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1 ific production of both interferon-gamma and beta-chemokine.
2 The soluble factor involved was not a beta-chemokine.
3 ate that Exodus represents a novel divergent beta-chemokine.
4 the previously described HIV R5-suppressive beta chemokines.
5 d protein, designated MCK-1, has homology to beta chemokines.
6 tion of HIV-1-suppressive factors, including beta chemokines.
7 rated an increased migratory response to the beta chemokines.
8 laboration of interferon-gamma and antiviral beta chemokines.
9 microglia and astrocytes produced all three beta chemokines.
10 rved cysteine residues typical for mammalian beta chemokines.
11 easured by expression of TNF-alpha and three beta chemokines.
12 state levels of mRNA specific for these two beta-chemokines.
13 nsensitive to the antiviral effects of these beta-chemokines.
14 nd resistance was abrogated by antibodies to beta-chemokines.
15 ell surface and with increased production of beta-chemokines.
16 ial tumor Kaposi's sarcoma, encodes three CC/beta-chemokines.
17 ned media produced significant quantities of beta-chemokines.
18 CCR5 expression and increasing production of beta-chemokines.
19 addition to the four others conserved in all beta-chemokines.
20 s caused rapid and specific release of these beta-chemokines.
21 inactive in signal transduction mediated by beta-chemokines.
22 ever, had NSI viruses that were sensitive to beta-chemokines.
23 NSI HIV-1 strains and secrete high levels of beta-chemokines.
24 the presence of CD8+ T-cell supernatants or beta-chemokines.
25 T cells cannot be explained entirely by the beta-chemokines.
26 cycle in late G(1), contained high levels of beta-chemokines.
27 ed by changes in the levels of CD4, CCR5, or beta-chemokines.
28 activity of CAF that is not attributable to beta-chemokines.
29 normal individuals that synthesize antiviral beta-chemokines.
30 ecretion of gamma interferon (IFN-gamma) and beta-chemokines.
37 of African green monkeys (AGMs) avidly binds beta-chemokines and functions as a coreceptor for simian
39 orphine on gene expression of the alpha- and beta-chemokines and their receptors by the astrocytoma c
41 endogenous suppressive factors, such as the beta-chemokines, and HIV-inducing cytokines, such as tum
43 ugh endogenously produced factors, including beta-chemokines, and that beta-chemokine production by C
44 on, the frequency of CD8+ T cells expressing beta-chemokines, and the extent of CD8+-T-cell prolifera
51 ated protein-1 and -2, defines a subgroup of beta-chemokines based on two conserved cysteines in addi
52 monstrating that US28 is responsible for the beta-chemokine binding and induced calcium signaling in
55 nd CD8(+) T-cell subsets in tissues produced beta-chemokines both before and 21 days after SIV infect
59 ealed that the production of HIV-suppressive beta-chemokines by HIV antigen-stimulated PBMC was signi
62 ombined data demonstrate that TCA3 and other beta-chemokines can modulate vascular smooth muscle cell
63 es as immunomodulators, plasmid DNA encoding beta-chemokines CCL19 and CCL21 (CCR7L) was codelivered
64 st growth factor, transforming growth factor beta, chemokine CCL2, SDF-1, and complements C3, C4, and
65 y CD4(+) and CD8(+) T cells, upregulation of beta-chemokines (CCL2 and CCL22), basic fibroblast growt
67 tion causes an increase in the expression of beta-chemokines CCL3, CCL4, and CCL5, and their receptor
68 dent on IFNalpha receptor 1 (IFNAR1) and the beta-chemokine CCL4, as IFNAR1 deficiency and neutralizi
