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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 f cytokine expression, but not of TH-related lymphokines.
5 redominant mediators for a limited number of lymphokines.
6 h MalE-OVA-expressing bacteria produced both lymphokines.
7 inocytes in response to a cocktail of T cell 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
33 expressed on all C57BL/6 IL-2-activated NK (lymphokine-activated killer (LAK)) cells, all splenic an
34 tease that is expressed predominantly in the lymphokine-activated killer (LAK)/natural killer (NK) co
35 ese mAbs inhibited the anti-CD3-directed and lymphokine-activated killer activity of the P815 cell li
36 cell proliferative responses, generation of lymphokine-activated killer activity, and development of
37 (IL-2) nor the induction of IL-2-stimulated lymphokine-activated killer activity, however, was inhib
39 cytotoxic T lymphocyte, natural killer, and lymphokine-activated killer cell activities compared wit
40 hocyte activity, and both natural killer and lymphokine-activated killer cell activities of graft non
41 oxic assay of PBL indicated the induction of lymphokine-activated killer cell activity, but no eviden
47 uces production of IFN-gamma and augments NK/lymphokine-activated killer cell proliferation and funct
49 tion of murine and human T cell-mediated and lymphokine-activated killer cell-mediated cytotoxicity,
50 otoxic lymphocytes, natural killer cells and lymphokine-activated killer cells depend primarily on th
51 ytotoxic T lymphocytes and natural killer or lymphokine-activated killer cells is not blocked by BCR-
52 ndothelium and cytotoxicity against tumor by lymphokine-activated killer cells were not affected by P
54 ions in T cell differentiation, induction of lymphokine-activated killer cells, and regulation of imm
55 actions of different human effector cells, (lymphokine-activated killer cells, gammadelta T cells, c
56 cid mice previously reconstituted with human lymphokine-activated killer cells, whereas treatment wit
61 mC and F genes in their MLR-derived CTLs and lymphokine-activated killer cells; removal of the PGK-ne
62 arge/zona occludens-1)-binding kinase/T-LAK (lymphokine-activated killer T cell) cell originating pro
64 de effects usually associated with classical lymphokine-activated killer therapy in association with
65 ities in a cytotoxic lymphocyte compartment (lymphokine-activated killer) and have normal lymphokine-
67 lymphokine-activated killer) and have normal lymphokine-activated killer-mediated cytotoxicity agains
68 ports of transformation of CTL into NK-like "lymphokine-activated killers" (LAK cells) under high dos
70 er each of four sequelae, with inhibition of lymphokine-activated killing induction being least sensi
71 cell-mediated cytotoxicity pathway, impairs lymphokine-activated killing, and decreases the proporti
73 stance to listerial infections of the liver, lymphokine-activated natural killer (LAK) cells were coc
74 in a wide variety of immune cells, including lymphokine-activated natural killer cells, resting T cel
75 ) that recognize only foreign MHC molecules, lymphokine-activated T cells that lack recognition speci
76 action (DTH) provided evidence for the first lymphokine activity: a lymphocyte-derived mediator calle
77 proliferation, and decreased expression of T lymphokines after stimulation by either anti-CD3 plus an
79 s, UUAUUUAU, present in the 3'-UTR of mature lymphokine and other cytokine transcripts, have been imp
80 ls are controlled by complex combinations of lymphokines and adhesion/costimulatory molecule signals.
81 h alpha beta T cells and are able to secrete lymphokines and express cytolytic activities in response
83 related to the secretory products (including lymphokines and proteinases) of the lymphocytic infiltra
84 al memory functions, such as secrete diverse lymphokines and provide cognate help to B cells, despite
85 rast to the selective and early reduction of lymphokines and the inducible form of nitric oxide synth
87 RNAs of many proto-oncogenes, cytokines and lymphokines are targeted for rapid degradation through A
90 gy can interfere with the delivery of helper lymphokines by T cells, resulting in a decreased capacit
91 To discover whether transgenic expression of lymphokines by the CTLs themselves might overcome these
92 ed by the finding that addition of exogenous lymphokines could restore PGE2-inhibited proliferation,
