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1 tors monocyte chemotactic protein-1 (MCP-1), macrophage inflammatory protein 1 (MIP-1), and macrophag
2 ral latent ORF73, immunomodulatory K5, viral macrophage inflammatory protein 1 (MIP-1), and viral MIP
3 arly disease stage was an increased level of macrophage inflammatory protein 1 alpha (MIP-1 alpha), a
4 enic mice deficient in interleukin-6 (IL-6), macrophage inflammatory protein 1 alpha (MIP-1alpha), IL
5 released 36% less nitric oxide and 82% less macrophage inflammatory protein 1 alpha and expressed 63
6 locyte macrophage colony-stimulating factor, macrophage inflammatory protein 1 alpha, and tumor necro
7 C3; and an increase in the levels of CD107a, macrophage inflammatory protein 1 beta (MIP-1beta), and
8 monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 1 beta (MIP-1beta), and
9 vated endothelium by its capacity to trigger macrophage inflammatory protein 1 beta from primary mono
10 rferon (IFN)-gamma-inducible protein 10, and macrophage inflammatory protein 1 beta levels were diffe
11 of PD-1 expression were required to inhibit macrophage inflammatory protein 1 beta production, lower
13 r functions; cardiac inflammation (increased macrophage inflammatory protein 1, interleukin-1, P-sele
14 o 3-fold greater amounts of IL-18, TNFalpha, macrophage inflammatory protein 1, macrophage inflammato
15 ed expression of T-cell-attracting chemokine macrophage inflammatory protein 1-alpha (MIP-1alpha/CCL3
16 o) mice have increased circulating levels of macrophage inflammatory protein 1-alpha and interleukin-
17 te macrophage colony-stimulating factor, and macrophage inflammatory protein 1-alpha were lower 14 da
18 ytic polypeptide 3 G/F/H) and CC chemokines (macrophage inflammatory protein 1-alpha, macrophage infl
19 es (macrophage inflammatory protein 1-alpha, macrophage inflammatory protein 1-beta, regulated on act
20 Genes encoding chemokines, including IL-8; macrophage inflammatory proteins 1, 3, and 4; and monocy
22 IL-6, as well as the migration-related genes macrophage inflammatory protein-1 (MIP-1alpha), MIP-2 an
23 athyroid hormone-related protein (PTHrP) and macrophage inflammatory protein-1 alpha (MIP-1 alpha) ar
24 nificant elevation in interleukin-6, whereas macrophage inflammatory protein-1 alpha and monocyte che
25 CCL2/monocyte chemotactic protein 1 and CCL3/macrophage inflammatory protein-1 alpha) were also prese
26 -1 receptor antagonist [IL-1Ra], IL-6, IL-8, macrophage inflammatory protein-1 beta [MIP-1beta]/C-C m
27 yte-macrophage colony-stimulating factor and macrophage inflammatory protein-1 beta levels in cocultu
28 whereas the levels of IL-6, IL-8, IL-10, and macrophage inflammatory protein-1 beta were higher in pa
29 interleukin-2, tumor necrosis factor-alpha, macrophage inflammatory protein-1 beta, and CD107a by CD
30 lysis, we found expression of the chemokine, macrophage inflammatory protein-1 delta (MIP-1 delta), t
31 mic proinflammatory chemokine levels such as macrophage inflammatory protein-1-gamma, B-lymphocyte ch
33 eptor that upon stimulation, particularly by macrophage inflammatory protein 1alpha (MIP-1alpha) and
34 pression of interleukin 1beta (IL-1beta) and macrophage inflammatory protein 1alpha (MIP-1alpha) in t
35 levels throughout infection, and had higher macrophage inflammatory protein 1alpha (MIP-1alpha) leve
36 erleukin-alpha1 (IL-1alpha), IL-12(p40), and macrophage inflammatory protein 1alpha (MIP-1alpha) para
38 tumor necrosis factor alpha (TNF-alpha), and macrophage inflammatory protein 1alpha (MIP-1alpha), in
39 factor (G-CSF), interferon alfa (IFN-alpha), macrophage inflammatory protein 1alpha (MIP-1alpha), MIP
41 ncluding IL-8, macrophage-derived chemokine, macrophage inflammatory protein 1alpha (MIP-1alpha), mon
42 of chemokines on RABV infection, chemokines macrophage inflammatory protein 1alpha (MIP-1alpha), RAN
43 SF), macrophage-derived chemokine (MDC), and macrophage inflammatory protein 1alpha (MIP-1alpha), wer
44 erleukin 6 (IL-6) and IL-8 and the chemokine macrophage inflammatory protein 1alpha (MIP-1alpha).
