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1 1 and Th2 cytokine network and systemic host allospecific Ab (allo-Ab) responses in the development o
2 notypically hostile NK cells that express an allospecific activating receptor without coexpressing an
3 vitro study quantified CD103+ T cells after allospecific activation with and without exogenous TGFbe
4 e findings highlight surprisingly asymmetric allospecific alterations in iNKT cells as they develop a
5 not be of donor origin, suggesting that both allospecific and non-allospecific mechanisms regulate en
6 freshly prepared primary MLRs, to determine allospecific and nonspecific inhibitory and Treg recruit
7 to investigate how immunosuppression affects allospecific and pathogen-specific memory B cells, and r
8 mulated with HLA class I antibody (W6/32) or allospecific antibodies from sensitized patients (n=6) w
10 f this study was to test the contribution of allospecific antibody-secreting cells (ASCs) from differ
11 (r=0.682, P=0.005) and inversely with IR of allospecific, antiinflammatory, CTLA4(+)Tc-M (r=-0.638,
15 alloantibody responses, with splenic GCs and allospecific bone marrow plasma cells readily detectable
16 estigated the development and maintenance of allospecific CD103 T cells within the tubular microenvir
17 sayed for allospecific CD154CD19 B cells and allospecific CD154 TcM in 16-hr live-cell mixed leukocyt
18 ed significantly with IR of proinflammatory, allospecific CD154(+)Tc-M (r=0.682, P=0.005) and inverse
20 ated monocytes correlated significantly with allospecific CD154+T-cytotoxic memory cells (Spearman r=
21 ng rATG concentrations, proportionately more allospecific CD154+T-cytotoxic memory cells (TcM) surviv
22 ic analyses, the rejection-risk threshold of allospecific CD154+T-cytotoxic memory cells (TcMs) assoc
30 d to the semi-direct pathway, as measured by allospecific CD4 (indirect) and CD8 T-cell clones (direc
33 fer model of TCR transgenic T cells to track allospecific CD4+ T cell expansion and trafficking chara
35 escribed factors affecting the generation of allospecific CD4CD25 forkhead/winged helix transcription
37 ergized to promote expansion and survival of allospecific CD8 CD103 T cells in vitro, but IL-15 down-
38 ions can strongly stimulate both NK cell and allospecific CD8 T cell responses, and these same effect
40 and adhesion molecules upon interaction with allospecific CD8 T suppressor cells or exposure to inhib
44 -1 reduced cytokine-induced proliferation of allospecific CD8+ cloned L3 T cells and OVA-reactive CD4
45 cytokine requirements for the generation of allospecific CD8+ CTL in vitro and have found that IL-4
47 In this study, we tested the role of IL-2 in allospecific CD8+ T cell memory by analyzing the long-te
48 endent inhibitory effect on proliferation of allospecific CD8+ T cells in mixed lymphocyte culture.
50 entical type 2 cytokine-inducing conditions, allospecific CD8+ T cells were primed to become IL-4, IL
54 95-ligand pathway; therefore the deletion of allospecific cells by donor spleen cells may be induced
55 1 partially protects HUVECs against lysis by allospecific class I MHC-restricted cytolytic T lymphocy
56 he differentiation of purified CD8+ PBL into allospecific, class I MHC-restricted CTL that lyse EC, b
57 PCR assays to monitor the levels of putative allospecific clonotypes in posttransplant blood samples
58 tosis by sHLA was analyzed by adding sHLA to allospecific CTL 4 or for 24 hr before flow cytometric a
60 ime course studies showed that DSBM impaired allospecific CTL activity whether given on day -10 (3.3%
61 tion, they show that both CD4(+)- and CD8(+)-allospecific CTL can be isolated from rejected allogenic
65 nto F(1) hosts stimulates the development of allospecific CTL effectors that eliminate host lymphocyt
67 neal cells produced a profound inhibition of allospecific CTL, DTH, and mixed-lymphocyte responses.
68 ells produces a dose-dependent inhibition of allospecific CTL, DTH, and mixed-lymphocyte responses.
69 costimulation blockade are able to generate allospecific CTL- and IFN-gamma-producing T cells within
72 s, providing evidence that the generation of allospecific CTLs during acute LCMV infection is antigen
73 ed, cardiac allografts and the generation of allospecific CTLs were not impaired in the absence of IL
75 yme-linked immunospot assay for detection of allospecific cytokines produced by individual human PBLs
77 and engage MHC class I antigens, leading to allospecific cytolytic responses and graft rejection.
79 BM infusion significantly reduced intragraft allospecific cytolytic T-cell (CTL) activity compared wi
80 alloantibody levels correlated with in vivo allospecific cytotoxic activity in CD8 knockout hepatocy
82 ng the 19 clones analyzed: 1) TCR alphabeta+ allospecific cytotoxic cells, 2) TCR alphabeta+ nonspeci
84 mulated the proliferation and development of allospecific cytotoxic effectors in vitro and in vivo.
