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1  ligands than human interferon-gamma-induced monokine.
2  nuclear factor kappaB (NF-kappaB)-dependent monokines.
3 erent costimulatory signals from these three monokines.
4 on of the production of many proinflammatory monokines.
5 volved in regulating IFN-gamma production by monokine-activated NK cells are not clearly identified.
6                     Further, supernatants of monokine-activated NK cells obtained from both normal do
7 s by autologous NK cells and, hence, renders monokine-activated NK cells susceptible to NKp80-mediate
8                 Hlx expression is induced in monokine-activated NK cells, but with delayed kinetics c
9                    Here, we demonstrate that monokine-activated NK cells, isolated from both normal a
10 egative regulator of IFN-gamma production in monokine-activated NK cells.
11     Following trauma, increased inflammatory monokine activation and depressed APC function can occur
12  normal donors and subjected them to a novel monokine activation culture scheme.
13  of SHIP1 in CD56bright NK cells followed by monokine activation substantially lowered IFN-gamma prod
14 an important role in vivo in down-regulating monokine and IFN-gamma responses to acute intracellular
15 disruption suppressed IFN-gamma induction in monokine and/or CD16-stimulated NK cells.
16 -deficient mice, despite local expression of monokines and IFN-gamma.
17 protein-10 (IP-10), interferon-gamma-induced monokine, and interferon-inducible T cell alpha-chemoatt
18  in isolated human NK cells, proinflammatory monokines antagonize antiinflammatory TGF-beta signaling
19  preferentially targeted NF-kappaB-regulated monokines, ASA acted predominantly by suppressing IFNgam
20                      Exposure of NK cells to monokines associated with conversion into memorylike cel
21 en) can trigger the expression of these four monokines by murine inflammatory macrophages.
22                                          The monokine combination IL-12, IL-18, and IFN-alpha substit
23 cing high levels of IFN-gamma in response to monokine costimulation.
24  Whereas CSA activates monocytes (to secrete monokines), CSB activates B-cells (to proliferate).
25 ll proliferation and watershed production of monokines (e.g. tumor necrosis factor alpha, interleukin
26               IL-12 and IL-18, but not other monokines, elicited secretion of IFN-gamma and IFN-gamma
27 n the levels of FcgammaRs, HLA antigens, and monokines, elutriated HMOs and U937 cells were transfect
28                                      AICL on monokine-exposed NK cells elicits NKp80-dependent effect
29 for neutralized IL-1 alpha, suggesting the 2 monokines have separate roles in promoting IgG2.
30 protein (IP-10) and IFN-gamma- induced human monokine (HuMig), but with a significantly higher affini
31                                              Monokines (i.e., interleukin [IL]-12, -18, and -15) indu
32                             For example, the monokine IL-15 appears to be required for type 2 cytokin
33    We demonstrate that when activated by the monokines IL-12, IL-15, and IL-18, these NK cells promot
34 ytes with SAA stimulated the proinflammatory monokines IL-6 and IL-1beta concurrently with the M2 mar
35  Addition of NK cells that were activated by monokines (IL-12, IL-15, and IL-18) or by exposure to M.
36        Here we compared the effects of three monokines (IL-18, IL-15, and IL-12) on human NK cell cyt
37 wing stimulation with the combination of two monokines, IL-15 plus IL-12.
38                                        These monokines in turn favor expansion of Tc1 CD8+ T cells.
39 rgdorferi antigens modulated lymphokines and monokines in vitro.
40  mice produced more IFN-gamma in response to monokines in vivo than did NK cells from wild-type mice.
41 fer cells in association with the release of monokines including TNF, which causes activation of circ
42                                     Although monokines increased NK cell expression of the activating
43 r, IL-10, which is inhibitory for most other monokines, increased levels of IL-15 mRNA found after st
44 kin-12 (IL-12), since neutralization of this monokine increases susceptibility to infection.
