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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
16                                        Human lymphokine-activated cells (LAK cells) and interferon al
17                             NK (P =.042) and lymphokine-activated killer (LAK) (P =.016) activity was
18 ripheral blood (APB) MNCs in terms of NK and lymphokine-activated killer (LAK) activities and cytokin
19                In addition, M40403 increased lymphokine-activated killer (LAK) cell cytotoxicity in v
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
24                              Contact between lymphokine-activated killer (LAK) cells and natural kill
25                                              Lymphokine-activated killer (LAK) cells generated from p
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 rtially protected targets from lysis by bulk lymphokine-activated killer (LAK) cells.
32 B interferon (IFN)-gamma production, NK, and lymphokine-activated killer (LAK) cytotoxicity.
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
38 ed to stimulate lymphocyte proliferation and lymphokine-activated killer cell activation.
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
42 induction of Ag-independent MHC-unrestricted lymphokine-activated killer cell activity.
43 traction of CD8+ T cells, and stimulation of lymphokine-activated killer cell activity.
44  exhibited a marked decrease in IL-2-induced lymphokine-activated killer cell activity.
45 eral downstream orphan granzyme genes in the lymphokine-activated killer cell compartment.
46                 We now show that NO inhibits lymphokine-activated killer cell killing of K562 target
47 uces production of IFN-gamma and augments NK/lymphokine-activated killer cell proliferation and funct
48 delivered into living tumor cells and during lymphokine-activated killer cell-mediated attack.
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
53                                              Lymphokine-activated killer cells were sorted into diffe
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
57 xic T lymphocytes, natural killer cells, and lymphokine-activated killer cells.
58  cytotoxic T-lymphocytes, natural killer, or lymphokine-activated killer cells.
59  IL-4 was required to limit the induction of lymphokine-activated killer cells.
60 d in perforin- and granzyme-resistant CTL or lymphokine-activated killer cells.
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
63 t cells, as well as NK target cells, but not lymphokine-activated killer target cells.
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-
66 cell targets, indicating that ISG15 enhanced lymphokine-activated killer-like activity.
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
69 enotype with respect to 14 NK receptors, and lymphokine-activated killing (LAK) function.
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
72 antibody-dependent cellular cytotoxicity and lymphokine-activated killing.
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
78 y T cells proliferated and secreted the same lymphokines after stimulation with either Ag.
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
82  and Borrelia burgdorferi antigens modulated lymphokines and monokines in vitro.
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
86 nto memory cells that produce anti-microbial lymphokines, and migrate to sites of infection.
87  RNAs of many proto-oncogenes, cytokines and lymphokines are targeted for rapid degradation through A
88 from infected goats reflected differences in lymphokine balance associated with disease status.
89                Secretion of all of the above lymphokines by lymph node cells was inhibited by YCD3 tr
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.
94                                         This lymphokine-dependent expression of PGHS-2 is blocked by
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
98 oding many protooncoproteins, cytokines, and lymphokines for rapid degradation.
99  although RK has a role in the regulation of lymphokine gene expression in monocytes, it is not requi
100                                              Lymphokine gene expression is a precisely regulated proc
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
104 ly acquires the capacity to produce effector lymphokines if stimulated.
105 iii) absent responses to endogenous Th1 cell lymphokines (IFN-gamma and IL-2) but preserved responsiv
106 been associated with detection of the type 1 lymphokines, IFN-gamma and IL-2.
107 10 blockade or stimulation with antagonistic lymphokine IL-12 normalized baseline and CD3/CD28-induce
108 t can be rescued in vitro and in vivo by the lymphokine IL-7.
109 unted response of its progeny to the central lymphokine IL-7.
110                                              Lymphokine (IL-2)-activated-killer (LAK) cells were capa
111                            Recently, a novel lymphokine (IL-21) and its receptor (IL-21R alpha) were
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
114 tory mRNA production, we conclude that other lymphokine-induced factors play a role.
115       Although the JAK/STAT pathway mediates lymphokine-induced transcriptional regulation in NK cell
116 to investigate the interplay between the Th1 lymphokine interferon-gamma (IFNgamma) and pivotal cytok
117 oid tissues that produced the anti-microbial lymphokine interferon-gamma.
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
120                                              Lymphokines interleukin-4 (IL4) and IL13 exert overlappi
121          Such production of an intracellular lymphokine is not typical of other soluble interleukin s
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.
