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1 d amounts of tumor necrosis factor alpha and macrophage inflammatory protein 1alpha.
2 vation in monocyte chemotactic protein-1 and macrophage inflammatory protein-1alpha.
3 pha, monocyte chemoattractant protein-1, and macrophage inflammatory protein-1alpha.
4 production of the relevant chemoattractant, macrophage inflammatory protein-1alpha.
5 TNF and IL-1beta and the chemokines IL-8 and macrophage inflammatory protein-1alpha.
6 3 and partially desensitized the response to macrophage inflammatory protein-1alpha.
7 L-6, IL-12, tumor necrosis factor alpha, and macrophage inflammatory protein-1alpha.
8 okines, including IL-1, IL-6, IL-8, TNF, and macrophage-inflammatory protein-1alpha.
9 cyte-chemoattractant protein-1, eotaxin, and macrophage-inflammatory protein-1alpha.
10 tein 10; monocyte chemoattractant protein 1; macrophage inflammatory proteins 1alpha, 1beta, and 2; a
11 , days 17-19), intra-allograft expression of macrophage-inflammatory protein-1alpha, -1beta, and thei
12 luding cytokine (G-CSF, 14-fold), chemokine (macrophage-inflammatory protein 1alpha, 5-fold), immunor
15 terleukin-7, interleukin-13, interleukin-17, macrophage inflammatory protein 1alpha and 1beta, granul
16 L-8, monocyte chemoattractant protein 1, and macrophage inflammatory protein 1alpha and elevated urin
17 ta in murine BPD and an involvement for MIP (macrophage inflammatory protein)-1alpha and TREM (trigge
18 anges in the steady state levels of mRNA for macrophage inflammatory protein-1alpha and -1beta and mo
19 ophosphate-induced release of the chemokines macrophage inflammatory protein-1alpha and -1beta and RA
20 etion of RANTES alone or in combination with macrophage inflammatory protein-1alpha and -1beta block
21 , IL-10, monocyte chemotactic protein-1, and macrophage inflammatory protein-1alpha and -1beta increa
23 n, normal T cell expressed and secreted) and macrophage inflammatory protein-1alpha and -1beta) from
24 te chemoattractant protein-1, interleukin-8, macrophage inflammatory protein-1alpha and -1beta, and i
25 sulted in the production of large amounts of macrophage inflammatory protein-1alpha and -1beta, and R
27 s, but failed to stimulate the production of macrophage inflammatory protein-1alpha and -1beta; regul
28 axin, JE/monocyte chemoattractant protein-1, macrophage inflammatory protein-1alpha and -2, and mRNA,
29 giotensin II (Ang II) vascular inflammation (macrophage inflammatory protein-1alpha and beta) were al
30 uced ICAM-1 and CXCR3 transcript expression, macrophage inflammatory protein-1alpha and CXCL10 levels
31 oint scale) exhibited significantly elevated macrophage inflammatory protein-1alpha and IL-10 and a t
33 hase mRNA was decreased in GKO mice, whereas macrophage inflammatory protein-1alpha and interleukin-4
35 secretion of the chemoattractant chemokines, macrophage inflammatory protein-1alpha and macrophage ch
37 protein-2 and KC as well as the CC chemokine macrophage inflammatory protein-1alpha and the proinflam
38 espondence between the ability of RANTES and macrophage inflammatory proteins 1alpha and 1beta to act
39 osis factor [TNF], interleukins 1beta and 6, macrophage inflammatory proteins 1alpha and 1beta) from
40 induces the production of two CC-chemokines, macrophage inflammatory proteins 1alpha and 1beta, by HI
42 in part with decreased levels of TNF-alpha, macrophage inflammatory proteins-1alpha and -2, and KC i
