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1 oxicity compared with higher doses of either lymphokine.
2 ny, IL-5 receptors and do not respond to the lymphokine.
3 ed by massive production of IL-5, a Th2-type lymphokine.
4 redominant mediators for a limited number of lymphokines.
5 h MalE-OVA-expressing bacteria produced both lymphokines.
6 inocytes in response to a cocktail of T cell lymphokines.
7 f cytokine expression, but not of TH-related lymphokines.
8 nd Th2 (interleukin 4 [IL-4] and IL-10) type lymphokines.
9 d psoriatic skin, in combination with T cell lymphokines.
10 irect CD4(+)-CD8(+) T cell communication via lymphokines.
11 emoved using Abs specific for the respective lymphokines.
12 ess A2ARs than are cells that do not produce lymphokines.
13 n of a continuously growing B cell line with lymphokines, a switch to Ig micrometer secretory mRNA an
14 ural killer (NK) cells, NK cytotoxicity, and lymphokine activated killer (LAK) cytoxicity, and a sign
15 or T cell fraction derived from heterologous lymphokine activated killer cells kills those tumor cell
18 ripheral blood (APB) MNCs in terms of NK and lymphokine-activated killer (LAK) activities and cytokin
20 al killer (NK) cell number and cytotoxicity, lymphokine-activated killer (LAK) cell number and activi
21 jugate formation is an essential step during lymphokine-activated killer (LAK) cell-mediated cytotoxi
22 cant (P <.01) decrease in natural killer and lymphokine-activated killer (LAK) cell-mediated cytotoxi
23 ytokine production and cytotoxic activity of lymphokine-activated killer (LAK) cells and determined w
26 erein describe immunotherapy with autologous lymphokine-activated killer (LAK) cells in seven patient
27 intratumor adenosine impairs the ability of lymphokine-activated killer (LAK) cells to kill tumor ce
28 rleukin-2 (IL-2)-induced natural killer (NK)/lymphokine-activated killer (LAK) cells use perforin and
29 of baboon and human natural killer (NK) and lymphokine-activated killer (LAK) cells were compared.
30 om conventional natural killer (NK) cells or lymphokine-activated killer (LAK) cells, because they co
31 CAR) T cells, CAR natural killer (NK) cells, lymphokine-activated killer (LAK) cells, gammadelta T ce
35 expressed on all C57BL/6 IL-2-activated NK (lymphokine-activated killer (LAK)) cells, all splenic an
36 tease that is expressed predominantly in the lymphokine-activated killer (LAK)/natural killer (NK) co
37 ese mAbs inhibited the anti-CD3-directed and lymphokine-activated killer activity of the P815 cell li
38 cell proliferative responses, generation of lymphokine-activated killer activity, and development of
39 (IL-2) nor the induction of IL-2-stimulated lymphokine-activated killer activity, however, was inhib
41 cytotoxic T lymphocyte, natural killer, and lymphokine-activated killer cell activities compared wit
42 hocyte activity, and both natural killer and lymphokine-activated killer cell activities of graft non
43 oxic assay of PBL indicated the induction of lymphokine-activated killer cell activity, but no eviden
49 uces production of IFN-gamma and augments NK/lymphokine-activated killer cell proliferation and funct
51 tion of murine and human T cell-mediated and lymphokine-activated killer cell-mediated cytotoxicity,
52 otoxic lymphocytes, natural killer cells and lymphokine-activated killer cells depend primarily on th
53 ytotoxic T lymphocytes and natural killer or lymphokine-activated killer cells is not blocked by BCR-
54 ndothelium and cytotoxicity against tumor by lymphokine-activated killer cells were not affected by P
56 ions in T cell differentiation, induction of lymphokine-activated killer cells, and regulation of imm
57 actions of different human effector cells, (lymphokine-activated killer cells, gammadelta T cells, c
58 atory research and clinical investigation of lymphokine-activated killer cells, tumour-infiltrating l
59 cid mice previously reconstituted with human lymphokine-activated killer cells, whereas treatment wit
64 mC and F genes in their MLR-derived CTLs and lymphokine-activated killer cells; removal of the PGK-ne