45 cyte chemoattractant protein 1 (MCP-1/CCL2), macrophage inflammatory protein 1alpha (MIP-1alpha/CCL3)
46 zes the binding of the chemokines RANTES and macrophage inflammatory protein 1alpha (MIP-1alpha; CCL3
47 on normal T cell expressed and secreted) and macrophage inflammatory protein 1alpha (MIP1-alpha).
48 whereas BDR was associated with high plasma macrophage inflammatory protein 1alpha (P = .002) and sp
50 cytokine (IL-1beta and IL-6) and chemokine (macrophage inflammatory protein 1alpha [MIP-1alpha] and
51 ory cytokines (interleukin-1beta [IL-1beta], macrophage inflammatory protein 1alpha [MIP-1alpha], and
53 terleukin-7, interleukin-13, interleukin-17, macrophage inflammatory protein 1alpha and 1beta, granul
54 L-8, monocyte chemoattractant protein 1, and macrophage inflammatory protein 1alpha and elevated urin
55 pO2 negatively correlated with CD68 mRNA and macrophage inflammatory protein 1alpha secretion (R = -0
56 inflammatory cytokines (TNF-alpha, IL-8, and macrophage inflammatory protein 1alpha) and augmented pr
58 mulating factor, monocyte chemoattractant 1, macrophage inflammatory protein 1alpha, and interleukin
59 enase-2, monocyte chemoattractant protein-1, macrophage inflammatory protein 1alpha, and macrophage i
60 d, while monocyte chemoattractant protein 1, macrophage inflammatory protein 1alpha, and RANTES were
61 d with elevated tumor necrosis factor alpha, macrophage inflammatory protein 1alpha, IL-6, and IL-8.
62 nses were characterized by the production of macrophage inflammatory protein 1alpha, interferon gamma
63 tors, including tumor necrosis factor alpha, macrophage inflammatory protein 1alpha, interleukin 1bet
65 6 (IL-6), tumor necrosis factor alpha, IL-8, macrophage inflammatory protein 1alpha/beta, and monocyt
67 chemoattractant protein 1], MIP-1alpha/beta [macrophage inflammatory protein 1alpha/beta], IL-6 [inte
68 s (monocyte chemoattractant protein 1/CCL-2, macrophage inflammatory protein 1alpha/CCL-3, and IP-10)
69 nes monocyte chemoattractant protein 1/CCL2, macrophage inflammatory protein 1alpha/CCL3, and RANTES/
70 ta in murine BPD and an involvement for MIP (macrophage inflammatory protein)-1alpha and TREM (trigge
71 ly induced the expression of two chemokines, macrophage inflammatory protein-1alpha (MIP-1alpha) and
72 flammatory cytokine IL-1alpha and chemokines macrophage inflammatory protein-1alpha (MIP-1alpha) and
74 mokines IL-8, growth-regulated protein-beta, macrophage inflammatory protein-1alpha (MIP-1alpha), and
75 8 (IL-8), and decreased production of IL-10, macrophage inflammatory protein-1alpha (MIP-1alpha), and
76 gE/antigen, and CCR1, using recombinant CCL3/macrophage inflammatory protein-1alpha (MIP-1alpha), inc
77 ry cytokines interleukin-1alpha (IL-1alpha), macrophage inflammatory protein-1alpha (MIP-1alpha), MIP
78 mma, interleukin (IL)-2, IL-9, IL-12, IL-17, macrophage inflammatory protein-1alpha (MIP-1alpha), mon
79 inflammation (IL-1RA, -6, -8, -10, and -18; macrophage inflammatory protein-1alpha and -1beta; tumor
