ester (CFSE) were adoptively transferred into IL-15(-/-) mice a

76 oxyfluorescein diacetate succinimidyl ester (CFSE) were cultured with Bahia grass pollen.

77 oxyfluorescein diacetate succinimidyl ester (CFSE), dioctadecyl-tetramethylindo carbocyanine perchlor

78 xy-fluorescein diacetate succinimidyl ester (CFSE), their division history has been studied by monito

79 ped a carboxyfluorescein succinimidyl ester (CFSE)-based flow-cytometric assay that can detect differ

80 xyfluorescein diacetate, succinimidyl ester (CFSE)-labeled naive CD4(+) T cells in LDLR(-/-) recipien

81 oxyfluorescein diacetate succinimidyl ester (CFSE)-labeled T lymphocytes in acutely SIVmac251-infecte

82 oxyfluorescein diacetate succinimidyl ester (CFSE)-stained splenocytes from cloned LG-6 donor frogs i

83 oxyfluorescein diacetate succinimidyl ester (CFSE).

84 ansfer of carboxyfluorescein succinyl ester (CFSE)-labeled T-cell receptor (TCR)-transgenic T cells a

85 xyfluorescein diacetate succinimidyl ester- (CFSE) labeled to allow detection, immunohistochemistry w

86 In addition, very few CFSE-labeled BDC2.5 T cells divide in the recipient's pa

87 Furthermore, CFSE labeling demonstrates impaired proliferation of nai

88 luorescein succinimidyl ester (CFSE) groups, CFSE-high (indicating low proliferation activity; 34.2%

89 marker CD38 compared with B cells (CD19(hi) CFSE(mid) CD27(lo) ) that were slow to divide.

90 nt more than eight proliferations (CD43(high)CFSE(neg)) and promptly secreted IFN-gamma upon contact

91 ed ICOShigh and ICOSlow Treg was assessed in CFSE-based suppression assays with autologous CD4+CD25-

92 d tissue in SIV infection, no differences in CFSE+ T-lymphocyte frequencies or cell compartmentalizat

93 Quantification of HIV DNA in CFSE(low) cells showed a reduction of strong-stop and fu

94 Finally, in CFSE T cell proliferation assays using anti-CD3 mAb or T

95 tion by ELISA and for suppressor function in CFSE inhibition assays plus or minus anti-IL-10 or anti-

96 pression of RC proliferation was measured in CFSE assays.

97 ection was monitored by intracellular p24 in CFSE(low) population.

98 in (MAP) kinase was significantly reduced in CFSE-high, SB-HCV-infected Molt-4 cells.

99 he in vivo clearance of autologously-infused CFSE-labeled erythrocytes from circulating blood was fas

100 in vivo, dual-label system using intranasal CFSE and BrdU administration to identify virus-specific

101 An in situ intrathymic CFSE injection labeled developing thymocytes and allowed

102 The ligand inducing largest CFSE results in the strongest effect on the coercivity o

103 vo, higher numbers of immature and Ag-loaded CFSE-labeled DC are present in the draining lymph nodes

104 hoid organs contained both resting (CD43(low)CFSE(high)) and virus-specific cells at different stages

105 we used the intracellular fluorescent marker CFSE (5-(and-6)-carboxyfluorescein diacetate succinimidy

106 dividing allergen-driven B cells (CD19(mid) CFSE(lo) CD27(hi) ) showed higher expression of the plas

107 Primed anti-LG-15 but not naive CFSE T cells accumulated and divided in the spleen of al

108 However, by following the fate of naive, CFSE-labeled, islet Ag-specific CD8+ (HA-specific clone-

109 sily detected in IL-15(+/-) mice, whereas no CFSE(+) NK cells survived in IL-15(-/-) mice.

110 Each group of (non-CFSE labeled) MLR-generated cells were then added as thi

111 ly reduced the number of viable, nondividing CFSE bright cells remaining after imatinib exposure.

112 Analysis of CFSE-labeled cells proliferating in the allogeneic hosts

113 Analysis of CFSE-labeled RTE and control unlabeled naive CD4 cells i

114 Analysis of CFSE-staining profiles established that resting tetramer

115 cytotoxicity was determined by clearance of CFSE-labeled target cells.

116 found that this increased the efficiency of CFSE-labeled parasite entry into monocytes (84.6% +/- 8.

117 gene therapy, we first followed the fate of CFSE-labeled B cell blasts.

