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1 d with impaired glycolysis and signaling via interleukin 2.
2 f both the magnitude of the TCR stimulus and Interleukin 2.
3 le by exogenous PD-1 blockade or addition of interleukin 2.
4 modified vaccinia Ankara expressing MUC1 and interleukin 2.
5 cells, by enhancing their responsiveness to interleukin-2.
6 ecrosis factor-alpha, and to a lesser extent interleukin-2.
7 regulate CD69 surface expression and secrete interleukin-2.
8 liferation in vitro that could be rescued by interleukin-2.
11 eased, were interleukin-4 (18.0 [6.0-54.2]), interleukin-2 (11.8 [4.3-32.2]), angiopoietin-2 (6.4 [1.
12 or the synthesis of N-(4-(18)F-fluorobenzoyl)interleukin-2 ((18)F-FB-IL2) and the in vitro and in viv
13 which include interferon alpha and gamma and interleukin 2, 2R, 6, 7, 12, 15, 17, and 18, across diff
14 forming cells (SFCs) of interferon gamma and interleukin 2, 4, 5, and 6 were counted by means of enzy
17 ce was reported had higher concentrations of interleukin 2, 6, and 10, interferon gamma, tumor necros
21 -type cells and bypassed the requirement for interleukin-2 administration to sustain in vivo activity
23 defects in allogeneic T-cell proliferation, interleukin 2 and interferon gamma (IFN-gamma) productio
25 CCL2, CCL4, CCL13, CCL17, CXCL8, CXCL10; and interleukin 2 and interferon gamma than children who sur
26 nefit from immunotherapies such as high-dose interleukin 2 and ipilimumab, which, by contrast with BR
27 evelopment of CD4(+) T cells that coproduced interleukin 2 and tumor necrosis factor alpha and were a
28 coproteins form supramolecular clusters with interleukin-2 and -15 receptors in lipid rafts of T cell
29 n T cells (T-bet) expression and recovery of interleukin-2 and interferon-gamma production and cytoly
31 po crystal structure; iii) visualisations of interleukin-2 and its homologues highlight conserved poc
32 od-stage specific CD4(+) T cells coproducing interleukin-2 and tumor necrosis factor alpha (P = .003)
33 sus controls) and lower levels of binding to interleukins 2 and 10 core promoter regions of the trans
34 interferon-gamma/tumor necrosis factor-alpha/interleukin-2), and proliferation-related markers (CD119
35 d the expression of T-bet, interferon gamma, interleukin 2, and the antiapoptotic molecule Bcl-2, whe
36 cterized for expression of interferon-gamma, interleukin 2, and tumor necrosis factor alpha and surfa
37 f CD4(+) T cells for detection of IFN-gamma, interleukin 2, and tumor necrosis factor alpha was perfo
38 culating levels of type 1 (interferon gamma, interleukin 2, and tumor necrosis factor alpha) and type
39 in vitro T cell expansion in the presence of interleukin-2, and ex vivo staining with HCV peptide-loa
42 medically relevant proteins--beta-lactamase, interleukin-2, and RNase H--even in the absence of any l
44 ed intracellular levels of interferon gamma, interleukin-2, and tumor necrosis factor alpha in HBV-sp
47 lls produced tumor necrosis factor alpha and interleukin 2 at the intrahepatic level significantly mo
48 ascular endothelial growth factor A (VEGFA), interleukin-2, bone morphogenetic protein-10, VEGFC, and
50 ation and production of interferon-gamma and interleukin-2 by intrahepatic and peripheral T cells fro
53 enhanced CD25 and CD69 expression, increased interleukin-2 expression, and improved proliferation of
54 EDA-fibronectin (EDA-Fn), when conjugated to interleukin-2 (F8-IL2) can effectively inhibit the growt
55 t the first use to our knowledge of low-dose interleukin 2 for treating severe AA by promoting the re
58 l killer (NK)-cell differentiation defect in interleukin-2 gamma-chain receptor (IL2RG)/JAK3 severe c
61 responses were screened by gamma interferon/interleukin-2 (IFN-gamma/IL-2) FluoroSpot using autologo
62 of T-helper type 1 intracellular cytokines (interleukin 2, IFN-gamma, and tumor necrosis factor alph
63 ting of dacarbazine, cisplatin, vinblastine, interleukin-2, IFN alfa-2b (IFN-alpha-2b) and granulocyt
64 equencies of interferon gamma (IFN-gamma(+))/interleukin 2 (IL-2(+))/tumor necrosis factor alpha (TNF
65 of regulatory T cells (Treg cells) requires interleukin 2 (IL-2) and agonist T cell antigen receptor