80 giotensin II (Ang II) vascular inflammation (macrophage inflammatory protein-1alpha and beta) were al
81 oint scale) exhibited significantly elevated macrophage inflammatory protein-1alpha and IL-10 and a t
82 tractants monocyte chemotactic protein-1 and macrophage inflammatory protein-1alpha but not RANTES or
83 ing factor, tumor necrosis factor alpha, and macrophage inflammatory protein-1alpha by LAK cells stim
84 IL-6, monocyte chemoattractant protein, and macrophage inflammatory protein-1alpha in GPR37-KO mice
86 ant, monocyte chemoattractant protein-1, and macrophage inflammatory protein-1alpha) that are signifi
87 tein-10, monocyte chemotactic protein-1, and macrophage inflammatory protein-1alpha) were associated
88 onocyte Chemoattractant Protein-1) and CCL3 (Macrophage Inflammatory Protein-1alpha), were upregulate
90 interacting signals comprising IL-10, IL-8, macrophage inflammatory protein-1alpha, and C-reactive p
91 emokines monocyte chemoattractant protein-1, macrophage inflammatory protein-1alpha, and interferon-g
92 lasma levels of tumor necrosis factor-alpha, macrophage inflammatory protein-1alpha, and monocyte che
93 mal T-cell expressed, and secreted (RANTES), macrophage inflammatory protein-1alpha, and monocyte che
94 tumor necrosis factor-alpha (TNF-alpha) and macrophage inflammatory protein-1alpha, as well as of ot
95 ation in plasma tumor necrosis factor-alpha, macrophage inflammatory protein-1alpha, monocyte chemoat
96 -1beta, IL-6, keratinocyte-derived cytokine, macrophage inflammatory protein-1alpha, monocyte chemota
97 eron-gamma-inducible protein of 10 kDa, CCL3/macrophage inflammatory protein-1alpha, or CCL5/RANTES (
99 was a potent stimulator of the CCR5 ligands macrophage inflammatory protein-1alpha/CCL-3 (MIP-1alpha
100 protein-1/CCL2, inducible protein-10/CXCL10, macrophage inflammatory protein-1alpha/CCL3, and interle
101 ple chemokines, including, most prominently, macrophage inflammatory protein-1alpha/CCL3, which is kn
102 Serum levels of tumor necrosis factor-alpha; macrophage inflammatory protein-1alpha; growth-related o
103 terleukin-6, interleukin-13, interleukin-17, macrophage inflammatory proteins-1alpha, and macrophage
104 ced protein 10 (approximately 2.0-fold), and macrophage inflammatory protein 1beta (approximately 1.5
105 ion of the cysteine-cysteine (C-C) chemokine macrophage inflammatory protein 1beta (MIP-1beta) and in
106 ity correlated with HIV-1-specific CD107a or macrophage inflammatory protein 1beta (MIP-1beta) expres
107 monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 1beta (MIP-1beta), and s
108 protein 10 (IP-10), interleukin 10 (IL-10), macrophage inflammatory protein 1beta (MIP-1beta), and s
109 rleukin-1beta (IL-1beta), IL-6, IL-8, CCL20, macrophage inflammatory protein 1beta (MIP-1beta), CXCL-
112 In support of this, there was an increase in macrophage inflammatory protein 1beta (MIP-1beta; CCL4)
113 mmatory protein 1alpha (P = .002) and sputum macrophage inflammatory protein 1beta (P = .001) levels.
