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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 mokines (monocyte chemoattractant protein 1, macrophage inflammatory protein 1 alpha [MIP-1alpha], MI
6 released 36% less nitric oxide and 82% less macrophage inflammatory protein 1 alpha and expressed 63
7 monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 1 beta (MIP-1beta), and
8 vated endothelium by its capacity to trigger macrophage inflammatory protein 1 beta from primary mono
9 rferon (IFN)-gamma-inducible protein 10, and macrophage inflammatory protein 1 beta levels were diffe
10 of PD-1 expression were required to inhibit macrophage inflammatory protein 1 beta production, lower
12 o 3-fold greater amounts of IL-18, TNFalpha, macrophage inflammatory protein 1, macrophage inflammato
13 related oncogene alpha (GROalpha), GROgamma, macrophage inflammatory protein 1, monocyte chemoattract
14 ed expression of T-cell-attracting chemokine macrophage inflammatory protein 1-alpha (MIP-1alpha/CCL3
15 o) mice have increased circulating levels of macrophage inflammatory protein 1-alpha and interleukin-
16 te macrophage colony-stimulating factor, and macrophage inflammatory protein 1-alpha were lower 14 da
17 ytic polypeptide 3 G/F/H) and CC chemokines (macrophage inflammatory protein 1-alpha, macrophage infl
18 es (macrophage inflammatory protein 1-alpha, macrophage inflammatory protein 1-beta, regulated on act
19 Genes encoding chemokines, including IL-8; macrophage inflammatory proteins 1, 3, and 4; and monocy
21 IL-6, as well as the migration-related genes macrophage inflammatory protein-1 (MIP-1alpha), MIP-2 an
22 athyroid hormone-related protein (PTHrP) and macrophage inflammatory protein-1 alpha (MIP-1 alpha) ar
23 nificant elevation in interleukin-6, whereas macrophage inflammatory protein-1 alpha and monocyte che
24 CCL2/monocyte chemotactic protein 1 and CCL3/macrophage inflammatory protein-1 alpha) were also prese
25 yte-macrophage colony-stimulating factor and macrophage inflammatory protein-1 beta levels in cocultu
26 whereas the levels of IL-6, IL-8, IL-10, and macrophage inflammatory protein-1 beta were higher in pa
27 interleukin-2, tumor necrosis factor-alpha, macrophage inflammatory protein-1 beta, and CD107a by CD
28 lysis, we found expression of the chemokine, macrophage inflammatory protein-1 delta (MIP-1 delta), t
29 mic proinflammatory chemokine levels such as macrophage inflammatory protein-1-gamma, B-lymphocyte ch
31 eptor that upon stimulation, particularly by macrophage inflammatory protein 1alpha (MIP-1alpha) and
32 pression of interleukin 1beta (IL-1beta) and macrophage inflammatory protein 1alpha (MIP-1alpha) in t
33 levels throughout infection, and had higher macrophage inflammatory protein 1alpha (MIP-1alpha) leve
34 erleukin-alpha1 (IL-1alpha), IL-12(p40), and macrophage inflammatory protein 1alpha (MIP-1alpha) para
36 tumor necrosis factor alpha (TNF-alpha), and macrophage inflammatory protein 1alpha (MIP-1alpha), in
37 factor (G-CSF), interferon alfa (IFN-alpha), macrophage inflammatory protein 1alpha (MIP-1alpha), MIP
39 natural ligands of CCR5, the beta-chemokines macrophage inflammatory protein 1alpha (MIP-1alpha), MIP
40 L-1beta), IL-6, tumor necrosis factor 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).
46 cyte chemoattractant protein 1 (MCP-1/CCL2), macrophage inflammatory protein 1alpha (MIP-1alpha/CCL3)
47 zes the binding of the chemokines RANTES and macrophage inflammatory protein 1alpha (MIP-1alpha; CCL3
48 on normal T cell expressed and secreted) and macrophage inflammatory protein 1alpha (MIP1-alpha).