67 ria monocytogenes epitope, elicited distinct interleukin 2 (IL-2) and phosphorylated kinase Erk respo
68 er levels of interferon gamma (IFN-gamma) or interleukin 2 (IL-2) ELISpot responses compared with eac
70 e introduction of a targeted mutation in the interleukin 2 (IL-2) receptor common gamma chain (IL2rg(
76 CD8(+) T cells by inflammatory mediators and interleukin 2 (IL-2) via pathways dependent on the metab
77 ncludes simian immunodeficiency virus (SIV), interleukin 2 (IL-2), and IL-15 DNAs, recombinant modifi
78 d secretion of interferon gamma (IFN-gamma), interleukin 2 (IL-2), and tumor necrosis factor alpha (T
80 rted their regulatory function by inhibiting interleukin 2 (IL-2)-dependent de novo differentiation o
85 d levels of interferon gamma (IFN-gamma) and interleukin 2 (IL-2; markers of VZV-specific cell-mediat
87 compared to CD8(+) T cells) that coexpressed interleukin-2 (IL-2) (66.4%) and/or tumor necrosis facto
88 tumor necrosis factor alpha (TNF-alpha), and interleukin-2 (IL-2) (P < 0.001) and splenic and lung CD
89 nfiltrating lymphocytes (TILs) and high-dose interleukin-2 (IL-2) administered to lymphodepleted pati
92 maintained CD25 expression and responded to interleukin-2 (IL-2) and CD27, which together programmed
93 ne function via changes to cytokines such as interleukin-2 (IL-2) and IL-10 and may predict disease p
95 to selectively up-regulate the production of interleukin-2 (IL-2) and interferon-gamma (IFN-gamma) an
96 -associated CXCR3/CCR5 and TNFalpha/IFNgamma/interleukin-2 (IL-2) and less TH2-associated CCR3/CCR4,
97 of antigen-specific Treg cells induced with interleukin-2 (IL-2) and transforming growth factor beta
98 vation from latency but inhibits CD3-induced interleukin-2 (IL-2) and tumor necrosis factor alpha (TN
99 roliferative capacity and ability to secrete interleukin-2 (IL-2) and tumor necrosis factor alpha (TN
100 ccination induced an increased expression of interleukin-2 (IL-2) by Gp120-specific CD4(+) T cells in
102 tumor necrosis factor-alpha (TNF-alpha) and interleukin-2 (IL-2) cytokines with a rate of approximat
103 e data obtained with overlapping peptides in interleukin-2 (IL-2) enzyme-linked immunosorbent spot (E
104 ay, normally activated by cytokines from the interleukin-2 (IL-2) family to promote cell proliferatio
105 consisting of the immunostimulatory cytokine interleukin-2 (IL-2) genetically fused to an antibody sp
107 ifferentiation and in particular the role of interleukin-2 (IL-2) in promoting or inhibiting Th diffe
117 tigen on ACT cells (Thy1.1) or an engineered interleukin-2 (IL-2) molecule on an Fc framework as targ
118 ly, antibody-mediated blockade of IFN-gamma, interleukin-2 (IL-2) or interleukin-15 receptor beta (IL
121 hrough the T-cell antigen receptor (TCR) and interleukin-2 (IL-2) provide major inputs for mTORC1 act
122 ex virus 1 (HSV-1) constitutively expressing interleukin-2 (IL-2) provokes central nervous system (CN
123 Treg cells led to reduced expression of the interleukin-2 (IL-2) receptor alpha subunit CD25, accumu
124 udies now highlight deficiencies in both the interleukin-2 (IL-2) receptor and its downstream signali
125 ymocyte globulin (r-ATG), alemtuzumab, or an interleukin-2 (IL-2) receptor blocker and were discharge
126 t of human AML cells in NOD-SCID gamma (with interleukin-2 (IL-2) receptor gamma chain deficiency) mi
127 ody, Toll-like receptor 7 (TLR7) agonist and interleukin-2 (IL-2) reduced T cell apoptosis but did no
129 multiple sclerosis (RRMS) because of altered interleukin-2 (IL-2) secretion and IL-2 receptor (IL-2R)
130 T cells inhibited T cell receptor (TCR) and interleukin-2 (IL-2) signaling and upregulated PD-1, lea
131 tion of kynurenine correlates with defective interleukin-2 (IL-2) signaling in memory CD4 T cells fro
133 iation of pathogenic Trm cells revealed that interleukin-2 (IL-2) signaling was required for residenc
134 ase 1 studies identified a low daily dose of interleukin-2 (IL-2) that was well tolerated, did not ex
136 ering therapeutic doses of recombinant human interleukin-2 (IL-2) to AGMs, we show here that this mec
139 frequency of interferon-gamma (IFN-gamma)(+) interleukin-2 (IL-2)(-) CD8(+) T cells (r = -0.6, P = 0.