114 s (e.g., monocyte chemoattractant protein 1, macrophage inflammatory protein 1beta [MIP-1beta], and M
115 lecules by means of immunoblotting, PGD2 and macrophage inflammatory protein 1beta generation by usin
116 cytotoxic (CD107a expression) and cytokine (macrophage inflammatory protein 1beta secretion) effecto
117 osphorylation, inflammatory gene expression, macrophage inflammatory protein 1beta secretion, COX-2 u
119 nd chemokines (such as interleukin-6 [IL-6], macrophage inflammatory protein 1beta, and beta interfer
120 eukin-2 (IL-2), tumor necrosis factor alpha, macrophage inflammatory protein 1beta, and gamma interfe
121 monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 1beta, and tumor necrosi
122 nd produced interferon gamma, interleukin 2, macrophage inflammatory protein 1beta, and tumor necrosi
123 rticular YKL-40, matrix metalloproteinase 3, macrophage inflammatory protein 1beta, IL-8, and IL-1bet
124 Ngamma, interleukin 2, granzyme B, perforin, macrophage inflammatory protein 1beta, interleukin 10, a
125 e genes affected by NS1 are those coding for macrophage inflammatory protein 1beta, interleukin-12 p3
126 nctions (degranulation and gamma interferon, macrophage inflammatory protein 1beta, tumor necrosis fa
127 T-cell activation (CD107a, gamma interferon, macrophage inflammatory protein 1beta, tumor necrosis fa
129 IFN-gamma, tumor necrosis factor alpha, and macrophage inflammatory protein 1beta; and had an activa
130 -alpha); monocyte chemoattractant protein 1; macrophage inflammatory protein 1beta; and regulated upo
131 CC chemokine receptor type 5 (CCR5) ligand (macrophage-inflammatory protein 1beta) levels increased
132 0(-9); H. influenzae, P = 5.9 x 10(-7)), and macrophage inflammatory protein-1beta (M. catarrhalis, P
133 roduced a covalent dimer of the CC chemokine macrophage inflammatory protein-1beta (MIP-1beta) by pla
134 ing tumor necrosis factor-alpha (TNF-alpha), macrophage inflammatory protein-1beta (MIP-1beta), and C
135 C) is associated with decreased secretion of macrophage inflammatory protein-1beta by NK cells in the
136 tumor necrosis factor, interferon-gamma and macrophage inflammatory protein-1beta expression, cytoto
137 Furthermore, tumor necrosis factor-alpha and macrophage inflammatory protein-1beta production from so
138 n-1beta, monocyte chemotactic protein-1, and macrophage inflammatory protein-1beta production from th
139 iously, our structure of the vCCI.MIP-1beta (macrophage inflammatory protein-1beta) complex indicated
140 )-alpha, IL-1ra, IL-2, IL-13, and MIP-1beta (macrophage inflammatory protein-1beta) responses were si
141 and 3DL1, reduced secretion of the cytokine macrophage inflammatory protein-1beta, and a significant
142 granulocyte colony stimulating factor, IL-8, macrophage inflammatory protein-1beta, and interferon-ga
143 (IL)-1beta, IL-1RA, IL-6, IL-8, IL-10, IL-17,macrophage inflammatory protein-1beta, and monocyte chem
144 ein, and monocyte chemoattractant protein-1, macrophage inflammatory protein-1beta, and monokine indu
145 ation of monocyte chemoattractant protein-1, macrophage inflammatory protein-1beta, IL-1beta, and IL-
146 of vascular cell adhesion molecule-1, IL-8, macrophage inflammatory protein-1beta, regulated on acti
147 , normal T cell expressed and secreted), and macrophage inflammatory protein-1beta, together with cel
148 macrophage inflammatory proteins-1alpha, and macrophage inflammatory proteins-1beta) when CD73 was la
149 les of patients with acute renal injury, and macrophage inflammatory protein-1Delta and osteoproteger
150 centrations of C-reactive protein, IL-8, and macrophage inflammatory protein-1delta did not differ be
151 erferon-gamma-inducible protein (IP-10), and macrophage inflammatory protein-1delta) were measured in
153 expressing WNV envelope protein and produced macrophage inflammatory protein 1ss, interferon gamma, a
154 ein kinase phosphorylation and expression of macrophage inflammatory protein 2 (an interleukin-8 homo
155 We measured levels of myeloperoxidase and macrophage inflammatory protein 2 (CXCL2), trypsinogen a