43 + CTL secrete the proinflammatory chemokines macrophage-inflammatory protein-1alpha and -1beta, IL-16
44 ese CTL clones secrete IFN-gamma, TNF-alpha, macrophage-inflammatory protein-1alpha and -1beta, IL-16
46 or CCR5; acquired specific binding sites for macrophage-inflammatory protein-1alpha and eotaxin (the
47 tants monocyte chemoattractant protein-1 and macrophage-inflammatory protein-1alpha and impaired clea
48 that IL-4 and IL-5 induced higher levels of macrophage-inflammatory protein-1alpha and KC; IL-4 also
49 reases P. acnes-induced granuloma formation, macrophage-inflammatory protein-1alpha and macrophage-in
50 SF stimulates PMN and macrophages to secrete macrophage-inflammatory protein-1alpha and MCP-1, which
51 o IgG1- and IgG3-GXM complexes regarding: 1) macrophage-inflammatory protein-1alpha and monocyte chem
52 ges, which correlated with expression of the macrophage-inflammatory protein-1alpha and the monocyte
53 inflammatory cytokines (TNF-alpha, IL-8, and macrophage inflammatory protein 1alpha) and augmented pr
54 -inducible chemokine (interleukin [IL]-8 and macrophage inflammatory protein-1alpha) and cytokine (IL
56 eady-state levels of TNF-alpha, IL-5, IL-13, macrophage inflammatory protein 1alpha, and granulocyte-
57 enase-2, monocyte chemoattractant protein-1, macrophage inflammatory protein 1alpha, and macrophage i
58 d, while monocyte chemoattractant protein 1, macrophage inflammatory protein 1alpha, and RANTES were
59 interacting signals comprising IL-10, IL-8, macrophage inflammatory protein-1alpha, and C-reactive p
60 on of proinflammatory proteins such as IL-8, macrophage inflammatory protein-1alpha, and eotaxin sugg
61 emokines monocyte chemoattractant protein-1, macrophage inflammatory protein-1alpha, and interferon-g
62 s selective for monocytes, including RANTES, macrophage inflammatory protein-1alpha, and macrophage i
63 s IP-10 and Mig and the CCR5 ligands RANTES, macrophage inflammatory protein-1alpha, and macrophage i
64 ion of normal T cell expressed and secreted, macrophage inflammatory protein-1alpha, and macrophage i
65 IP-10, Mig, monocyte chemotactic protein-1, macrophage inflammatory protein-1alpha, and macrophage i
66 activation normal T expressed and secreted), macrophage inflammatory protein-1alpha, and monocyte che
67 f IL-1beta, IL-1Ra, IL-8, IL-12 p40, RANTES, macrophage inflammatory protein-1alpha, and monocyte che
69 lasma levels of tumor necrosis factor-alpha, macrophage inflammatory protein-1alpha, and monocyte che
70 mal T-cell expressed, and secreted (RANTES), macrophage inflammatory protein-1alpha, and monocyte che
71 ollagen up-regulates the production of IL-8, macrophage inflammatory protein-1alpha, and monocyte che
72 lpha, macrophage inflammatory protein-2, KC, macrophage inflammatory protein-1alpha, and monocyte che
74 okines macrophage chemoattractant protein-1, macrophage inflammatory protein-1alpha, and RANTES prece
75 of MCP-3/FIC and other CC chemokines (MCP-1, macrophage inflammatory protein-1alpha, and RANTES) was
76 d, including monocyte chemotactic protein-1, macrophage inflammatory protein-1alpha, and stromal cell
77 terleukin-6, interleukin-13, interleukin-17, macrophage inflammatory proteins-1alpha, and macrophage
78 flammatory cytokines TNF-alpha, IL-1, IL-12, macrophage-inflammatory protein-1alpha, and IFN-gamma, b
80 tumor necrosis factor-alpha (TNF-alpha) and macrophage inflammatory protein-1alpha, as well as of ot
81 expression of mRNA for MCP-1, MCP-3/FIC, and macrophage inflammatory protein-1alpha at 2 and/or 24 h.