141 py with cisplatin, vinblastine, dacarbazine, interleukin-2 (IL-2), and interferon alfa as part of a c
142 with reduced expression of interferon-gamma, interleukin-2 (IL-2), and soluble IL-2Ralpha, but did no
143 d through the in vitro addition of exogenous interleukin-2 (IL-2), and the in vivo blockade of the re
145 ly, and very few cells produce IFN-gamma and interleukin-2 (IL-2), compared with transgenic T cells i
146 OT-II T cells to proliferate and to secrete interleukin-2 (IL-2), demonstrating a functional consequ
147 unctional and able to simultaneously produce interleukin-2 (IL-2), gamma interferon (IFN-gamma), and
148 re elevated frequencies of T cells producing interleukin-2 (IL-2), IL-10, and IL-17 and decreased IL-
150 e show that the T cell homeostatic cytokines interleukin-2 (IL-2), IL-7, and IL-15 can induce CD4 dow
151 4+ T cells was induced in vitro by anti-CD3, interleukin-2 (IL-2), IL-7, or IL-15 but not by Toll-lik
152 confer susceptibility to type 1 diabetes at interleukin-2 (IL-2), IL2/4q27 (rs2069763) and renalase,
153 at distinguished LTBI from controls included interleukin-2 (IL-2), monocyte chemotactic protein 2 (MC
155 the activation markers CD40 ligand (CD40L), interleukin-2 (IL-2), tumor necrosis factor alpha (TNF-a
157 PB CD4(+) T cells produced predominantly interleukin-2 (IL-2), whereas CD4(+) and CD8(+) T-cell s
158 h factor-beta (TGF-beta)-activated Smad3 and interleukin-2 (IL-2)-activated Stat5 facilitated Tet1 an
160 e investigated the regulation of the size of interleukin-2 (IL-2)-producing CD4(+) T cell (IL-2p) poo
165 with DNA simian immunodeficiency virus (SIV)/interleukin-2 (IL-2)/IL-15, SIV Gag/Pol/Env recombinant
166 n FOXP3(hi), CD127(lo) Tregs), expresses the interleukin-2 (IL-2)/STAT5 pathway and cell-cycle commit
167 tumor necrosis factor alpha [TNF-alpha], and interleukin 2 [IL-2]) and cytolytic molecules (granzyme
168 or [gammadelta-TCR]) and cytokines examined (interleukin 2 [IL-2], IL-4, IL-10, IL-17A, and gamma int
169 revealed a defect in the expression of CD25 (interleukin-2 [IL-2] receptor alpha chain) on Ad5-elicit
170 tumor necrosis factor alpha [TNF-alpha], and interleukin-2 [IL-2]) and type 17 (IL-17A and/or IL-17F)
171 tumor necrosis factor alpha [TNF-alpha], and interleukin-2 [IL-2]), and the cytolytic mediator granzy
172 ma and/or tumor necrosis factor [TNF] and/or interleukin-2 [IL-2])-producing CD4(+) and CD8(+) T cell
173 secretion of candidate cytokines/chemokines (interleukin-2 [IL-2], IL-6, IL-10, MIP-1alpha, and RANTE
174 yze T-cell activation markers (CD107, CD154, interleukin-2 [IL-2], tumor necrosis factor [TNF], and I
175 PREX1-Rac1-signaling pathway that stabilizes interleukin-2(IL-2), IL-4, and IL-10 messenger RNA (mRNA
179 SCM cells had increased abilities to secrete interleukin-2 in response to viral antigen, while secret
182 hibitor of both Bruton's tyrosine kinase and interleukin-2 inducible kinase (ITK), has been used to t
