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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.
31       CD8+ lymphocytes are a major source of beta-chemokines [3], but the stimulus for chemokine rele
32                                 Alignment of beta-chemokine amino acid sequences revealed the presenc
33                Although AOP-RANTES and other beta-chemokine analogs are potent inhibitors, the extrem
34                                          The beta chemokines and antibodies to CCR3 failed to affect
35               CCR5 is a receptor for several beta chemokines and the entry coreceptor used by macroph
36 gH contributes to this process by modulating beta-chemokine and interleukin 6 (Il6) expression.
37 of African green monkeys (AGMs) avidly binds beta-chemokines and functions as a coreceptor for simian
38 shows a differential effect on production of beta-chemokines and gamma interferon.
39 orphine on gene expression of the alpha- and beta-chemokines and their receptors by the astrocytoma c
40                                              beta-Chemokines and their receptors mediate the traffick
41  endogenous suppressive factors, such as the beta-chemokines, and HIV-inducing cytokines, such as tum
42                 Here, we show that all three beta-chemokines, and MIP-1alpha in particular, inhibit p
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
45 be partially reversed by treatment with anti-beta-chemokine antibodies.
46 n found in the macrophage-rich lesions where beta-chemokines are being produced.
47                                              Beta-chemokines are expressed by tubular epithelial cell
48             These observations indicate that beta-chemokines are responsible for a major proportion o
49         The findings indicate that alpha and beta chemokine as well as classical chemoattractant rece
50                To examine the potency of two beta-chemokines as immunomodulators, plasmid DNA encodin
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
53 CR5 NH2 terminus was important for efficient beta-chemokine binding.
54  cytolytic mechanisms include the release of beta-chemokines blocking entry of R5 HIV-1 strains.
55 nd CD8(+) T-cell subsets in tissues produced beta-chemokines both before and 21 days after SIV infect
56                                Production of beta-chemokines, but not of cytokines, was increased by
57                We show that secretion of the beta-chemokines by activated lymphocytes starts before c
58                  Maximal production of these beta-chemokines by activated peripheral blood cells was
59 ealed that the production of HIV-suppressive beta-chemokines by HIV antigen-stimulated PBMC was signi
60 n of antigen by T cells to the production of beta-chemokines by macrophages.
61                 The synergistic induction of beta-chemokines by non-CpG-ODN was phosphorothioate (PS)
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
66                   Therefore, drugs targeting beta-chemokines (CCL2 and CCL22), FGF-basic, HGF, or MIF
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
71                        A new member of human beta-chemokine cDNA was isolated and named leukotactin-1
72                     Two new members of human beta-chemokine cDNA were isolated based on structural an
73 th severe malaria have a distinct profile of beta-chemokines characterized by increased circulating l
74                              Two novel human beta-chemokines, Ck beta-8 or myeloid progenitor inhibit
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
78                            Thus, even though beta-chemokines decrease HIV replication in Mphi, these
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
84                                          CSF beta chemokine elevation is consistent with the macropha
85                         The release of these beta-chemokines explains both the specificity for R5 HIV
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
91 as at the level of inflammatory cytokine and beta-chemokine expression within the joint.
92  infection, monocyte brain infiltration, and beta-chemokine expression.
93 is, monocyte transendothelial migration, and beta-chemokine expression.
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
99 roduced similar amounts of IL-12, IL-10, and beta-chemokines, following stimulation.
100  an alternative splicing produces two active beta-chemokines from a single gene.
101 volved in the post-inflammatory clearance of beta-chemokines from cutaneous sites.
102  induce the secretion of specific alpha- and beta-chemokines from human umbilical vein endothelial ce
103 ycoproteins and by augmenting the release of beta-chemokines from NK cells.
104                                              beta-chemokine gene expression and release was determine
105 at least in part, from Hz-induced changes in beta-chemokine gene expression in blood mononuclear cell
106                                              Beta-chemokine gene expression profiles in blood mononuc
107 (NHPs) showed a better balance of alpha- and beta-chemokine gene expression with higher levels of bet
108  (beta-hematin) promote a similar pattern of beta-chemokine gene expression.
109                   The synthesis of antiviral beta-chemokines has joined cytolysis as a potential mech
110 ponsible for inducing macrophages to produce beta-chemokines have not been established.
111                  Two subfamilies, alpha- and beta-chemokines, have been described, based on structura
112 udies show that MCMV encodes and expresses a beta chemokine homolog with a novel predicted structure.
113         Murine cytomegalovirus carries a CC (beta) chemokine homolog gene giving rise to two related
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
116                                 In contrast, beta chemokines in plasma were either nondetectable or s
117                           However, levels of beta-chemokines in AIDS patients are comparable to and c
118 s observed upon neutralization of endogenous beta-chemokines in CD8-depleted or CD4+ PBMCs from most
119                                  The role of beta-chemokines in HIV infection was evaluated.
120 ings is discussed in relation to the role of beta-chemokines in HIV pathogenesis.