82 6 (IL-6), tumor necrosis factor alpha, IL-8, macrophage inflammatory protein 1alpha/beta, and monocyt
84 chemoattractant protein 1], MIP-1alpha/beta [macrophage inflammatory protein 1alpha/beta], IL-6 [inte
85 tractants monocyte chemotactic protein-1 and macrophage inflammatory protein-1alpha but not RANTES or
86 ing factor, tumor necrosis factor alpha, and macrophage inflammatory protein-1alpha by LAK cells stim
87 s (monocyte chemoattractant protein 1/CCL-2, macrophage inflammatory protein 1alpha/CCL-3, and IP-10)
88 was a potent stimulator of the CCR5 ligands macrophage inflammatory protein-1alpha/CCL-3 (MIP-1alpha
90 f these studies was to determine the role of macrophage inflammatory protein 1alpha/CCL3 in pulmonary
91 nes monocyte chemoattractant protein 1/CCL2, macrophage inflammatory protein 1alpha/CCL3, and RANTES/
92 protein-1/CCL2, inducible protein-10/CXCL10, macrophage inflammatory protein-1alpha/CCL3, and interle
93 ple chemokines, including, most prominently, macrophage inflammatory protein-1alpha/CCL3, which is kn
95 CL10 (IFN-gamma-inducible protein-10), CCL3 (macrophage-inflammatory protein-1alpha), CCL7 (monocyte
96 erences in monocyte chemotactic protein-1 or macrophage inflammatory protein-1alpha chemokine levels
97 or necrosis factor alpha, interleukin-1, and macrophage inflammatory protein 1alpha compared to that
98 fic calcium flux and chemotaxis responses to macrophage-inflammatory protein-1alpha, eotaxin, and oth
99 ective because no changes were observed when macrophage-inflammatory protein-1alpha, eotaxin, or MCP-
100 n, normal T cell expressed and secreted, and macrophage inflammatory protein-1alpha genes in tubercul
101 IL-4, and IFN-gamma, whereas mRNA levels for macrophage inflammatory protein-1alpha, GM-CSF, and IL-1
102 Serum levels of tumor necrosis factor-alpha; macrophage inflammatory protein-1alpha; growth-related o
103 vation, normal T expressed and secreted) and macrophage inflammatory protein-1alpha, have also been i
104 oma patients was recently screened and human macrophage inflammatory protein-1alpha (hMIP-1alpha) was
105 d with elevated tumor necrosis factor alpha, macrophage inflammatory protein 1alpha, IL-6, and IL-8.
108 nses were characterized by the production of macrophage inflammatory protein 1alpha, interferon gamma
109 tors, including tumor necrosis factor alpha, macrophage inflammatory protein 1alpha, interleukin 1bet
111 expression for tumor necrosis factor-alpha, macrophage inflammatory protein-1alpha, macrophage infla
112 8 and IL-12 for NK cell production of IL-10, macrophage inflammatory protein-1alpha, macrophage infla
113 duced proliferation and chemokine secretion (macrophage inflammatory protein-1alpha, macrophage infla
114 receptor for the leukocyte chemoattractants macrophage inflammatory protein-1alpha, macrophage infla
115 -chemokines (monocyte chemotactic protein-1, macrophage inflammatory protein-1alpha, macrophage infla
116 es the activation of cells by the chemokines macrophage inflammatory protein-1alpha, macrophage infla
117 cluding IFN-gamma-inducible protein (IP)-10, macrophage inflammatory protein-1alpha, macrophage infla
118 everal members of the chemokine gene family: macrophage inflammatory protein-1alpha, macrophage infla
119 and chemokine-related cytokine/lymphotactin, macrophage-inflammatory protein 1alpha, macrophage-infla
120 macrophages produced only limited amounts of macrophage-inflammatory protein 1alpha, macrophage-infla
121 g to an enhanced secretion of the chemokines macrophage-inflammatory protein-1alpha, macrophage-infla
122 bserved during rejection of these grafts: 1) macrophage-inflammatory protein-1alpha, macrophage-infla
124 nd IL-6, as well as levels of the chemokines macrophage inflammatory protein 1alpha (MIP-1alpha) and
125 eptor that upon stimulation, particularly by macrophage inflammatory protein 1alpha (MIP-1alpha) and
126 rely burned patients (91%) failed to produce macrophage inflammatory protein 1alpha (MIP-1alpha) in c
127 pression of interleukin 1beta (IL-1beta) and macrophage inflammatory protein 1alpha (MIP-1alpha) in t