49 whereas BDR was associated with high plasma macrophage inflammatory protein 1alpha (P = .002) and sp
51 cytokine (IL-1beta and IL-6) and chemokine (macrophage inflammatory protein 1alpha [MIP-1alpha] and
52 ory cytokines (interleukin-1beta [IL-1beta], macrophage inflammatory protein 1alpha [MIP-1alpha], and
54 terleukin-7, interleukin-13, interleukin-17, macrophage inflammatory protein 1alpha and 1beta, granul
55 L-8, monocyte chemoattractant protein 1, and macrophage inflammatory protein 1alpha and elevated urin
56 pO2 negatively correlated with CD68 mRNA and macrophage inflammatory protein 1alpha secretion (R = -0
57 inflammatory cytokines (TNF-alpha, IL-8, and macrophage inflammatory protein 1alpha) and augmented pr
58 enase-2, monocyte chemoattractant protein-1, macrophage inflammatory protein 1alpha, and macrophage i
59 d, while monocyte chemoattractant protein 1, macrophage inflammatory protein 1alpha, and RANTES were
60 d with elevated tumor necrosis factor alpha, macrophage inflammatory protein 1alpha, IL-6, and IL-8.
61 nses were characterized by the production of macrophage inflammatory protein 1alpha, interferon gamma
62 tors, including tumor necrosis factor alpha, macrophage inflammatory protein 1alpha, interleukin 1bet
64 6 (IL-6), tumor necrosis factor alpha, IL-8, macrophage inflammatory protein 1alpha/beta, and monocyt
66 chemoattractant protein 1], MIP-1alpha/beta [macrophage inflammatory protein 1alpha/beta], IL-6 [inte
67 s (monocyte chemoattractant protein 1/CCL-2, macrophage inflammatory protein 1alpha/CCL-3, and IP-10)
68 nes monocyte chemoattractant protein 1/CCL2, macrophage inflammatory protein 1alpha/CCL3, and RANTES/
69 ta in murine BPD and an involvement for MIP (macrophage inflammatory protein)-1alpha and TREM (trigge
70 ly induced the expression of two chemokines, macrophage inflammatory protein-1alpha (MIP-1alpha) and
71 flammatory cytokine IL-1alpha and chemokines macrophage inflammatory protein-1alpha (MIP-1alpha) and
74 ocyte chemoattractant protein-1 (MCP-1), and macrophage inflammatory protein-1alpha (MIP-1alpha) than
75 mokines IL-8, growth-regulated protein-beta, 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 giotensin II (Ang II) vascular inflammation (macrophage inflammatory protein-1alpha and beta) were al
80 oint scale) exhibited significantly elevated macrophage inflammatory protein-1alpha and IL-10 and a t
81 tractants monocyte chemotactic protein-1 and macrophage inflammatory protein-1alpha but not RANTES or
82 ing factor, tumor necrosis factor alpha, and macrophage inflammatory protein-1alpha by LAK cells stim
84 ant, monocyte chemoattractant protein-1, and macrophage inflammatory protein-1alpha) that are signifi
85 tein-10, monocyte chemotactic protein-1, and macrophage inflammatory protein-1alpha) were associated
86 onocyte Chemoattractant Protein-1) and CCL3 (Macrophage Inflammatory Protein-1alpha), were upregulate
88 interacting signals comprising IL-10, IL-8, macrophage inflammatory protein-1alpha, and C-reactive p
89 emokines monocyte chemoattractant protein-1, macrophage inflammatory protein-1alpha, and interferon-g
90 lasma levels of tumor necrosis factor-alpha, macrophage inflammatory protein-1alpha, and monocyte che
91 mal T-cell expressed, and secreted (RANTES), macrophage inflammatory protein-1alpha, and monocyte che
92 tumor necrosis factor-alpha (TNF-alpha) and macrophage inflammatory protein-1alpha, as well as of ot
93 ation in plasma tumor necrosis factor-alpha, macrophage inflammatory protein-1alpha, monocyte chemoat
94 -1beta, IL-6, keratinocyte-derived cytokine, macrophage inflammatory protein-1alpha, monocyte chemota