121             We sought to clarify the role of beta-chemokines in nonprogressors and AIDS patients by e
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-
125             Screening for epithelial-derived beta-chemokines indicated that IFN-gamma treatment cause
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
128                              The kinetics of beta-chemokine induction in T cells were slow (3 to 4 da
129 infection helps to explain viral tropism and beta-chemokine inhibition of primary HIV-1 isolates.
130              A soluble factor believed to be beta-chemokine is responsible for the inhibition of M-tr
131    Although the inhibition of HIV-1 entry by beta-chemokines is well documented, their effects on pos
132                                          The beta chemokine known as 6-C-kine, secondary lymphoid-tis
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
136                  To test the hypothesis that beta-chemokine levels may be relevant to the control of
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
140 ns are inhibited by their natural alpha- and beta-chemokine ligands.
141        Met-Ckbeta7 is a modified form of the beta-chemokine macrophage inflammatory protein (MIP) 4 (
142                                          The beta-chemokine macrophage inflammatory protein (MIP)-1al
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
146 ed CD8(+) T cell clone and identified as the beta-chemokine macrophage-derived chemokine (MDC).
147 esize and secrete substantial amounts of the beta-chemokines macrophage inflammatory protein (MIP)-1
148             The natural ligands of CCR5, the beta-chemokines macrophage inflammatory protein 1alpha (
149       We characterized the expression of the beta-chemokines macrophage inflammatory protein 1alpha (
150 he level of interferon-gamma (IFN-gamma) and beta-chemokines macrophage inflammatory protein-1alpha (
151             This study demonstrates that the beta-chemokines macrophage inflammatory proteins 1 alpha
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
154                The specific receptor for the beta-chemokines (macrophage-inflammatory protein (MIP)-1
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
158                  These findings suggest that beta-chemokines may affect HIV replication when an NSI v
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
161                                     The high beta-chemokine-mediated anti-HIV activity was against th
162  The sensitivity of an individual's virus to beta-chemokine-mediated inhibition correlated with the N
163 pagation of infection by failing to activate beta-chemokine-mediated inhibition of HIV-1 entry.
164                       These data reveal that beta-chemokine-mediated inhibition of virus replication
165 ugh its interactions with astrocytes induces beta-chemokine-mediated monocyte migration in HAD.
166                     Our results suggest that beta-chemokine-mediated resistance may be an important c
167 onocyte chemotactic protein-1 (MCP-1), a CC (beta) chemokine, mediates airway hyperreactivity in norm
168 usly described as a receptor for the related beta chemokine MIP-3beta (ELC or Exodus-3).
169 rus (HIV) biology was the discovery that the beta-chemokines MIP-1 alpha (macrophage inflammatory pro
170         In contrast, increased levels of the beta-chemokines MIP-1 alpha and -beta were seen early in
171                                          The beta-chemokines MIP-1alpha, MIP-1beta and RANTES inhibit
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
177             We studied the expression of the beta-chemokines: monocyte chemoattractant protein (gene
178 experiments demonstrated that the release of beta-chemokines, most likely through FcgammaR triggering
179 own to occur in dementia and with studies of beta chemokine mRNA expression in the brain.
180                        We assessed alpha and beta chemokine mRNA expression patterns and leukocyte ac
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
184                              In these cells, beta-chemokine mRNA was upregulated within 30 min and pr
185                                              beta-Chemokine neutralization enhanced HIV infection in
186 ells remained low despite increased entry by beta-chemokine neutralization, suggesting postentry HIV
187                                Finally, anti-beta-chemokine-neutralizing antibodies caused a more rap
188            However, the inhibitory effect of beta-chemokines on HIV-1 infection of macrophages has be
189                          Characterization of beta-chemokines on native macaque CCR3 on eosinophils wa
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
192                                              beta-chemokines play an important role in the developmen
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
196                    The suppressive effect of beta-chemokines, principally RANTES, on certain HIV-1 is
197 n response to P. falciparum and suggest that beta-chemokines produced by maternal cells contribute to
198                              The majority of beta-chemokine-producing CD8(+) T cells also produced IF
199                        Macrophages are major beta-chemokine-producing cells during T-cell directed, d
200 nti-HIV effects of PTX/PTX-B were not due to beta -chemokine production or coreceptor down-modulation
201            Moreover, we asked whether higher beta chemokine production could be demonstrated with cel
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
207 a primary source for the observed pattern of beta-chemokine production during acute malaria.
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
216 t also by the balance of CCR5 expression and beta-chemokine production.
217 ining or enhancing inflammatory cytokine and beta-chemokine production.
218 train ADA revealed an inverse correlation to beta-chemokine production; clones from nonprogressors we
219              Increased concentrations of the beta -chemokine RANTES were found in BAL fluid from the
220                 N-Formyl-Met-Leu-Phe and the beta-chemokine RANTES (regulated on activation normal T
221                                          The beta-chemokine RANTES (regulated on activation, normal T
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
224                                          The beta-chemokines RANTES (regulated on activation, normal
225 kines interferon-gamma and interleukin-2 and beta-chemokines RANTES (regulated upon activation, norma
226                                          The beta-chemokines RANTES, macrophage inflammatory protein
227                                          The beta-chemokines RANTES, MIP-1 alpha, and MIP-1 beta have
228 ins of HIV-1 is CC-CKR-5, a receptor for the beta-chemokines RANTES, MIP-1alpha and MIP-1beta.