118 By contrast, a higher frequency of CFSE+ T lymphocytes in the small intestine was detected

119 h traditional assays involving inhibition of CFSE dilution and cytokine production.

120 IR of CFSE(low) Tc correlated significantly with IR of proinfl

121 roduction in vitro and by in vivo killing of CFSE-labeled targets.

122 ls of chemokines and can induce migration of CFSE-labeled macrophages and splenocytes.

123 By 5 days, similar numbers of CFSE(+) NK cells were still easily detected in IL-15(+/-

124 Furthermore, the proliferation of CFSE-labeled OT-1 cells in response to OVA cross-present

125 effector systems mediating the rejection of CFSE-labeled allogeneic splenocytes after an infection o

126 T cells was examined using the technique of CFSE dye dilution and flow cytometry.

127 Using adoptive transfer of CFSE-labeled cells, we first demonstrated that alloreact

128 bacterial infection by adoptive transfer of CFSE-labeled monoclonal and polyclonal T cells.

129 ems, as well as in vivo adoptive transfer of CFSE-labeled OT-II cells, we demonstrated the presence o

130 Adoptive transfer of CFSE-labeled TCR-transgenic T cells into B6 recipients t

131 ation was estimated using (3) H-thymidine or CFSE labeling and ICAM-1 blocking.

132 he CD4+CD25+ T cells using [3H]TdR uptake or CFSE dilution.

133 significantly more (P <.003) CFSE-positive (CFSE(+)) NK cells were found in control mice than in IL-

134 antigens, the survival and growth of primary CFSE-labeled CLL cells in vivo is achieved and quantifie

135 er counts were observed for all proliferated CFSE(low) T-cell subsets among rejectors, compared with

136 ramer(+) and allergen-induced proliferating (CFSE(lo) ) CD4(+) T cells by flow cytometry.

137 onor- and third-party-induced proliferation (CFSE(low)) of the T cells was reported as the immunoreac

138 We have used purified CFSE-labeled B cells and an adoptive transfer model syst

139 timates can be obtained from the more recent CFSE data which allow to track the number of divisions e

140 Proliferative responses of recipient CFSE-labeled T cells to donor or third party DC, cytokin

141 males, and vaccinated males failed to reject CFSE-labeled male splenocytes in vivo.

142 ion (MLR) culture, we have found that sorted CFSE(bright) (5-(and-6)-carboxyfluorescein diacetate suc

143 s was assessed by propidium iodide staining, CFSE labeling profiles, [(3)H]thymidine uptake, and up-r

144 In contrast, allergen-stimulated CFSE(lo) CD4(+) T cells contain extremely high fractions

145 boxyfluorescein-diacetate-succinimidylester (CFSE) dilution assay.

146 was no difference in cell survival or in the CFSE dilution profiles.

147 ubstantial clonal expansion, and loss of the CFSE label.

148 Of the CFSE-high cells, 82.4% were positive for the HCV protein

149 e HCV protein NS5A, whereas only 1.2% of the CFSE-low cells were positive for this protein.

150 hereas in nontumor-challenged recipients the CFSE(+) Th1 cells localized only within the T cell zones

151 Significantly, the CFSE(bright) CD25(-) cells recovered from these cultures

152 Thus, CFSE-labeled OT-I cells greatly proliferated in these ti

153 cells were then added as third components to CFSE-labeled responding cells in freshly prepared primar

154 illustrate this technique by applying it to CFSE data taken from the literature.

155 In vivo tracking of adoptively transferred CFSE-labeled splenocytes from LTS showed equivalent FACS

156 ivo, we boosted BALB/c hosts of transferred, CFSE-labeled HA-specific memory CD4 T cells with native

157 Separation of proliferating cells based upon CFSE fluorescence intensity showed that daughter cells f

158 We measured T-cell responses using CFSE-labeled recipient lymphocytes in a direct one-way M

159 irculating human B cell subsets, an in vitro CFSE dilution assay was used for the assessment of proli

160 an in vitro coculture system and an in vivo CFSE-based adoptive transfer model indicate that lymphoc

161 ed recombinant allergens in conjunction with CFSE staining allow the dissection of allergen-specific

162 B cells from human tonsils were labeled with CFSE and stimulated in vitro with complement-coated anti

163 with the D(b)NP(366) tetramer, labeled with CFSE, and transferred into normal Thy-1.2(+) recipients.

164 confirmed by adoptive transfer studies with CFSE-labeled T cells.

165 eral pro- and anti-apoptotic proteins within CFSE-labeled cultures.