95 eron-gamma-inducible protein of 10 kDa, CCL3/macrophage inflammatory protein-1alpha, or CCL5/RANTES (
98 was a potent stimulator of the CCR5 ligands macrophage inflammatory protein-1alpha/CCL-3 (MIP-1alpha
99 protein-1/CCL2, inducible protein-10/CXCL10, macrophage inflammatory protein-1alpha/CCL3, and interle
100 ple chemokines, including, most prominently, macrophage inflammatory protein-1alpha/CCL3, which is kn
101 Serum levels of tumor necrosis factor-alpha; macrophage inflammatory protein-1alpha; growth-related o
102 terleukin-6, interleukin-13, interleukin-17, macrophage inflammatory proteins-1alpha, and macrophage
103 ced protein 10 (approximately 2.0-fold), and macrophage inflammatory protein 1beta (approximately 1.5
104 ion of the cysteine-cysteine (C-C) chemokine macrophage inflammatory protein 1beta (MIP-1beta) and in
105 ity correlated with HIV-1-specific CD107a or macrophage inflammatory protein 1beta (MIP-1beta) expres
106 monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 1beta (MIP-1beta), and s
107 protein 10 (IP-10), interleukin 10 (IL-10), macrophage inflammatory protein 1beta (MIP-1beta), and s
108 rleukin-1beta (IL-1beta), IL-6, IL-8, CCL20, macrophage inflammatory protein 1beta (MIP-1beta), CXCL-
111 In support of this, there was an increase in macrophage inflammatory protein 1beta (MIP-1beta; CCL4)
112 mmatory protein 1alpha (P = .002) and sputum macrophage inflammatory protein 1beta (P = .001) levels.
113 s (e.g., monocyte chemoattractant protein 1, macrophage inflammatory protein 1beta [MIP-1beta], and M
114 lecules by means of immunoblotting, PGD2 and macrophage inflammatory protein 1beta generation by usin
115 cytotoxic (CD107a expression) and cytokine (macrophage inflammatory protein 1beta secretion) effecto
116 osphorylation, inflammatory gene expression, macrophage inflammatory protein 1beta secretion, COX-2 u
118 nd chemokines (such as interleukin-6 [IL-6], macrophage inflammatory protein 1beta, and beta interfer
119 eukin-2 (IL-2), tumor necrosis factor alpha, macrophage inflammatory protein 1beta, and gamma interfe
120 monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 1beta, and tumor necrosi
121 nd produced interferon gamma, interleukin 2, macrophage inflammatory protein 1beta, and tumor necrosi
122 e genes affected by NS1 are those coding for macrophage inflammatory protein 1beta, interleukin-12 p3
123 nctions (degranulation and gamma interferon, macrophage inflammatory protein 1beta, tumor necrosis fa
124 T-cell activation (CD107a, gamma interferon, macrophage inflammatory protein 1beta, tumor necrosis fa
126 IFN-gamma, tumor necrosis factor alpha, and macrophage inflammatory protein 1beta; and had an activa
127 -alpha); monocyte chemoattractant protein 1; macrophage inflammatory protein 1beta; and regulated upo
128 CC chemokine receptor type 5 (CCR5) ligand (macrophage-inflammatory protein 1beta) levels increased
129 0(-9); H. influenzae, P = 5.9 x 10(-7)), and macrophage inflammatory protein-1beta (M. catarrhalis, P
130 roduced a covalent dimer of the CC chemokine macrophage inflammatory protein-1beta (MIP-1beta) by pla
131 ing tumor necrosis factor-alpha (TNF-alpha), macrophage inflammatory protein-1beta (MIP-1beta), and C
132 C) is associated with decreased secretion of macrophage inflammatory protein-1beta by NK cells in the
133 tumor necrosis factor, interferon-gamma and macrophage inflammatory protein-1beta expression, cytoto
134 Furthermore, tumor necrosis factor-alpha and macrophage inflammatory protein-1beta production from so
135 n-1beta, monocyte chemotactic protein-1, and macrophage inflammatory protein-1beta production from th
136 iously, our structure of the vCCI.MIP-1beta (macrophage inflammatory protein-1beta) complex indicated