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
232               Furthermore, neither the human beta-chemokines RANTES, MIP-1alpha, MIP-1beta, and MCP-1
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
236                                   At the CC (beta) chemokine receptor 2 (CCR2) and CCR5 loci, combina
237 32-nucleotide deletion (delta 32) within the beta-chemokine receptor 5 (CCR5) gene has been described
238 ro produced an increase in the expression of beta-chemokine receptor 5 (CCR5).
239                                          The beta-chemokine receptor C-C chemokine receptor 3 (CCR3)
240                            Expression of the beta-chemokine receptor CC-CKR-5 in CD4+, non-permissive
241                                          The beta-chemokine receptor CCR-5 is an essential co-factor
242 n this study, we evaluated the expression of beta-chemokine receptor CCR1 in the immature and adult r
243                                          The beta-chemokine receptor CCR3, which recognizes the ligan
244 me to inflamed tissues typically express the beta-chemokine receptor CCR5 and exhibit a Th1 cytokine
245                                          The beta-chemokine receptor CCR5 has been shown to modulate
246                                    The human beta-chemokine receptor CCR5 is an important cofactor fo
247                                          The beta-chemokine receptor CCR5 is required as a coreceptor
248  alpha-chemokine receptor fusin (CXCR-4) and beta-chemokine receptor CCR5 serve as entry cofactors fo
249            Surface expression of CD4 and the beta-chemokine receptor CCR5 was reduced on MDM in respo
250 hage-tropic (M-tropic) HIV-1 strains use the beta-chemokine receptor CCR5, but not CCR2b, as a cofact
251                       Here, we show that the beta-chemokine receptor CKR-5 serves as a cofactor for M
252  cytokine and beta-chemokine production, and beta-chemokine receptor expression in monocyte-derived m
253                       A mutant allele of the beta-chemokine receptor gene CCR5 bearing a 32-basepair
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
256                                          The beta-chemokine receptors CKR-3 and CKR-2b support HIV-1
257 fferent gp120 isolates bind to the alpha- or beta-chemokine receptors CXCR4 and CCR5, respectively.
258               An array of no less than eight beta-chemokine receptors has been identified, four of wh
259                        The data suggest that beta-chemokine receptors may influence FIV infection by
260                           Detection of these beta-chemokine receptors on microglia and some of their
261 d dual-tropic strains can also utilize other beta-chemokine receptors, such as CCR2b and CCR3.
262                 We demonstrate here that the beta chemokines, recombinant human macrophage inflammato
263                                Whereas three beta chemokines, regulated-on-activation normal T-cell e
264 TCR) following binding of antigen results in beta-chemokine release from CTLs in addition to cytolyti
265 d candidiasis is not secondary to suboptimal beta-chemokine release.
266                      Neutralization of these beta-chemokines rendered memory CD4(+) cells highly sens
267  beta-chemokine expression and the number of beta-chemokine responsive cells (i.e. microglia) accumul
268              Altered patterns of circulating beta-chemokines result, at least in part, from Hz-induce
269 increased extracellular levels of anti-HIV-1 beta-chemokines resulting from transient prolongation of
270 sisting of activated CD4(+) T cells, DC, and beta-chemokine-secreting cells.
271       To determine the in vivo importance of beta-chemokine secretion and CD8+-T-cell proliferation i
272 s replication were associated with increased beta-chemokine secretion and there is no evidence that b
273                                              beta-Chemokines serve to attract various types of blood
274 ach, using assays that measure the effect of beta-chemokines solely on Env-mediated fusion.
275                   Specific receptors for the beta-chemokine TCA3 have been identified on mouse monocy
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
278                            MCP-1 is a potent beta-chemokine that recruits monocytes and T cells and p
279 and macrophage inflammatory protein-1 alpha, beta-chemokines that have been suggested to have anti-HI
280                               High levels of beta-chemokines, the natural ligands of the CCR5 corecep
281 and MAdCAM as well as a number of alpha- and beta-chemokines was induced or upregulated and preceded
282                    The induction of CD83 and beta-chemokines was tyrosine phosphorylation dependent.
283                                              Beta-chemokines were expressed predominantly at the baso
284                        Significant levels of beta-chemokines were produced by both CD4+ and CD8+ PBMC
285         The monocyte- and macrophage-derived beta-chemokines were sufficient to block CCR5-dependent
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
288                  This receptor is ligated by beta chemokines, which influence HIV type 1 (HIV-1) repl
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
291                        Astrocytic release of beta-chemokines, which are relatively less selective for
292                                        Three beta-chemokines, which can be secreted by activated CD8+
293              Nevertheless, neutralization of beta-chemokines with specific antibodies did not abolish

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