156 sed expression of the chemoattractants CXCL2/macrophage inflammatory protein 2 (MIP-2) and CXCL1/kera
157 -induced neutrophil chemoattractant (KC) and macrophage inflammatory protein 2 (MIP-2) in murine plas
158 tor alpha (TNF-alpha), interleukin-6 (IL-6), macrophage inflammatory protein 2 (MIP-2), and CXCL5/LIX
159 Tumor necrosis factor alpha, interleukin-6, macrophage inflammatory protein 2 (MIP-2), and keratinoc
160 vels of Keratinocyte-derived chemokine (KC), macrophage inflammatory protein 2 (MIP-2), and MIP-1alph
162 a, IL-22, or IL-17, including genes encoding macrophage inflammatory protein 2 (MIP-2), inducible nit
163 recruitment accompanied by induction of KC, macrophage inflammatory protein 2 (MIP-2), NOS-2, interl
164 (FKS) stimulate mouse macrophages to secret macrophage inflammatory protein 2 (MIP-2), which suggest
165 ulator of proinflammatory cytokines, such as macrophage inflammatory protein 2 (MIP-2), which, in tur
168 dulation/and or potentiation of RANTES/CCL5, macrophage inflammatory protein 2 (MIP-2)/CXCL2, IP-10/C
169 rum levels of the neutrophil chemoattractant macrophage inflammatory protein 2 (MIP-2); however, pulm
171 gulation of interleukin-6 (IL-6), IL-10, and macrophage inflammatory protein 2 alpha in the intestine
172 tion resulting in increased airway levels of macrophage inflammatory protein 2 and KC, and higher lun
174 addition, mRNA levels of the CXC chemokines macrophage inflammatory protein 2 and keratinocyte-deriv
175 nal concentrations of inflammatory mediators macrophage inflammatory protein 2 and tumor necrosis fac
176 In vivo neutralization of highly induced macrophage inflammatory protein 2 did not affect clinica
177 cyte derived cytokine and was independent of macrophage inflammatory protein 2 expression, whereas su
179 or necrosis factor alpha, interleukin-6, and macrophage inflammatory protein 2 not inhibited by polym
180 hesion molecule 1, Toll-like receptor 4, and macrophage inflammatory protein 2 were all up-regulated.
181 ntaining sequences based on beta-amyloid and macrophage inflammatory protein 2 were synthesized and c
183 ding, RelA nuclear translocation, and MIP-2 (macrophage inflammatory protein 2) and keratinocyte-deri
184 okine interleukin-6 and the chemokine MIP-2 (macrophage inflammatory protein 2) but impair levels of
185 a], tumor necrosis factor alpha), chemokine (macrophage inflammatory protein 2), Th1/Th2 indicator (I
186 1beta, a major proinflammatory cytokine, and macrophage inflammatory protein 2, a chemokine involved
187 TNFalpha, macrophage inflammatory protein 1, macrophage inflammatory protein 2, and IFNgamma upon sti
189 stimulated gamma interferon, interleukin 6, macrophage inflammatory protein 2, and monocyte chemoatt
191 including keratinocyte-derived chemokine and macrophage inflammatory protein 2, and severe lung neutr
192 genes encoding interleukin-1beta [IL-1beta], macrophage inflammatory protein 2, IL-12, and gamma inte
193 showed that keratinocyte-derived chemokine, macrophage inflammatory protein 2, RANTES, tumor necrosi
194 the keratinocyte-derived chemokine, RANTES, macrophage inflammatory protein 2, tumor necrosis factor
195 olecule 1, keratinocyte chemoattractant, and macrophage inflammatory protein 2, which favored neutrop
198 red for 10 days increased neutrophil counts, macrophage inflammatory protein-2 (MIP-2) and chemokine
199 sma levels of the neutrophil chemoattractant macrophage inflammatory protein-2 (MIP-2) and pulmonary
200 ages with increasing amounts of NaCl induced macrophage inflammatory protein-2 (MIP-2) and tumor necr
201 s in keratinocyte-derived chemokine (KC) and macrophage inflammatory protein-2 (MIP-2) production as
202 in mice, keratinocyte-derived cytokine (KC), macrophage inflammatory protein-2 (MIP-2), and TNF-alpha
203 uced production of several cytokines such as macrophage inflammatory protein-2 (MIP-2), ILs, TNFalpha
204 ulation of proinflammatory cytokines such as macrophage inflammatory protein-2 (MIP-2), upregulation
207 y cytokines tumor necrosis factor- alpha and macrophage inflammatory protein-2 and with a decrease in