45                      Monocyte cytokines (ie, monokines) induce natural killer (NK) cells to produce i
46 on-inducible protein 10 [IP-10 (CXCL10)] and monokine induced by gamma interferon (IFN-gamma) [MIG (C
47 presented here demonstrate the expression of monokine induced by gamma interferon (IFN-gamma; Mig/CXC
48 ly member 14 (TNFSF14, also known as LIGHT), monokine induced by gamma interferon (MIG), and granzyme
49  RANTES and eotaxin, and of the CXCR3 ligand monokine induced by gamma interferon (MIG).
50 lated oncogene alpha [GRO-alpha], IP-10, and monokine induced by gamma interferon [MIG]), were upregu
51 in 3beta and proinflammatory chemokine CXCL9/monokine induced by gamma interferon in secondary lympho
52 vels of the Th1-associated chemokines CXCL9 (monokine induced by gamma interferon), CXCL10 (interfero
53             These studies revealed that Mig (monokine induced by gamma interferon), cytokine-responsi
54  chemokines interferon-inducible protein 10, monokine induced by gamma interferon, and platelet facto
55 , including interferon-inducible protein 10, monokine induced by gamma interferon, macrophage-induced
56 ines monocyte chemotactic protein-1/CCL2 and monokine induced by gamma interferon/CXCL9 in the hypote
57 ro-alpha, IFN-inducible protein-10, and mig (monokine induced by gamma-IFN), and of the adhesion mole
58 ed the expression and function of CXC (human monokine induced by gamma-interferon [HuMig], interleuki
59 -1), intercellular adhesion molecule-1, Mig (monokine induced by gamma-interferon), and RANTES (regul
60  IL-7, IL-8, IL-10, MCP-1, MCP-2, MCP-3, and monokine induced by gamma-interferon.
61  (10-kDa interferon-inducible protein), MIG (monokine induced by human interferon-gamma), and I-TAC (
62 ucible T cell alpha chemoattractant (I-TAC), monokine induced by IFN (Mig), and their receptor CXCR3
63                                       CXCL9 (monokine induced by IFN gamma [Mig]) and CXCL10 (interfe
64 ing mAbs to IFN-induced protein-10 (CXCL10), monokine induced by IFN-gamma (CXCL9), and IFN-inducible
65 IFN-gamma-inducible protein-10 (CXCL10), and monokine induced by IFN-gamma (CXCL9).
66 ial hemopoietic suppressive effects of human monokine induced by IFN-gamma (HuMig), a CXC chemokine t
67                                 In contrast, monokine induced by IFN-gamma (HuMig), which like HuIP-1
68 IP10 (OR 4.62, 95% CI 1.69-12.65, P = .003), monokine induced by IFN-gamma (MIG) (OR 3.11, 95% CI 1.1
69             The IFN-gamma-inducible proteins monokine induced by IFN-gamma (Mig) and chemokine respon
70 ed tumor cell clones that produce both CXCL9/monokine induced by IFN-gamma (Mig) and CXCL10/IFN-gamma
71 to mouse chromosome 5 close to the genes for monokine induced by IFN-gamma (MIG) and IP10.
72    This effect was associated with decreased monokine induced by IFN-gamma (Mig) and secondary lympho
73 hemokines IFN-gamma-inducible protein-10 and monokine induced by IFN-gamma (Mig) are expressed in all
74 n (IFN)-gamma-induced protein 10 (IP-10) and monokine induced by IFN-gamma (Mig) in a pool of human a
75 s IFN-gamma inducible protein 10 (IP-10) and monokine induced by IFN-gamma (Mig) in acute rejection o
76 n; peak levels of soluble TNF receptor 2 and monokine induced by IFN-gamma (MIG) on days 10-11 after
77 low or undetectable levels; and 2) IP-10 and monokine induced by IFN-gamma (Mig) were expressed in th
78 ets and the expression of its ligands CXCL9 (monokine induced by IFN-gamma (Mig)) and CXCL10 (IFN-gam
79 sion of T helper 1-associated CXCR3 ligands, monokine induced by IFN-gamma (Mig), and IFN-gamma-induc
80 nes IFN-inducible protein of 10 kDa (IP-10), monokine induced by IFN-gamma (Mig), and IFN-inducible T
81 N)-gamma-inducible protein of 10 kD (IP-10), monokine induced by IFN-gamma (Mig), and IFN-inducible T
82 hemokines--IFN-inducible protein 10 (IP-10), monokine induced by IFN-gamma (Mig), and IFN-inducible T
83 kines IFN-induced protein of 10 kDa (IP-10), monokine induced by IFN-gamma (Mig), and IFN-inducible T
84 k liver expression of another chemokine, the monokine induced by IFN-gamma (Mig), depended upon prese
85     Expression of inducible protein (IP)-10, monokine induced by IFN-gamma (Mig), interferon inducibl
86 feron (IFN)-gamma inducible protein (IP)-10, monokine induced by IFN-gamma (Mig), interferon-inducibl
87 GF), IFN-gamma-inducible protein 10 (IP-10), monokine induced by IFN-gamma (MIG), monocyte chemotacti
88 the current study was to test the ability of monokine induced by IFN-gamma (Mig)-specific antibodies
89 emokines IFN-gamma inducible protein 10, and monokine induced by IFN-gamma (MIG).