93 D40-independent DC sensitization, and direct lymphokine-dependent CD4(+)-CD8(+) T cell communication.
95 tes synthesis of IFN-gamma, while the latter lymphokine directly controls parasite growth and diminis
96 or alpha, interleukin 1, interleukin 6), and lymphokines (e.g. tumor necrosis factor beta, interleuki
97 y factor (MIF) is a secreted proinflammatory lymphokine essential for elicitation of delayed-type hyp
99 although RK has a role in the regulation of lymphokine gene expression in monocytes, it is not requi
101 ng its ability to block the transcription of lymphokine genes in activated T cells through formation
102 ctivation by preventing the transcription of lymphokine genes through binding to the intracellular pr
103 target genes, such as CD4 and CD8 as well as lymphokine genes, during the specialization of naive CD4
105 iii) absent responses to endogenous Th1 cell lymphokines (IFN-gamma and IL-2) but preserved responsiv
107 10 blockade or stimulation with antagonistic lymphokine IL-12 normalized baseline and CD3/CD28-induce
112 ns, enhanced production of mRNA encoding Th1 lymphokines in draining lymph nodes, and increased gamma
113 r patients can proliferate and form Th1 type lymphokines in the presence of autologous tumor cell whe
116 to investigate the interplay between the Th1 lymphokine interferon-gamma (IFNgamma) and pivotal cytok
118 IL-6, and tumor necrosis factor [TNF]-alpha; lymphokines: interferon-gamma, IL-2, IL-4, and TNF-beta)
119 s and the production of the T-helper-1 (Th1) lymphokines interleukin-2 (IL-2) and interferon-gamma (I
122 ssion of many proto-oncogenes, cytokines and lymphokines is regulated by targeting their messenger RN
123 tingly, IL-15, which licenses NKG2D-mediated lymphokine killer activity in CTLs, cooperates with NKG2
124 or status determine whether IL-15 can confer lymphokine killer activity-like properties to T cells.
126 press CD40, suggesting that T cell-CD40L and lymphokines may be involved in regulating FDC-CD23.
127 regions of many protooncogene, cytokine, and lymphokine messages target them for rapid degradation.
130 expressed constitutively elevated levels of lymphokine mRNA, including IL-4, IL-5, and IL-10, and we
131 ct of fibronectin in combination with T cell lymphokines on psoriatic uninvolved basal keratinocyte p
132 n along with proliferation (CD40 ligand plus lymphokines or Staphylococcus aureus protein A) induces
134 did not reveal any significant difference in lymphokine output, and isotype expression was not altere
135 in cultures of L929 cells treated with crude lymphokine preparations (LK) or with gamma interferon (I
136 tes to signals for proliferation provided by lymphokines produced by intralesional T lymphocytes in p
137 elper cell subsets (TH1 and TH2) reveal that lymphokine-producing cells are much more likely to expre
138 on in this gene lacks the ability to inhibit lymphokine production and lymphocyte proliferation.
139 documented by lower overall antigen-induced lymphokine production and proliferation, as well as dimi
141 These defects in thymocyte maturation and lymphokine production are IL-12 driven, since they are p
143 ropathogenic Escherichia coli (EPEC) inhibit lymphokine production by mitogen-activated human periphe
145 .2, 14.1, and 15.1-positive T cells, and the lymphokine production from the activated T cells is beli
149 ells (MDSCs) inhibited the proliferation and lymphokine production of wild-type CD4+ T cells in vitro
153 stimulation with vigorous proliferation and lymphokine production while retaining their specificity,
155 The T cells were assayed for proliferation, lymphokine production, and immunosuppressive activity.
156 anti-LFA-1 treatments on NSDC, intrahepatic lymphokine production, and the homing of lymphocytes to
165 In keeping with this, regulation of the lymphokine profile of CD4+ cells by CD8+ cells was consi
172 We conclude that an early CCR2-dependent Th1 lymphokine response predominates in normal DVT resolutio
173 favors certain signals that contribute to a lymphokine response that can mediate allergic inflammati
174 genic mice were primed by PCC injection, the lymphokine responses measured after in vitro antigen res
176 et gene promoters and might evoke their same lymphokine-responsive profile in immortalized progenitor
178 ns in vivo may lead to different patterns of lymphokine secretion and accumulation of cytokines (e.g.
180 d the antigen-specific antibody isotypes and lymphokine secretion by CD4+ T cells in BALB/c mice immu
182 mplex molecule ligands that induce selective lymphokine secretion or anergy in mature T cells in asso
183 Crohn's disease) is associated with altered lymphokine secretion profiles, as recently found in vari
185 de cytotoxicity, inhibition of viral growth, lymphokine secretion, and support of humoral and CD8 res
188 est that stimulation of OVA-specific CTLs by lymphokines seems to be more important to maintaining me
189 e expression is induced by the delivery of a lymphokine signal to antigen-activated B cells in a prim
190 ttractant protein-1 (MCP-1) in Ag-stimulated lymphokine synthesis and proliferation by CD4+ T cells d
191 ron-gamma (IFN-gamma) is an immunoregulatory lymphokine that is primarily produced by T cells and nat
192 mice correlated with the failure to produce lymphokines that lead to the recruitment of monocytes/gr
195 Prospects for the use of IFN-gamma and other lymphokines to enhance the safety and efficacy of live a
198 nfected animals responded primarily with Th1 lymphokines, whereas lymphocytes from patenly infected m
199 nterferon-gamma (IFN-gamma) is a pleiotropic lymphokine whose production is restricted to activated T
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