65 arge/zona occludens-1)-binding kinase/T-LAK (lymphokine-activated killer T cell) cell originating pro
67 de effects usually associated with classical lymphokine-activated killer therapy in association with
68 ities in a cytotoxic lymphocyte compartment (lymphokine-activated killer) and have normal lymphokine-
70 lymphokine-activated killer) and have normal lymphokine-activated killer-mediated cytotoxicity agains
71 ports of transformation of CTL into NK-like "lymphokine-activated killers" (LAK cells) under high dos
73 er each of four sequelae, with inhibition of lymphokine-activated killing induction being least sensi
74 cell-mediated cytotoxicity pathway, impairs lymphokine-activated killing, and decreases the proporti
76 stance to listerial infections of the liver, lymphokine-activated natural killer (LAK) cells were coc
77 in a wide variety of immune cells, including lymphokine-activated natural killer cells, resting T cel
78 ) that recognize only foreign MHC molecules, lymphokine-activated T cells that lack recognition speci
79 action (DTH) provided evidence for the first lymphokine activity: a lymphocyte-derived mediator calle
80 proliferation, and decreased expression of T lymphokines after stimulation by either anti-CD3 plus an
82 s, UUAUUUAU, present in the 3'-UTR of mature lymphokine and other cytokine transcripts, have been imp
83 ls are controlled by complex combinations of lymphokines and adhesion/costimulatory molecule signals.
84 h alpha beta T cells and are able to secrete lymphokines and express cytolytic activities in response
86 related to the secretory products (including lymphokines and proteinases) of the lymphocytic infiltra
87 al memory functions, such as secrete diverse lymphokines and provide cognate help to B cells, despite
88 rast to the selective and early reduction of lymphokines and the inducible form of nitric oxide synth
90 RNAs of many proto-oncogenes, cytokines and lymphokines are targeted for rapid degradation through A
93 gy can interfere with the delivery of helper lymphokines by T cells, resulting in a decreased capacit
94 To discover whether transgenic expression of lymphokines by the CTLs themselves might overcome these
95 ed by the finding that addition of exogenous lymphokines could restore PGE2-inhibited proliferation,
96 D40-independent DC sensitization, and direct lymphokine-dependent CD4(+)-CD8(+) T cell communication.
98 tes synthesis of IFN-gamma, while the latter lymphokine directly controls parasite growth and diminis
99 or alpha, interleukin 1, interleukin 6), and lymphokines (e.g. tumor necrosis factor beta, interleuki
100 y factor (MIF) is a secreted proinflammatory lymphokine essential for elicitation of delayed-type hyp
102 although RK has a role in the regulation of lymphokine gene expression in monocytes, it is not requi
104 ng its ability to block the transcription of lymphokine genes in activated T cells through formation
105 ctivation by preventing the transcription of lymphokine genes through binding to the intracellular pr
106 target genes, such as CD4 and CD8 as well as lymphokine genes, during the specialization of naive CD4
108 iii) absent responses to endogenous Th1 cell lymphokines (IFN-gamma and IL-2) but preserved responsiv
110 10 blockade or stimulation with antagonistic lymphokine IL-12 normalized baseline and CD3/CD28-induce
115 ns, enhanced production of mRNA encoding Th1 lymphokines in draining lymph nodes, and increased gamma
116 r patients can proliferate and form Th1 type lymphokines in the presence of autologous tumor cell whe
119 to investigate the interplay between the Th1 lymphokine interferon-gamma (IFNgamma) and pivotal cytok
121 IL-6, and tumor necrosis factor [TNF]-alpha; lymphokines: interferon-gamma, IL-2, IL-4, and TNF-beta)
122 s and the production of the T-helper-1 (Th1) lymphokines interleukin-2 (IL-2) and interferon-gamma (I
125 ssion of many proto-oncogenes, cytokines and lymphokines is regulated by targeting their messenger RN
126 tingly, IL-15, which licenses NKG2D-mediated lymphokine killer activity in CTLs, cooperates with NKG2
127 or status determine whether IL-15 can confer lymphokine killer activity-like properties to T cells.