90 IFN-gamma inducible protein-10 (IP-10) or to monokine induced by IFN-gamma (MIG).
91                          The CXC chemokines (monokine induced by IFN-gamma (MIG)/CXC chemokine ligand
92 mmatory protein-10/CXC ligand (CXCL) 10, and monokine induced by IFN-gamma (MIG)/CXCL9 were significa
93 N-gamma and the IFN-gamma-induced chemokines monokine induced by IFN-gamma (Mig, CXCL9) and IFN-induc
94 ha-chemoattractant (I-TAC; CXCL11), and then monokine induced by IFN-gamma (Mig, CXCL9).
95 -gamma)-inducible protein 10 (IP-10/CXCL10), monokine induced by IFN-gamma (Mig/CXCL9), and interfero
96 n a radial diffusion assay, only recombinant monokine induced by IFN-gamma (MIG/CXCL9), IFN-gamma-ind
97                                              Monokine induced by IFN-gamma (Mig; CXC chemokine ligand
98                                              Monokine induced by IFN-gamma (MIG; CXC chemokine ligand
99 s of gamma interferon (IFN-gamma) and CXCL9 (monokine induced by IFN-gamma [MIG]) were found to be si
100 e expression of IFN-inducible protein 10 and monokine induced by IFN-gamma and cellular infiltration
101  elaboration of Th1 cytokines and chemokines monokine induced by IFN-gamma and IFN-gamma-inducible pr
102  protein of 10 kDa (IP-10), in contrast with monokine induced by IFN-gamma and IFN-inducible T cell-a
103 lity; (b) other ELR-negative CXC chemokines, monokine induced by IFN-gamma and platelet factor 4 that
104 rked induction of mRNAs for STAT1, IL-8, and monokine induced by IFN-gamma during the first day of tr
105 vation of IFN-gamma-inducible protein-10 and monokine induced by IFN-gamma expression in IFN-alpha-pr
106 hemokines IFN-gamma-inducible protein-10 and monokine induced by IFN-gamma in response to Klebsiella
107 tic increase in IFN-inducible protein 10 and monokine induced by IFN-gamma production.
108 inflammatory markers D-dimer, IFN-gamma, and monokine induced by IFN-gamma than i.v. challenged contr
109      The plasma levels of IL-17A, MCP-1, and monokine induced by IFN-gamma were increased in infants
110                Induced protein of 10 kDa and monokine induced by IFN-gamma were significantly elevate
111 ll alpha chemoattractant) (CXCL11), and Mig (monokine induced by IFN-gamma) (CXCL9), T-lymphocyte che
112  Conversely, the Th1-type chemokines, CXCL9 (monokine induced by IFN-gamma) and CXCL10 (IFN-gamma-ind
113                    The CXCR3 ligands, CXCL9 (monokine induced by IFN-gamma) and CXCL10 (IFN-inducible
114 ounts of the IFN-inducible chemokines CXCL9 (monokine induced by IFN-gamma) and CXCL11 (IFN-gamma-ind
115 ; IP-10 (interferon-inducible protein); Mig (monokine induced by IFN-gamma) and decreased neutrophil
116 y that expression of the CXC chemokines Mig (monokine induced by IFN-gamma) and IP-10 (inducible prot
117 (IFN-gamma-inducible protein-10), and CXCL9 (monokine induced by IFN-gamma) and their corresponding c
118 or the T cell chemoattractant chemokine Mig (monokine induced by IFN-gamma) in contributing to a Th1
119 CL)10 (IFN inducible protein 10 kDa), CXCL9 (monokine induced by IFN-gamma), and CC chemokine ligand
120                   Blocking of IP-10, but not monokine induced by IFN-gamma, aborts severity of Ag-spe
121  flagellin and IFN-inducible protein-10 kDa, monokine induced by IFN-gamma, and IFN-inducible T cell
122 L-8, RANTES, IFN-gamma inducible protein 10, monokine induced by IFN-gamma, and MIP-1alpha, specifica
123 h increased circulating levels of IFN-gamma, monokine induced by IFN-gamma, and RANTES.