125 ation and leukotriene secretion) and dampen (lymphokine) mast cell effector responses.
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.
128                              Moreover, liver lymphokine mRNA levels in these animals and IL-4 KO mice
129                                              Lymphokine mRNA profiles in SU-stimulated PBMC were depe
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
133  of B, T, and NK cells in concert with other lymphokines or stimuli.
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
140 vity is required for the induction of T cell lymphokine production and proliferation.
141    These defects in thymocyte maturation and lymphokine production are IL-12 driven, since they are p
142                   Moreover, TR6-Fc modulates lymphokine production by alloantigen-stimulated mouse T
143 ropathogenic Escherichia coli (EPEC) inhibit lymphokine production by mitogen-activated human periphe
144                            Proliferation and lymphokine production dramatically increased in the pres
145 .2, 14.1, and 15.1-positive T cells, and the lymphokine production from the activated T cells is beli
146 ces with the adaptor SLP-76 and up-regulates lymphokine production in T-cells.
147 timulation, suggesting a role for endogenous lymphokine production in the induction of bcl-2.
148 hat it induced the proliferation but not the lymphokine production of Ld 61-80-primed T cells.
149 ells (MDSCs) inhibited the proliferation and lymphokine production of wild-type CD4+ T cells in vitro
150                        Similarly, studies of lymphokine production suggested that T cell function in
151                                    Increased lymphokine production was observed with most clinical is
152                    In one T cell clone (E6), lymphokine production was reduced in part because of an
153  stimulation with vigorous proliferation and lymphokine production while retaining their specificity,
154 ytes, including a rise in cytosolic calcium, lymphokine production, and cell division.
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
157              In further studies centering on lymphokine production, we showed that LP T cells from in
158  signal crucial for T cell proliferation and lymphokine production.
159  influencing the direction of T-cell-derived lymphokine production.
160 lymphocyte proliferative response as well as lymphokine production.
161  receptors to signaling pathways involved in lymphokine production.
162 tissues and is capable of immediate effector lymphokine production.
163 e Ag receptor-initiated signaling events and lymphokine production.
164 ine and the clone elaborated an unrestricted lymphokine profile in vitro.
165      In keeping with this, regulation of the lymphokine profile of CD4+ cells by CD8+ cells was consi
166                   However, the phenotype and lymphokine profile of populations arising in aged animal
167 of CD4+ T cell subpopulations with differing lymphokine profiles are well established.
168                                              Lymphokine profiles suggested that the peptides may favo
169       Interleukin-15 (IL-15) is an important lymphokine regulating natural killer (NK) activity, T-ce
170        One of these mAbs specifically blocks lymphokine release by T cells responsive to this complex
171 nic mice displayed reduced proliferation and lymphokine release.
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
175 mmatory processes, as well as conferring Th1 lymphokine responses.
176 et gene promoters and might evoke their same lymphokine-responsive profile in immortalized progenitor
177                              The kinetics of lymphokine secretion after stimulation by E.
178 ns in vivo may lead to different patterns of lymphokine secretion and accumulation of cytokines (e.g.
179 latory signal promotes T-cell proliferation, lymphokine secretion and effector function.
180 d the antigen-specific antibody isotypes and lymphokine secretion by CD4+ T cells in BALB/c mice immu
181 pagation of TCR-triggered signals needed for lymphokine secretion by T cells.
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
184 ts ability to elicit different cytolytic and lymphokine secretion responses.
185 de cytotoxicity, inhibition of viral growth, lymphokine secretion, and support of humoral and CD8 res
186  than B7.1 and induces a distinct pattern of lymphokine secretion.
187 liferation, T cell signaling activation, and lymphokine secretion.
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
193                       Herein, we report that lymphokines that promote allergic inflammation, like MCP
194 ecific T cells capable of producing effector lymphokines throughout the body.
195 Prospects for the use of IFN-gamma and other lymphokines to enhance the safety and efficacy of live a
196 tokines reveals that IL-2 is the predominant lymphokine utilized by memory cells.
197 s MCP-1 was significantly increased, and Th2 lymphokines were unaffected.
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
200                                      Passive lymphokine withdrawal death may result from the cytoplas
201 at least two major forms: antigen-driven and lymphokine withdrawal.

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