186 Given its critical role in T-cell signaling, interleukin-2-inducible kinase (ITK) is an appealing the
192 Tato et al. demonstrate that high amounts of interleukin-2 inhibit production of this critical T effe
194 by intracellular staining for the cytokines interleukin 2, interferon gamma, and tumor necrosis fact
195 Expression of proinflammatory cytokines interleukin 2, interferon gamma, tumor necrosis factor a
196 week 24 with appearance of HIV gag-specific interleukin 2, interferon-gamma, and CD107a responses in
197 have been conjugated via this method include interleukin-2, interferon-alpha, ubiquitin, antibodies a
198 f proinflammatory and profibrotic cytokines (interleukin-2, interferon-gamma, and interleukin-17) whe
199 m antigen, and interferon gamma (IFN-gamma), interleukin 2, interleukin 10, and tumor necrosis factor
201 vels of interferon gamma, interleukin 1beta, interleukin 2, interleukin 6, and interleukin 13 were si
202 terferon gamma (IFNgamma), interleukin1beta, interleukin 2, interleukin 6, interleukin 10 (IL-10), an
204 gnificantly higher admission serum levels of interleukin-2, interleukin-12, interferon-gamma, and tum
206 active protein, tumor necrosis factor-alpha, interleukin-2, interleukin-6, and interleukin-8) have be
207 at this infection leads to the production of interleukin-2, interleukin-6, and transforming growth fa
209 lysis further implicates IFNgamma, IFNalpha, interleukin-2, interleukin-7, CTLA-4 (cytotoxic T-lympho
210 ependent type I interferon signaling and the interleukin-2/interleukin-2 receptor alpha pathway for t
211 ith Leishmania-specific interferon gamma and interleukin 2 levels, and negatively with Leishmania ski
213 explored 2 means to increase Tregs in cGVHD: interleukin-2/monoclonal antibody (IL-2/mAb) complexes a
214 h and without preactivation by interleukins (interleukin-2 or interleukin-6), was evaluated in the pr
217 m the fMLP signal, while only 15.2 or 22.2% (interleukin-2-or interleukin-6-activated) of preactivate
219 d NKp30/MAPK/IL-12 (interleukin-12) or IL-2 (interleukin-2) pathway was susceptible to NK lysis.
220 tumor necrosis factor-alpha [TNF-alpha] and interleukin-2 pathways), and research on intravitreal bi
221 oly(I . C)LC induced potent multifunctional (interleukin 2-positive [IL-2(+)], tumor necrosis factor
222 n levels of interferon gamma (IFN-gamma) and interleukin 2 produced by T-helper 1 cells when comparin
224 interferon, tumor necrosis factor alpha, and interleukin-2 production and CD107(a/b) cytotoxic degran
225 activated T-cells (NFAT) transcription, and interleukin-2 production in Jurkat or primary T-cells.
227 imilarly, we found that lenalidomide-induced interleukin-2 production in T cells is due to depletion
228 Old observations, such as the decreased interleukin-2 production, are better understood with our
229 e normal T cell receptor (TCR) signaling and interleukin-2 production, WASHout T cells demonstrate si