124 matory cytokines IL-6, IL-12, CXCL10, MCP-1, monokine induced by IFN-gamma, and TNF-alpha in macropha
125 tractants IFN-gamma-inducible protein-10 and monokine induced by IFN-gamma, cellular infiltration int
126 (IFN-gamma)-inducible chemokine mRNAs (CXCL9/monokine induced by IFN-gamma, CXCL10/IFN-gamma-inducibl
127        CD4-depleted mice had lower levels of monokine induced by IFN-gamma, IFN protein-10 (IP-10), a
128 tokines and chemokines, including IFN-gamma, monokine induced by IFN-gamma, IFN-gamma-inducible prote
129 er levels than IFN-induced protein-10 or the monokine induced by IFN-gamma, it was the principal chem
130                                              Monokine induced by IFN-gamma, MCP-1, and IFN-gamma prod
131 hemokines IFN-gamma-inducible protein 10 and monokine induced by IFN-gamma, suggesting that macrophag
132 P-10, cutaneous T-cell-attracting chemokine, monokine induced by IFN-gamma, tumor necrosis factor-rel
133 enic chemokines IFN-inducible protein 10 and monokine induced by IFN-gamma.
134  interferon-inducible protein-10 (IP-10) and monokine induced by IFN-gamma.
135 vities of IFN-gamma inducible protein 10 and monokine induced by IFN-gamma.
136 hemokines IFN-gamma-inducible protein-10 and monokine induced by IFN-gamma.
137  the inflammatory chemokine receptors CXCR3 (monokine induced by IFN-gamma/CXC ligand (CXCL)9) and CX
138 CL11 mRNA in the CNS and decreased levels of monokine induced by IFN-gamma/CXCL9 mRNA in draining lym
139 y the other high affinity ligands for CXCR3, monokine induced by IFN-gamma/CXCL9, and I-TAC/CXCL11.
140  cells (IFN-inducible protein-10 kDa/CXCL10, monokine induced by IFN-gamma/CXCL9, IFN-inducible T cel
141 ssed IFNgamma-induced expression of the MIG (monokine induced by IFNgamma) gene, a C-X-C chemokine, i
142 (gamma-interferon-inducible protein (IP-10), monokine induced by INF-gamma (MIG), macrophage inflamma
143 tory protein 1alpha (MIP-1alpha), MIP-1beta, monokine induced by interferon (MIG)-gamma, and interfer
144 kines interferon gamma inducible protein 10, monokine induced by interferon gamma, and platelet facto
145 t concentrations of the CXCR3 ligands CXCL9 (monokine induced by interferon gamma, MIG) and CXCL10 (i
146 , KC (mouse analog of interleukin-8 [IL-8]), monokine induced by interferon-gamma (CXCL9), and IL-1 r
147 colony-stimulating factor, stem cell factor, monokine induced by interferon-gamma (CXCL9), intercellu
148 )-inducible chemokine CXC chemokine ligand 9/monokine induced by interferon-gamma (CXCL9/Mig) was one
149                        We combined IL-10 and monokine induced by interferon-gamma (derived from the 2
150 nflammatory protein-1Delta, osteoprotegerin, monokine induced by interferon-gamma (IFN), and IFN-gamm
151 , particularly the T-cell recruiting factors monokine induced by interferon-gamma (Mig) and inducible
152 FN-gamma inducible protein ([Crg2]IP-10) and monokine induced by interferon-gamma (Mig) are rapidly a
153 n-gamma-inducible protein-10 (IP-10) and the monokine induced by interferon-gamma (Mig) caused tissue
154 on-gamma-inducible 10-kd protein (IP-10) and monokine induced by interferon-gamma (MIG) constituted 2
155 feron-gamma inducible protein-10 (IP-10) and monokine induced by interferon-gamma (Mig) were determin
156 acrophage migration inhibitory factor (MIF), monokine induced by interferon-gamma (MIG), and matrix m
157 n-gamma-inducible protein of 10 kDa (IP-10); monokine induced by interferon-gamma (Mig); and regulate
158 odies (mAbs) to neutralize the CXCR3 ligands monokine induced by interferon-gamma (MIG, CXCL9) and in
159                        Chemokines, including monokine induced by interferon-gamma (Mig/CXCL9), are pr
160          We hypothesized that the chemokine, monokine induced by interferon-gamma (MIG/CXCL9), which
161 fically, monocyte chemoattractant protein-1, monokine induced by interferon-gamma, and interferon-gam
162 es (interferon-inducible protein 10 [IP-10], monokine induced by interferon-gamma, and interferon-ind
163 nterferon-gamma-inducible protein-10 (IP10), monokine induced by interferon-gamma, and monocyte chemo
164                                     Mig, the monokine induced by interferon-gamma, is a CXC chemokine
165 kine (interferon-gamma-inducible protein-10, monokine induced by interferon-gamma, macrophage-inflamm
166       Of these transcripts, only four (human monokine induced by interferon-gamma, T-cell receptor ac
167 , macrophage inflammatory protein-1beta, and monokine induced by interferon-gamma.