69 treated 32D-BCR/ABL cells, we identified the beta-chemokine CCL9 as a gene regulated by BCR/ABL in a
70 monkeys had significantly higher numbers of beta-chemokine(+) CD8+ T cells than did vaccinated, prot
73 th severe malaria have a distinct profile of beta-chemokines characterized by increased circulating l
75 s identical to the previously isolated human beta-chemokine, CKbeta8, whereas the other is a splicing
76 kine secretion and there is no evidence that beta-chemokines contributed to the SHIV89.6-mediated con
77 of HIV-specific Th responses associated with beta-chemokines could mediate nonlytic inhibition of inf
79 that: (i) CD8+ T-cell supernatants did, but beta-chemokines did not, suppress HIV replication in the
80 (iii) the CD8+ T-cell supernatants did, but beta-chemokines did not, suppress HIV-1 IIIB replication
81 RK and MEK through R2, whereas MIP-1alpha, a beta chemokine, does not activate these kinases through
82 utative amino-terminal signal sequence and a beta chemokine domain, followed by a carboxyl-terminal d
83 addition of antibodies that neutralize these beta-chemokines, either alone or in combination, only pa
86 IV infection markedly altered the pattern of beta chemokine expression elicited by tumor necrosis fac
87 ations of lymphocytes, this dysregulation of beta chemokine expression may influence the trafficking
88 us, there was a positive correlation between beta-chemokine expression and the number of beta-chemoki
89 -specific IL-2 and CTL responses, as well as beta-chemokine expression in HIV-infected and uninfected
90 mokine gene expression with higher levels of beta-chemokine expression relative to nonvaccinated anim
94 xpected four cysteines characteristic of the beta chemokine family plus two additional carboxyl-termi
95 motactic agent 4 (TCA4), a new member of the beta-chemokine family, was cloned from a mouse thymic cD
96 secreted) is a cytokine that belongs to the beta-chemokine family; it is chemoattractant for CD4+/CD
97 y CD4(+) and CD8(+) T cells, upregulation of beta-chemokines, fibroblast growth factor-basic, hepatoc
98 peripheral blood mononuclear cells secreted beta-chemokines following stimulation with HBa, and this
102 induce the secretion of specific alpha- and beta-chemokines from human umbilical vein endothelial ce
105 at least in part, from Hz-induced changes in beta-chemokine gene expression in blood mononuclear cell
107 (NHPs) showed a better balance of alpha- and beta-chemokine gene expression with higher levels of bet
112 udies show that MCMV encodes and expresses a beta chemokine homolog with a novel predicted structure.
114 r cells closely matched those of circulating beta-chemokines, illustrating that PBMCs are a primary s
115 Little is known about the participation of beta chemokines in inflammatory processes within the cen
118 s observed upon neutralization of endogenous beta-chemokines in CD8-depleted or CD4+ PBMCs from most
122 e been reported to be important producers of beta-chemokines in the lymph nodes of HIV-1-infected ind
123 le of soluble effector molecules, especially beta-chemokines, in antiviral immunity is still controve
124 ith a combination of anti-CCR5 antibodies or beta-chemokines increased their fusion with X4 envelope-
126 ostentry levels and imply the involvement of beta-chemokine-induced signaling in postentry inhibition
127 ntrast, stimulation with TCA3, but not other beta-chemokines, induces proliferation of vascular smoot
129 infection helps to explain viral tropism and beta-chemokine inhibition of primary HIV-1 isolates.