129 levels throughout infection, and had higher macrophage inflammatory protein 1alpha (MIP-1alpha) leve
130 erleukin-alpha1 (IL-1alpha), IL-12(p40), and macrophage inflammatory protein 1alpha (MIP-1alpha) para
131 oformans immune complexes as the stimuli and macrophage inflammatory protein 1alpha (MIP-1alpha) prod
136 mma-interferon-inducible protein 10 (IP-10), macrophage inflammatory protein 1alpha (MIP-1alpha), and
137 cell expressed and secreted (RANTES), murine macrophage inflammatory protein 1alpha (MIP-1alpha), and
138 leukin-1alpha (IL-1alpha), IL-4, IL-6, IL-8, macrophage inflammatory protein 1alpha (MIP-1alpha), and
139 of tumor necrosis factor, gamma interferon, macrophage inflammatory protein 1alpha (MIP-1alpha), and
140 tion, normal T cell expressed and secreted), macrophage inflammatory protein 1alpha (MIP-1alpha), and
143 tumor necrosis factor alpha (TNF-alpha), and macrophage inflammatory protein 1alpha (MIP-1alpha), in
144 erized the expression of the beta-chemokines macrophage inflammatory protein 1alpha (MIP-1alpha), MIP
145 species induced secretion of high levels of macrophage inflammatory protein 1alpha (MIP-1alpha), MIP
146 ealed much higher levels of RNA specific for macrophage inflammatory protein 1alpha (MIP-1alpha), MIP
147 -8), monocyte chemotactic protein 1 (MCP-1), macrophage inflammatory protein 1alpha (MIP-1alpha), MIP
148 ral ligands for the CCR5 chemokine receptor, macrophage inflammatory protein 1alpha (MIP-1alpha), MIP
149 ) and interleukin-8 (IL-8) but not mRNAs for macrophage inflammatory protein 1alpha (MIP-1alpha), MIP
150 pecifically, levels of pulmonary and hepatic macrophage inflammatory protein 1alpha (MIP-1alpha), MIP
151 factor (G-CSF), interferon alfa (IFN-alpha), macrophage inflammatory protein 1alpha (MIP-1alpha), MIP
153 natural ligands of CCR5, the beta-chemokines macrophage inflammatory protein 1alpha (MIP-1alpha), MIP
154 L-1beta), IL-6, tumor necrosis factor alpha, macrophage inflammatory protein 1alpha (MIP-1alpha), MIP
156 ncluding IL-8, macrophage-derived chemokine, macrophage inflammatory protein 1alpha (MIP-1alpha), mon
157 of chemokines on RABV infection, chemokines macrophage inflammatory protein 1alpha (MIP-1alpha), RAN
158 SF), macrophage-derived chemokine (MDC), and macrophage inflammatory protein 1alpha (MIP-1alpha), wer
159 erleukin 6 (IL-6) and IL-8 and the chemokine macrophage inflammatory protein 1alpha (MIP-1alpha).
160 r inflammation modulated by the CC chemokine macrophage inflammatory protein 1alpha (MIP-1alpha).
164 cyte chemoattractant protein 1 (MCP-1/CCL2), macrophage inflammatory protein 1alpha (MIP-1alpha/CCL3)
165 zes the binding of the chemokines RANTES and macrophage inflammatory protein 1alpha (MIP-1alpha; CCL3
167 nocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1alpha (MIP-1alpha) aid
169 dent growth-related oncogene homologue (KP), macrophage inflammatory protein-1alpha (MIP-1alpha) and
171 IL-10), and the T-cell-regulatory chemokines macrophage inflammatory protein-1alpha (MIP-1alpha) and
172 strocyte cultures resulted in the release of macrophage inflammatory protein-1alpha (MIP-1alpha) and
174 te the following proinflammatory chemokines: macrophage inflammatory protein-1alpha (MIP-1alpha) and
175 ors is blocked by the suppressive chemokines macrophage inflammatory protein-1alpha (MIP-1alpha) and
176 te monocyte/macrophage production of IL-8 or macrophage inflammatory protein-1alpha (MIP-1alpha) and
177 ells, expressed, probably secreted (RANTES), macrophage inflammatory protein-1alpha (MIP-1alpha) and
178 ly induced the expression of two chemokines, macrophage inflammatory protein-1alpha (MIP-1alpha) and
179 flammatory cytokine IL-1alpha and chemokines macrophage inflammatory protein-1alpha (MIP-1alpha) and
180 istration of plasmids encoding the chemokine macrophage inflammatory protein-1alpha (MIP-1alpha) and
186 infiltration, the expression of ICAM-1, and macrophage inflammatory protein-1alpha (MIP-1alpha) in t