208 ne-induced neutrophil chemoattractant-1, and macrophage inflammatory protein-2 contents were increase
209 eater monocyte chemoattractant protein-1 and macrophage inflammatory protein-2 expression; (2) more m
210 hemoattractant protein-1, interleukin-6, and macrophage inflammatory protein-2 following stimulation
211 less tumor necrosis factor-alpha, IL-6, and macrophage inflammatory protein-2 in bronchial alveolar
212 l production of KC and the related chemokine macrophage inflammatory protein-2 is decreased in both B
213 erleukin-1beta, neutrophil chemokine KC, and macrophage inflammatory protein-2 messenger RNA by polym
214 erleukin-1beta, neutrophil chemokine KC, and macrophage inflammatory protein-2 messenger RNA expressi
215 r the tumor necrosis factor-alpha, IL-6, and macrophage inflammatory protein-2 production in LPS-stim
216 ificantly increased neutrophil infiltration, macrophage inflammatory protein-2 production, and lung m
217 atment of primary wild-type hepatocytes with macrophage inflammatory protein-2 revealed that low conc
218 of airway keratinocyte-derived chemokine and macrophage inflammatory protein-2 significantly improves
219 hemokines keratinocyte-derived chemokine and macrophage inflammatory protein-2 were significantly low
220 t cytokines such as interleukin-1a, MIG, and macrophage inflammatory protein-2 within the tumor and t
221 ut it reduced levels of bacteremia and serum macrophage inflammatory protein-2) (MIP-2), interleukin-
222 macrophages, both alarmins increased MIP-2 (macrophage inflammatory protein-2) chemokine expression,
224 ediators, including TNF-alpha, IL-1beta, and macrophage inflammatory protein-2, and decreases interst
225 s, such as interleukin-1beta, interleukin-6, macrophage inflammatory protein-2, and keratinocyte chem
226 C chemokine, monocyte chemotactic protein-1, macrophage inflammatory protein-2, granulocyte colony-st
227 hemoattractant protein-1, interleukin-6, and macrophage inflammatory protein-2, important for neutrop
228 lung, and decreased levels of blood amylase, macrophage inflammatory protein-2, interleukin 6, and hi
230 mortalized murine melanocytes overexpressing macrophage inflammatory protein-2, was inhibited or enha
231 e synthase, tumor necrosis factor alpha, and macrophage inflammatory protein-2, was significantly att
237 ha; IFN-inducible protein-10; interleukin-6; macrophage inflammatory protein-2; monocyte chemotactic
238 ating factor (G-CSF) and chemokines, such as macrophage-inflammatory protein-2 (MIP-2; CXCL2), can in
239 polizumab affected particularly RV16-induced macrophage inflammatory protein-3a, vascular endothelial
240 mulating factor (mGM-CSF), human CCL20/human macrophage inflammatory protein 3alpha (hCCL20/hMIP-3alp
241 inflammatory Th17-like phenotype and express macrophage inflammatory protein 3alpha and alpha4beta7 i
242 hrough the action of their chemoattractants, macrophage inflammatory protein 3alpha and chemerin.
243 tion contributed to increased mRNA levels of macrophage inflammatory protein 3alpha and more fluid ac
244 lation of monocyte chemotactic protein 1 and macrophage inflammatory protein 3alpha in the skin.
245 ory cytokine (keratinocyte-derived cytokine, macrophage inflammatory protein 3alpha, and IL-6) expres
246 n of neutrophils across the endothelium, and macrophage inflammatory protein 3alpha, which is a chemo
248 asthmatic patients increased sputum IL-6 and macrophage inflammatory protein 3alpha/CCL20 levels were
249 m neutrophil numbers and IL-1beta, IL-6, and macrophage inflammatory protein 3alpha/CCL20 levels were
250 The TH17-associated mediators IL-23 and macrophage inflammatory protein 3alpha/CCL20 were highly
251 (monocyte chemotactic protein 1), and CCL19 (macrophage inflammatory protein 3beta) in an independent
252 grate toward the lymph node-homing chemokine macrophage inflammatory protein 3beta, like LPS-matured
254 hemokine, monocyte chemotactic protein 1, or macrophage inflammatory protein alpha, compared with the