131 Although the inhibition of HIV-1 entry by beta-chemokines is well documented, their effects on pos
133 tory protein-1alpha (MIP-1alpha) and RANTES, beta chemokines known to block gp120 interactions with m
134 mals also had marked elevation of alpha- and beta-chemokines known to be active on eosinophils and mo
135 charide isolated from HBa (LPS-Ba) to elicit beta-chemokines, known to bind to the human immunodefici
137 cytostatic agents shown here to up-regulate beta-chemokine levels, our results provide an additional
138 ability of CCR5 to signal in response to its beta-chemokine ligands is necessary or sufficient for vi
139 fined, but we have shown previously that its beta-chemokine ligands prevent HIV-1 from fusing with th
143 he T cell subsets that secrete the antiviral beta-chemokine macrophage inflammatory protein (MIP)-1be
144 is interaction was partially competed by the beta-chemokine macrophage inflammatory protein 1 beta (M
145 y structural motifs mediating binding of the beta-chemokine macrophage inflammatory protein-1alpha (M
147 esize and secrete substantial amounts of the beta-chemokines macrophage inflammatory protein (MIP)-1
150 he level of interferon-gamma (IFN-gamma) and beta-chemokines macrophage inflammatory protein-1alpha (
152 udy compares the activity of TCA3 with other beta-chemokines (macrophage inflammatory protein (MIP)-1
153 A concomitant and marked upregulation of beta-chemokines (macrophage inhibitory proteins 1alpha a
155 hese factors primarily as a mixture of three beta chemokines [macrophage-derived chemokine (MDC), thy
156 with elevations in mRNA expression of three beta chemokines, macrophage-inflammatory protein 1 (MIP-
157 results of this in vitro study suggest that beta chemokines may play an important role in the traffi
159 ce of endotoxin only induced the mRNA of the beta-chemokine MCP-1, and its expression was delayed com
160 t biopsies were examined for the presence of beta-chemokines (MCP-1, MIP-1alpha, MIP-1beta, and RANTE
162 The sensitivity of an individual's virus to beta-chemokine-mediated inhibition correlated with the N
167 onocyte chemotactic protein-1 (MCP-1), a CC (beta) chemokine, mediates airway hyperreactivity in norm
169 rus (HIV) biology was the discovery that the beta-chemokines MIP-1 alpha (macrophage inflammatory pro
172 -alpha), but not to IFN-gamma, IFN-beta, the beta-chemokines MIP-1alpha, MIP-1beta, and RANTES, or in
173 alpha-chemokines IL-8 and SDF-1alpha and the beta-chemokines MIP-1alpha, RANTES, and MCP-1 along with
174 viously been reported, circulating levels of beta-chemokines (MIP-1alpha, MIP-1beta, and RANTES) and
175 0 production in vitro, whereas levels of the beta-chemokine monocyte chemoattractant protein-1 were s
176 ial cell line demonstrated that other murine beta-chemokines (monocyte chemotactic protein-1, macroph
178 experiments demonstrated that the release of beta-chemokines, most likely through FcgammaR triggering
181 and SI viruses was observed at the level of beta-chemokine mRNA as well as at the level of protein e
182 unprotected monkeys had significantly higher beta-chemokine mRNA expression levels and increased numb
183 d, unprotected (n = 11) monkeys by measuring beta-chemokine mRNA levels and protein expression, the f
186 ells remained low despite increased entry by beta-chemokine neutralization, suggesting postentry HIV
190 ion, C-18 mediated inhibition did not induce beta-chemokines or cause CCR5 downmodulation, suggesting
191 ites of allergic inflammation by a number of beta-chemokines, particularly eotaxin and RANTES, the re
193 that the early production of proinflammatory beta chemokines plays a major role in the severe, most o
194 A expression levels and increased numbers of beta-chemokine-positive cells than did vaccinated, prote
195 bition of HIV replication was not due to the beta-chemokines present in cocultures of cell lines with
197 n response to P. falciparum and suggest that beta-chemokines produced by maternal cells contribute to
200 nti-HIV effects of PTX/PTX-B were not due to beta -chemokine production or coreceptor down-modulation
202 This cellular immunotherapy can modulate beta chemokine production in patients with advanced HIV-
203 se data suggest that the effects of IL-12 on beta-chemokine production and chemokine-receptor express
204 gressors and AIDS patients by examination of beta-chemokine production and HIV-1 infection in patient