85 The demonstration of cloned, TCR alphabeta+, allospecific cytotoxic effectors provides the strongest
86 Administering IL-18 significantly enhanced allospecific cytotoxic function and expansion of CD8(+)
87 Moreover, mdr1a-/- T cells produced strong allospecific cytotoxic responses comparable to those of
88 alized splenic T lymphocyte subsets, reduced allospecific cytotoxic T lymphocyte activity, and increa
95 injected s.c. into naive recipients induced allospecific delayed hypersensitivity and elicited delay
99 ition to graft survival, graft infiltration, allospecific delayed-type hypersensitivity (DTH), and cy
107 T cells as helper cells in the generation of allospecific effector macrophages in corneal graft rejec
108 ransgenic model, blockade of TIM-3 increased allospecific effector T cells, enhanced Th1 and Th17 pol
110 However, DNA fragmentation induced by either allospecific FasL-defective CTL, or by perforin-deficien
111 ce from animal studies has demonstrated that allospecific FoxP3(+)CD4(+) regulatory T (Treg) cells ex
113 results indicate the importance of adequate allospecific helper as well as effector T cells for the
114 igen, we identified and cloned a TCR from an allospecific HLA-A2-restricted, HCV:NS3:1406-1415-reacti
116 accompanied by markedly increased numbers of allospecific, IFN-gamma-producing cells in the periphery
119 lockade, there was a diminished frequency of allospecific IL-10-producing cells and an increased freq
120 proved ability to define the strength of the allospecific immune response by enzyme-linked immunospot
125 atibility complex disparate skin grafts, the allospecific immunoglobulin (Ig)G response was markedly
127 skin transplantation, increased induction of allospecific iTregs and a reduction in T effector respon
128 The CD8(+) Ly49G2(+) population mediated no allospecific killing, nor was any NK-like killing observ
132 itro analyses revealed that the apoptosis of allospecific memory CD8(+) T cells is significantly incr
135 nswer this question, we investigated whether allospecific naive or memory T cells can mediate acute c
137 , cell-extrinsic signals appeared to dictate allospecific patterns of Ly49 receptor expression and li
138 -restricted T cell hybridoma (B4.2.3), or an allospecific, peptide-dependent, T cell hybridoma (3DT52
141 0-producing CD8 T cells strongly inhibit the allospecific proliferation of naive CD8 T cells to monoc
142 y, fully mismatched graft were performed and allospecific proliferation was measured after depletion
145 is assay can thereby be helpful in assessing allospecific regulatory effects of diverse immunosuppres
146 oughout the overall T-cell repertoire, one's allospecific repertoire is similarly made up of cells in
147 man cells and tested agents known to inhibit allospecific responses for their ability to inhibit xeno
149 grafts, the CD8+ Vbeta8+ cells demonstrated allospecific responses that were numerically larger than
150 d acute lung allograft rejection and reduced allospecific responsiveness by markedly decreasing monon
153 this drug interfere with the persistence of allospecific suppressor cells for 35 days after the graf
156 )) phenotype and were capable of suppressing allospecific T cell proliferation and IFN-gamma producti
157 eks following rejection, however, the memory allospecific T cell response became predominant in the r
158 of C5aR in both graft and recipient reduced allospecific T cell responses and prolonged renal allogr
159 T cells modulates their function, enhancing allospecific T cell responses that lead to allograft rej
161 llo-Ab responses and induction of peripheral allospecific T cell unresponsiveness both in vitro and i
162 g of donor Th2 cell therapy, host-anti-donor allospecific T cells acquired Th2 polarity, persisted po
164 olecules and were less potent at stimulating allospecific T cells after an additional 48-hour culture
166 tible with either deletion or suppression of allospecific T cells as possible mechanisms of tolerance
167 the DLN whether it contains naive or memory allospecific T cells as shown in experiments in which re
168 alysis of the phenotype and proliferation of allospecific T cells expanded in vitro in the presence o
170 directed to tissue antigens but differ from allospecific T cells in several important respects, refl
173 ining demonstrated that early recruitment of allospecific T cells into allografts around POD10 correl
174 ascularization and that early recruitment of allospecific T cells into the grafts promotes destructio
175 cells and/or soluble MHC Ags suppresses NIMA-allospecific T cells of the offspring, predisposing to o
176 ively, these results suggest that peripheral allospecific T cells undergo the initial stages of activ
177 These innate immune cells, in addition to allospecific T cells, can damage cardiomyocytes directly
183 llorecognition is responsible for generating allospecific T follicular helper cells remains unclear.
187 CMV characteristically induces an anti-H2(d) allospecific T-cell response that includes T-cell clones
188 T-cell costimulatory blocking agents inhibit allospecific T-cell responses in vitro and prevent allog
189 cooperation, CD154 has been used to identify allospecific T-cytotoxic memory cells (TcM) for rejectio
191 R alphabeta+ nonspecific cytotoxic cells, 3) allospecific TCR alphabeta+ noncytotoxic cells, 4) TCR a
193 ) infected with influenza A virus have lower allospecific Th1-cell stimulatory abilities than DCs act
194 s also developed vigorous primary and memory allospecific Th1/Th2 responses that exceeded the respons
195 , because neonatal antigen exposure triggers allospecific Th2 CD4 memory cells, whereas antigen expos
196 her show that LCMV prevents the induction of allospecific tolerance and mixed hematopoietic chimerism
197 es, without CD40-CD40L costimulation, induce allospecific tolerance but may trigger allo-independent
198 ade is most effective at inducing long-lived allospecific tolerance if anergy and regulation can be e
199 ese findings illustrate the robust nature of allospecific tolerance in prenatal mixed chimerism compa
201 CD40L-/- transplant recipients developed allospecific tolerance to the donor haplotype; second se
202 as an efficacious cellular therapy to induce allospecific tolerance to transplantation antigens.
205 tive NKT cells are required for induction of allospecific Tr cells and are essential for survival of
206 B/c mice, and the adoptive transfer of these allospecific Tr cells to Jalpha281 KO mice allowed a 50%
208 MMc) has been associated with development of allospecific transplant tolerance, antitumor immunity, a
211 s has demonstrated that adoptive transfer of allospecific Tregs offers greater protection from graft
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