255 ll-derived neutrophil-activating peptide-78, macrophage-inflammatory protein alpha, and interleukin-8
256 M-CSF, macrophage chemoattractant protein-1, macrophage inflammatory protein-alpha and -beta, and TNF
257 y, MRL/MpJ mice had lower gene expression of macrophage inflammatory proteins and macrophage-derived
258 rotein 10, macrophage-derived chemokine, and macrophage inflammatory protein-beta, were found in youn
259 ), IL6, IL8, the inflammasome NLRP3, and the macrophage inflammatory proteins CCL3 and CCL4 as well a
260 g a broad acting chemokine antagonist, viral macrophage inflammatory protein II (vMIP II), on graft s
264 A unique viral chemokine analogue, viral macrophage inflammatory protein-II (vMIP-II), encoded by
265 stromal cell-derived factor-1alpha or viral macrophage inflammatory protein-II as chemical probes of
266 stromal cell-derived factor-1alpha or viral macrophage inflammatory protein-II, can be modified to p
267 ce of mRNAs encoding the antiviral cytokines macrophage inflammatory proteins MIP-1alpha, MIP-1alphaP
268 hloride channel calcium-activated 3 (Clca3), macrophage inflammatory protein (MIP) 1alpha and 1beta,
269 oattractant, monocyte chemotactic protein-1, macrophage inflammatory protein (MIP) 1alpha, MIP-1beta,
270 f cytolysis) and production of IFN-gamma and macrophage inflammatory protein (MIP) 1beta were assesse
271 mor necrosis factor-alpha and the chemokines macrophage inflammatory protein (MIP)-1 alpha, MIP-1 bet
272 and produce very low levels of CCR5 ligands macrophage inflammatory protein (MIP)-1alpha and MIP-1be
274 and secreted (RANTES) at week 4 and week 8; macrophage inflammatory protein (MIP)-1alpha and MIP-1be
275 PD-1 engagement on iLCs reduced IL-6 and macrophage inflammatory protein (MIP)-1alpha cytokine pr
277 rmal T-cell expressed and secreted (RANTES), macrophage inflammatory protein (MIP)-1alpha, and MIP-1b
278 okines [keratinocyte cell-derived chemokine, macrophage inflammatory protein (MIP)-1alpha, and MIP-1b
279 rmal T-cell expressed and secreted (RANTES), macrophage inflammatory protein (MIP)-1alpha, and MIP-1b
280 10, macrophage migration inhibitory factor, macrophage inflammatory protein (MIP)-1alpha, and MIP-1b
281 eta, IL-6, matrix metalloproteinase (MMP)-8, macrophage inflammatory protein (MIP)-1alpha, and prosta
282 teins, such as IFN-gamma-induced protein 10, macrophage inflammatory protein (MIP)-1alpha, MIP-1beta,
283 rmal T cell expressed and secreted (RANTES), macrophage inflammatory protein (MIP)-1alpha, MIP-1beta,
284 (IFN)-gamma, IFN-alpha, IL-2, IL-2 R, IL-8, macrophage inflammatory protein (MIP)-1alpha, MIP-1beta,
285 ed vascular inflammatory repair occurs via a macrophage inflammatory protein (MIP)-1alpha- and MIP-2-
286 IP-10/CXCL10 (P<0.05), MCP-1/CCL2 (P<0.05), macrophage inflammatory protein (MIP)-1alpha/CCL3 (P<0.0
287 -6, IL-8, IL-10, interferon (IFN)-gamma, and macrophage inflammatory protein (MIP)-1beta were signifi
288 alpha, and interleukin (IL)-2, the chemokine macrophage inflammatory protein (MIP)-1beta, and surface
289 in-1, interleukin [IL]-8, IL-6, Fractalkine, macrophage inflammatory protein (MIP)-1beta, granulocyte
290 L-8, monocyte chemoattractant protein-1, and macrophage inflammatory protein (MIP)-1beta, the latter
291 IL-6, IL-10, IL-12, IL-17, interferon-gamma, macrophage inflammatory protein (MIP)-1beta, transformin
292 nificant elevation in the mRNA expression of macrophage inflammatory protein (MIP)-2 and an MIP-2 rec
293 he expression of hyaluronic acid, COX-2, and macrophage inflammatory protein (MIP)-2 was evaluated by
294 ice with control or CpG DNA; TLR9, IL-1beta, macrophage inflammatory protein (MIP)-2, IL-4, IL-10, IL
295 interferon-gamma inducible protein (IP)-10, macrophage inflammatory protein (MIP)-3alpha, and monoki
297 ines/chemokines in injured muscles: mRNAs of macrophage-inflammatory protein (MIP)-1alpha, MIP-1beta,
298 ase (monocyte chemotactic protein-1 [MCP-1], macrophage inflammatory protein [MIP] 1alpha, RANTES, tu
299 [IP-10], monocyte chemoattractant protein-1, macrophage inflammatory protein [MIP]-1alpha, MIP-1beta)