190 oratory have suggested that the CC chemokine macrophage inflammatory protein-1alpha (MIP-1alpha) may
191 ly to sites, in particular CCR1, shared with macrophage inflammatory protein-1alpha (MIP-1alpha) on t
192 distal region of mouse Chr 9 where the mouse macrophage inflammatory protein-1alpha (MIP-1alpha) rece
193 hage colony-stimulating factor (GM-CSF), and macrophage inflammatory protein-1alpha (MIP-1alpha) resu
194 ugh the TCR and incubated in the presence of macrophage inflammatory protein-1alpha (MIP-1alpha) show
195 ocyte chemoattractant protein-1 (MCP-1), and macrophage inflammatory protein-1alpha (MIP-1alpha) than
196 tifs mediating binding of the beta-chemokine macrophage inflammatory protein-1alpha (MIP-1alpha) to G
197 chemoattractant protein-1 (MCP-1), C10, and macrophage inflammatory protein-1alpha (MIP-1alpha) were
198 (monocyte chemoattractant protein-1), CCL3 (macrophage inflammatory protein-1alpha (MIP-1alpha)), CC
199 ed the renal cortical expression of the C-C (macrophage inflammatory protein-1alpha (MIP-1alpha)), mo
201 rmal T cell expressed and secreted (RANTES), macrophage inflammatory protein-1alpha (MIP-1alpha), and
202 a-inducible protein-10 (IP-10), Mig, RANTES, macrophage inflammatory protein-1alpha (MIP-1alpha), and
203 mokines IL-8, growth-regulated protein-beta, macrophage inflammatory protein-1alpha (MIP-1alpha), and
204 tion, normal T cell expressed and secreted), macrophage inflammatory protein-1alpha (MIP-1alpha), and
205 through covaccination with plasmids encoding macrophage inflammatory protein-1alpha (MIP-1alpha), fms
206 gE/antigen, and CCR1, using recombinant CCL3/macrophage inflammatory protein-1alpha (MIP-1alpha), inc
207 mRNA expression and protein production of macrophage inflammatory protein-1alpha (MIP-1alpha), MIP
208 is and RNase protection assays revealed that macrophage inflammatory protein-1alpha (MIP-1alpha), MIP
209 ficiency virus (HIV) entry into macrophages: macrophage inflammatory protein-1alpha (MIP-1alpha), MIP
210 rferon-gamma (IFN-gamma) and beta-chemokines macrophage inflammatory protein-1alpha (MIP-1alpha), MIP
211 dependently inhibit HA-induced expression of macrophage inflammatory protein-1alpha (MIP-1alpha), MIP
213 ion of 1 group of chemokine genes, including macrophage inflammatory protein-1alpha (MIP-1alpha), MIP
214 ry cytokines interleukin-1alpha (IL-1alpha), macrophage inflammatory protein-1alpha (MIP-1alpha), MIP
215 ncoding the chemokines interleukin-8 (IL-8), macrophage inflammatory protein-1alpha (MIP-1alpha), MIP
216 mma, interleukin (IL)-2, IL-9, IL-12, IL-17, macrophage inflammatory protein-1alpha (MIP-1alpha), mon
217 BX 471 was able to displace the CCR1 ligands macrophage inflammatory protein-1alpha (MIP-1alpha), RAN
218 receptor 5 (CCR5) and migrate in response to macrophage inflammatory protein-1alpha (MIP-1alpha), whe
219 s supplemented with interleukin-3 (IL-3) and macrophage inflammatory protein-1alpha (MIP-1alpha).
220 tumor necrosis factor-alpha (TNF-alpha), and macrophage inflammatory protein-1alpha (MIP-1alpha).
221 monocyte chemotactic protein-1 (MCP-1), and macrophage inflammatory protein-1alpha (MIP-1alpha).
222 astrocyte chemotaxis to the mouse chemokine macrophage inflammatory protein-1alpha (MIP-1alpha).
224 evaluated the expression of the CCR1 ligand macrophage inflammatory protein-1alpha (MIP-1alpha/CCL3)
225 oproteinase-2 activity and diminished plasma macrophage inflammatory protein-1alpha (MIP-1alpha; also
226 infiltration was an increased expression of macrophage-inflammatory protein 1alpha (MIP-1alpha), a l
227 s representing several chemokines, including macrophage-inflammatory protein 1alpha (MIP-1alpha), MIP
229 ults in the production of copious amounts of macrophage-inflammatory protein-1alpha (MIP-1alpha) and
230 tive was to define the role of the chemokine macrophage-inflammatory protein-1alpha (MIP-1alpha) in t
231 assessed, monocyte-chemotactic protein-1 and macrophage-inflammatory protein-1alpha (MIP-1alpha), onl
232 with HIV-1 produce high levels of M-CSF and macrophage-inflammatory protein-1alpha (MIP-1alpha).