168 d by the CXC chemokine ligand 9 (CXCL9, Mig [monokine induced by interferon-gamma]) that impressively
169  ligands interferon-inducible protein 10 and monokine-induced by gamma interferon were detected on si
170 ding gamma-IFN-inducible protein (IP-10) and monokine-induced by gamma-IFN (MIG), as well as down-reg
171 d expression of IFN-inducible protein-10 and monokine-induced by IFN-gamma and thereby promote the co
172  cells secreted IFN-inducible protein-10 and monokine-induced by IFN-gamma in response to stimulation
173 e CXCR3 ligands IFN-inducible protein-10 and monokine-induced by IFN-gamma were selectively up-regula
174 feron-gamma inducible protein 10 (IP-10) and monokine-induced by IFN-gamma, (Mig), in allogeneic hear
175 ymphocytes correlated with both Th2 and Th1 (monokine-induced by IFN-gamma, IFN-gamma-inducible prote
176    CD94(high)CD56(dim) NK cells produce less monokine-induced IFN-gamma than CD56(bright) NK cells bu
177 emokine (MCP-1, macrophage-derived cytokine, monokine-induced IFN-gamma, keratinocyte-derived chemoki
178 ature effector cells, but also via bystander monokine-induced maturation of immature T cells.
179  demonstrate that SHIP1 negatively regulates monokine-induced NK cell IFN-gamma production in vitro a
180  NK cells temporally controls and limits the monokine-induced production of IFN-gamma, in part throug
181 coding IFN-gamma inducible protein of 10 kD, monokine inducible by gamma and RANTES.
182 n soluble tachyzoite antigen responsible for monokine induction are heat stable at 100 degree C but d
183              Together, these data argue that monokine induction by T. gondii is mediated by glycoprot
184                       A further dichotomy in monokine induction signals was inferred from experiments
185  used to enumerate cytokine-producing cells (monokines: interleukin [IL]-1alpha, IL-1beta, IL-6, and
186 ne production may be governed in part by the monokine milieu induced during the early proinflammatory
187 t tumor necrosis factor-alpha (TNF-alpha), a monokine overexpressed in inflammatory myopathies, led t
188 es are shown to be dependent on the specific monokines present.
189 olerance, a state characterized by decreased monokine production and enhanced protection against endo
190       Notably, in the absence of significant monokine production by DenV-infected DC, it was the comb
191                                   Similarly, monokine production in vitro was reduced, whereas serum
192 ts of SLPI did not involve the modulation of monokine production since TNF-alpha and IL-10 were unaff
193 cytokines, regulated in part by differential monokine production.
194 itutively express monocyte-derived cytokine (monokine) receptors and secrete cytokines and chemokines
195 fector IFN-gamma(+) cells following a linear monokine-regulated pathway identical with that previousl
196 ction, whereas activation pathways for other monokine responses remain relatively intact.
197 an monocytes and suggest that stimulation of monokine secretion by bryo-1 may represent at least one
198 se to infection, monocyte-derived cytokines (monokines), stimulate natural killer (NK) cells to produ
199 ransduction 4 (STAT4), and STAT5 activity in monokine-stimulated NK cells, potentially contributing t
200 cantly enhanced IFN-gamma gene expression in monokine-stimulated NK cells.
201                    SET was up-regulated upon monokine stimulation of primary human NK cells.
202 tor, IL-10, and IL-13 protein in response to monokine stimulation than do CD56(dim) NK cells, which p
203 d secrete cytokines and chemokines following monokine stimulation, and are therefore a critical compo
204 and may be predominantly an antiinflammatory monokine stimulus.
205 monocytes produce proinflammatory cytokines (monokines) such as interleukin (IL)-12, IL-15, and IL-18
206                                     Enhanced monokine synthesis requires engagement of P-selectin gly
207 ducible NO synthase, and multiple neutrophil/monokine-targeted chemokine programs.
208 ls produce far more IFN-gamma in response to monokines than do CD56dim NK cells.
209 nd monocytes and required both IL-17 and the monokines TNF-alpha and IL-1beta.
210 Conversely, CD14(+) monocytes synergize with monokines to promote IFN-gamma production by these NK ce
211 ependent IFN-gamma production in response to monokine treatment.
212 rs responsible for the induction of all four monokines were found to be sensitive to periodate oxidat

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