233 Treg activity, by inducing the production of interleukin 2 proinflammatory cytokines in these cells.
234 , or a combination (29/37), elevated soluble interleukin 2 receptor (20/21), and elevated VEGF (16/20
235 genitors by augmenting responsiveness of the interleukin 2 receptor (IL-2R) and transcription factor
236 ells), which have abundant expression of the interleukin 2 receptor (IL-2R), are reliant on IL-2 prod
238 te (gamma interferon [IFN-gamma] and soluble interleukin 2 receptor alpha [sIL-2Ralpha]) and adaptive
239 le tumor necrosis factor receptor 2, soluble interleukin 2 receptor alpha, soluble gp130, soluble CD2
240 tandard immunosuppression with Thymoglobulin/interleukin 2 receptor blocker and mycophenolate mofetil
241 odeficiency (SCID-X1) caused by mutations in interleukin 2 receptor gamma (IL2RG) gene threatens the
243 2Mit80, an interval that includes Il2ra (for interleukin 2 receptor, alpha chain), a gene that is kno
247 tosis reporter system using a chimera of the interleukin-2 receptor alpha (previously referred to as
248 n, soluble interleukin-1 receptor I, soluble interleukin-2 receptor alpha, and tumor necrosis factor
249 e clearance was also similar between groups (interleukin-2 receptor antagonist group 56 +/- 20 mL/min
250 e low and similar between groups (10% in the interleukin-2 receptor antagonist group vs 6% in the RAT
251 The impact of induction (thymoglobulin, interleukin-2 receptor antagonists [IL-2RA], or alemtuzu
252 antithymocyte globulin (RATG) compared with interleukin-2 receptor antagonists in a racially diverse
253 tandard induction immunosuppression was with interleukin-2 receptor antagonists, and antithymocyte gl
255 isk of BPAR compared with induction with the interleukin-2 receptor antibodies (IL-2RAs): basiliximab
256 lso distinguished patients who received anti-interleukin-2 receptor antibodies from those who receive
257 phenolate mofetil, corticosteroids, and anti-interleukin-2 receptor antibody induction, results in im
258 phenolate mofetil, corticosteroids, and anti-interleukin-2 receptor antibody induction, was associate
261 tion treatments (alemtuzumab, thymoglobulin, interleukin-2 receptor blockers, and no induction) given
262 is due to mutations in the gene encoding the Interleukin-2 receptor gamma chain (IL-2Rgamma), leading
263 of iCD8alpha cells depends on expression of interleukin-2 receptor gamma chain (IL-2Rgammac), IL-15,
264 rus-based gamma-retrovirus vector expressing interleukin-2 receptor gamma-chain (gammac) complementar
265 r-like effector nucleases (TALENs) to target interleukin-2 receptor subunit gamma (IL2RG) in pronucle
266 ody that binds to CD25 (alpha subunit of the interleukin-2 receptor) and modulates interleukin-2 sign
268 1beta, and interleukin-7) as well as soluble interleukin-2 receptor-alpha were significantly elevated
269 ry group, whereas interleukin-1beta, soluble interleukin-2 receptor-alpha, interleukin-4, interleukin
275 eron gamma, tumor necrosis factor alpha, and interleukin 2) responses were discordant in frequency an
276 and CD8+ T cells and a higher proportion of interleukin 2-secreting cells (P = .01 and P = .002, res
277 and enhanced TCR-induced CD69 upregulation, interleukin-2 secretion, and proliferation to promote vi
281 alpha (tissue necrosis factor-alpha) and IL (interleukin)-2 soluble receptors and NT-proBNP (N-Termin
282 BTLA(-) T cells but more IFN-gamma, TNF, and interleukin-2 than the highly dysfunctional subset expre
283 y a rapid response team for complications of interleukin-2 therapeutic infusions were subsequently ex
284 ll differentiation by limiting the access of interleukin 2 to CD4(+) T cells, thereby enhancing Tfh c
285 co-operates with growth factor TGF-beta and interleukin-2 to activate Tet-mediated DNA demethylation
286 tumor necrosis factor alpha (TNF-alpha), and interleukin 2 together, compared with delayed vaccinatio
288 4 cytokines evaluated (ie, interferon gamma, interleukin 2, tumor necrosis factor alpha, and granzyme
289 the functional diversity (ie, CD107, CD154, interleukin 2, tumor necrosis factor, and interferon gam
290 vely studying five effector functions (i.e., interleukin-2, tumor necrosis factor-alpha, interferon-g
291 g aspartate-directed protease 3 (caspase-3), interleukin-2, tumor necrosis factor-related apoptosis-i
292 rophage colony-stimulating factor) and IL-2 (interleukin-2), two pleiotropic cytokines of the mammali
294 ng on the well-characterized T-cell cytokine interleukin-2, we show how cytokine secretion and compet
295 eron gamma, tumor necrosis factor alpha, and interleukin 2 were quantified using intracellular cytoki
297 lpha (TNF-alpha) but not interferon gamma or interleukin 2 which had a differentiated effector phenot
298 erative capacity and produced cytokines like interleukin-2, while revealing similar suppressive poten
299 or-antigen-targeting antibody, a recombinant interleukin-2 with an extended half-life, anti-PD-1 and
300 2 hours and then cultured in the presence of interleukin-2 with vehicle control or the SSRI (10(-6) m
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