233 id peroxidation), liver and lung chemokines (macrophage inflammatory protein 1alpha [MIP-1alpha] and
234 cytokine (IL-1beta and IL-6) and chemokine (macrophage inflammatory protein 1alpha [MIP-1alpha] and
235 ory cytokines (interleukin-1beta [IL-1beta], macrophage inflammatory protein 1alpha [MIP-1alpha], and
237 (tumor necrosis factor-alpha [TNF-alpha] and macrophage inflammatory protein-1alpha [MIP-1alpha]), si
238 leukin 1 [IL-1], and IL-16); and chemokines (macrophage inflammatory protein-1alpha [MIP-1alpha], MIP
239 rferon-inducible protein-10 [IP-10]) and CC (macrophage inflammatory protein-1alpha [MIP-1alpha], MIP
240 d CCR5 ligands (stromal-derived factor 1 and macrophage-inflammatory protein-1alpha [MIP-1alpha], MIP
241 on normal T cell expressed and secreted) and macrophage inflammatory protein 1alpha (MIP1-alpha).
243 a striking correlation between expression of macrophage-inflammatory protein 1alpha (MIP1alpha) and s
244 reatment with stromal cell-derived factor 1, macrophage-inflammatory protein-1alpha (MIP1alpha) or TG
245 ction of monocyte chemoattractant protein-1, macrophage inflammatory protein-1alpha, MMP-2, MMP-9, an
246 ontrol cells, responded to the CC chemokines macrophage inflammatory protein-1alpha, monocyte chemoat
247 ation in plasma tumor necrosis factor-alpha, macrophage inflammatory protein-1alpha, monocyte chemoat
248 -1beta, IL-6, keratinocyte-derived cytokine, macrophage inflammatory protein-1alpha, monocyte chemota
249 We earlier observed that two chemokines-macrophage inflammatory protein 1alpha/monocyte chemoatt
250 inflammatory response, and no production of macrophage inflammatory protein-1alpha or monocyte chemo
252 eron-gamma-inducible protein of 10 kDa, CCL3/macrophage inflammatory protein-1alpha, or CCL5/RANTES (
253 reatment with stromal cell-derived factor 1, macrophage-inflammatory protein-1alpha, or TGF-beta.
254 whereas BDR was associated with high plasma macrophage inflammatory protein 1alpha (P = .002) and sp
258 ), or C5a, but not stromal-derived factor-1, macrophage inflammatory protein-1alpha, RANTES, or eotax
259 kines (TNF-alpha, IFN-gamma) and chemokines (macrophage-inflammatory protein-1alpha, RANTES, monocyte
260 Galphai, Galphaq, and Galpha16, whereas the macrophage inflammatory protein-1alpha/RANTES (regulated
261 of one of the ligands for RANTES receptors, macrophage-inflammatory protein 1alpha, reduces only sli
262 pO2 negatively correlated with CD68 mRNA and macrophage inflammatory protein 1alpha secretion (R = -0
264 esponse to stromal cell-derived factor-1 and macrophage-inflammatory protein-1alpha, suggesting that
265 mma, monocyte chemoattractant protein-1, and macrophage-inflammatory protein-1alpha than parental mic
266 ant, monocyte chemoattractant protein-1, and macrophage inflammatory protein-1alpha) that are signifi
267 igration was specific, as another chemokine, macrophage inflammatory protein-1alpha, triggered astroc
269 ines, monocyte chemoattractant protein-1 and macrophage inflammatory protein-1alpha were induced with
270 onocyte chemoattractant protein-1 and murine macrophage inflammatory protein-1alpha were up-regulated
271 tein-10, monocyte chemotactic protein-1, and macrophage inflammatory protein-1alpha) were associated
272 ry cytokines (IFN-gamma, IL-1beta, IL-6, and macrophage inflammatory protein-1alpha) were lower after
273 -2 and IFN-gamma) and chemokines (RANTES and macrophage inflammatory protein-1alpha) were significant
274 onocyte Chemoattractant Protein-1) and CCL3 (Macrophage Inflammatory Protein-1alpha), were upregulate
275 ocyte chemoattractant protein-1 (MCP-1), and macrophage inflammatory protein-1alpha, whereas both sub
276 Here we report that local expression of macrophage inflammatory protein 1alpha, which results in
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