129 press CD40, suggesting that T cell-CD40L and lymphokines may be involved in regulating FDC-CD23.
130 regions of many protooncogene, cytokine, and lymphokine messages target them for rapid degradation.
133 expressed constitutively elevated levels of lymphokine mRNA, including IL-4, IL-5, and IL-10, and we
134 ct of fibronectin in combination with T cell lymphokines on psoriatic uninvolved basal keratinocyte p
135 n along with proliferation (CD40 ligand plus lymphokines or Staphylococcus aureus protein A) induces
137 did not reveal any significant difference in lymphokine output, and isotype expression was not altere
138 in cultures of L929 cells treated with crude lymphokine preparations (LK) or with gamma interferon (I
139 tes to signals for proliferation provided by lymphokines produced by intralesional T lymphocytes in p
140 elper cell subsets (TH1 and TH2) reveal that lymphokine-producing cells are much more likely to expre
141 on in this gene lacks the ability to inhibit lymphokine production and lymphocyte proliferation.
142 documented by lower overall antigen-induced lymphokine production and proliferation, as well as dimi
144 These defects in thymocyte maturation and lymphokine production are IL-12 driven, since they are p
146 ropathogenic Escherichia coli (EPEC) inhibit lymphokine production by mitogen-activated human periphe
148 .2, 14.1, and 15.1-positive T cells, and the lymphokine production from the activated T cells is beli
152 ells (MDSCs) inhibited the proliferation and lymphokine production of wild-type CD4+ T cells in vitro
156 stimulation with vigorous proliferation and lymphokine production while retaining their specificity,
158 The T cells were assayed for proliferation, lymphokine production, and immunosuppressive activity.
159 anti-LFA-1 treatments on NSDC, intrahepatic lymphokine production, and the homing of lymphocytes to
168 In keeping with this, regulation of the lymphokine profile of CD4+ cells by CD8+ cells was consi
175 We conclude that an early CCR2-dependent Th1 lymphokine response predominates in normal DVT resolutio
176 favors certain signals that contribute to a lymphokine response that can mediate allergic inflammati
177 genic mice were primed by PCC injection, the lymphokine responses measured after in vitro antigen res
179 et gene promoters and might evoke their same lymphokine-responsive profile in immortalized progenitor
181 ns in vivo may lead to different patterns of lymphokine secretion and accumulation of cytokines (e.g.
183 d the antigen-specific antibody isotypes and lymphokine secretion by CD4+ T cells in BALB/c mice immu
185 mplex molecule ligands that induce selective lymphokine secretion or anergy in mature T cells in asso
186 Crohn's disease) is associated with altered lymphokine secretion profiles, as recently found in vari
188 de cytotoxicity, inhibition of viral growth, lymphokine secretion, and support of humoral and CD8 res
191 est that stimulation of OVA-specific CTLs by lymphokines seems to be more important to maintaining me
192 e expression is induced by the delivery of a lymphokine signal to antigen-activated B cells in a prim
193 ttractant protein-1 (MCP-1) in Ag-stimulated lymphokine synthesis and proliferation by CD4+ T cells d
194 ron-gamma (IFN-gamma) is an immunoregulatory lymphokine that is primarily produced by T cells and nat
195 mice correlated with the failure to produce lymphokines that lead to the recruitment of monocytes/gr
198 Prospects for the use of IFN-gamma and other lymphokines to enhance the safety and efficacy of live a
201 nfected animals responded primarily with Th1 lymphokines, whereas lymphocytes from patenly infected m
202 nterferon-gamma (IFN-gamma) is a pleiotropic lymphokine whose production is restricted to activated T