205 factors, including beta-chemokines, and that beta-chemokine production by CD4+, but not CD8+, T cells
206 summary, phenotype, cytokine secretion, and beta-chemokine production by DC from HIV+ individuals we
208 aluation of the effect of HIV replication on beta-chemokine production indicated that acute infection
209 gressing individuals, indicating that global beta-chemokine production may have little effect on HIV-
210 These findings suggest that constitutive beta-chemokine production may play an important role in
211 a-inducing (NSI) viruses generally increased beta-chemokine production two to eightfold, whereas with
212 imulated cell proliferation nor cytokine and beta-chemokine production was associated with the expres
213 tide-specific IL-2 responses associated with beta-chemokine production were detectable at birth in th
214 combinant CD40 ligand (CD40LT), cytokine and beta-chemokine production were similar by DC from HIV- d
215 red productive viral infection, cytokine and beta-chemokine production, and beta-chemokine receptor e
218 train ADA revealed an inverse correlation to beta-chemokine production; clones from nonprogressors we
222 pression of a critical immune regulator, the beta-chemokine RANTES (regulated upon activation, normal
223 rocytes, and macrophages/microglia, that the beta-chemokines RANTES (regulated on activation, normal
225 kines interferon-gamma and interleukin-2 and beta-chemokines RANTES (regulated upon activation, norma
229 ct likely was due to the increased levels of beta-chemokines RANTES, MIP-1alpha, and MIP-1beta becaus
230 Recent studies have demonstrated that the beta-chemokines RANTES, MIP-1alpha, and MIP-1beta suppre
231 the memory cells produced high levels of the beta-chemokines RANTES, MIP-1alpha, and MIP-1beta upon s
233 ce protein R1, plus upregulation of exodus 2 beta-chemokine, RDC1 alpha-chemokine receptor, and trans
234 in the presence of its cognate receptor, the beta chemokine receptor 2 (CCR2), produces neural activi
235 The recent identification of the CC-CKR5 beta chemokine receptor as a major cofactor for entry of
237 32-nucleotide deletion (delta 32) within the beta-chemokine receptor 5 (CCR5) gene has been described
242 n this study, we evaluated the expression of beta-chemokine receptor CCR1 in the immature and adult r
244 me to inflamed tissues typically express the beta-chemokine receptor CCR5 and exhibit a Th1 cytokine
248 alpha-chemokine receptor fusin (CXCR-4) and beta-chemokine receptor CCR5 serve as entry cofactors fo
250 hage-tropic (M-tropic) HIV-1 strains use the beta-chemokine receptor CCR5, but not CCR2b, as a cofact
252 cytokine and beta-chemokine production, and beta-chemokine receptor expression in monocyte-derived m
254 tor (TNF)-alpha-like receptor gene, the US28 beta-chemokine receptor gene, and the UL55 envelope glyc
255 investigate the relative contribution of the beta-chemokine receptors CCR3 and CCR5 to viral infectio
257 fferent gp120 isolates bind to the alpha- or beta-chemokine receptors CXCR4 and CCR5, respectively.
264 TCR) following binding of antigen results in beta-chemokine release from CTLs in addition to cytolyti
267 beta-chemokine expression and the number of beta-chemokine responsive cells (i.e. microglia) accumul
269 increased extracellular levels of anti-HIV-1 beta-chemokines resulting from transient prolongation of
272 s replication were associated with increased beta-chemokine secretion and there is no evidence that b
276 h HIV-1-associated dementia and that, of the beta-chemokines tested, only MCP-1 could be detected in
277 e have isolated and characterized a human C6 beta-chemokine that is a potent agonist at CCR1 and CCR3
279 and macrophage inflammatory protein-1 alpha, beta-chemokines that have been suggested to have anti-HI
281 and MAdCAM as well as a number of alpha- and beta-chemokines was induced or upregulated and preceded
286 kines, but not antiinflammatory cytokines or beta-chemokines, were found to inhibit CMV expression, D
287 onocyte chemoattractant protein-1 (MCP-1), a beta chemokine which attracts cells of monocytic origin
289 as neutrophil chemoattractants, and the beta(beta)-chemokines, which function primarily as monocyte c
290 iased cytokine response; 3) the secretion of beta-chemokines, which are known to inhibit the use of t
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