137 )-alpha, IL-1ra, IL-2, IL-13, and MIP-1beta (macrophage inflammatory protein-1beta) responses were si
138 and 3DL1, reduced secretion of the cytokine macrophage inflammatory protein-1beta, and a significant
139 granulocyte colony stimulating factor, IL-8, macrophage inflammatory protein-1beta, and interferon-ga
140 (IL)-1beta, IL-1RA, IL-6, IL-8, IL-10, IL-17,macrophage inflammatory protein-1beta, and monocyte chem
141 ein, and monocyte chemoattractant protein-1, macrophage inflammatory protein-1beta, and monokine indu
142 ation of monocyte chemoattractant protein-1, macrophage inflammatory protein-1beta, IL-1beta, and IL-
143 of vascular cell adhesion molecule-1, IL-8, macrophage inflammatory protein-1beta, regulated on acti
144 , normal T cell expressed and secreted), and macrophage inflammatory protein-1beta, together with cel
145 macrophage inflammatory proteins-1alpha, and macrophage inflammatory proteins-1beta) when CD73 was la
146 les of patients with acute renal injury, and macrophage inflammatory protein-1Delta and osteoproteger
147 centrations of C-reactive protein, IL-8, and macrophage inflammatory protein-1delta did not differ be
148 erferon-gamma-inducible protein (IP-10), and macrophage inflammatory protein-1delta) were measured in
150 expressing WNV envelope protein and produced macrophage inflammatory protein 1ss, interferon gamma, a
151 ein kinase phosphorylation and expression of macrophage inflammatory protein 2 (an interleukin-8 homo
152 We measured levels of myeloperoxidase and macrophage inflammatory protein 2 (CXCL2), trypsinogen a
153 sed expression of the chemoattractants CXCL2/macrophage inflammatory protein 2 (MIP-2) and CXCL1/kera
155 -induced neutrophil chemoattractant (KC) and macrophage inflammatory protein 2 (MIP-2) in murine plas
156 tor alpha (TNF-alpha), interleukin-6 (IL-6), macrophage inflammatory protein 2 (MIP-2), and CXCL5/LIX
157 Tumor necrosis factor alpha, interleukin-6, macrophage inflammatory protein 2 (MIP-2), and keratinoc
158 vels of Keratinocyte-derived chemokine (KC), macrophage inflammatory protein 2 (MIP-2), and MIP-1alph
160 a, IL-22, or IL-17, including genes encoding macrophage inflammatory protein 2 (MIP-2), inducible nit
161 recruitment accompanied by induction of KC, macrophage inflammatory protein 2 (MIP-2), NOS-2, interl
162 ulator of proinflammatory cytokines, such as macrophage inflammatory protein 2 (MIP-2), which, in tur
165 dulation/and or potentiation of RANTES/CCL5, macrophage inflammatory protein 2 (MIP-2)/CXCL2, IP-10/C
166 rum levels of the neutrophil chemoattractant macrophage inflammatory protein 2 (MIP-2); however, pulm
168 gulation of interleukin-6 (IL-6), IL-10, and macrophage inflammatory protein 2 alpha in the intestine
169 tion resulting in increased airway levels of macrophage inflammatory protein 2 and KC, and higher lun
171 addition, mRNA levels of the CXC chemokines macrophage inflammatory protein 2 and keratinocyte-deriv
172 nal concentrations of inflammatory mediators macrophage inflammatory protein 2 and tumor necrosis fac
173 In vivo neutralization of highly induced macrophage inflammatory protein 2 did not affect clinica
174 cyte derived cytokine and was independent of macrophage inflammatory protein 2 expression, whereas su
176 or necrosis factor alpha, interleukin-6, and macrophage inflammatory protein 2 not inhibited by polym
177 hesion molecule 1, Toll-like receptor 4, and macrophage inflammatory protein 2 were all up-regulated.
178 ntaining sequences based on beta-amyloid and macrophage inflammatory protein 2 were synthesized and c
180 ding, RelA nuclear translocation, and MIP-2 (macrophage inflammatory protein 2) and keratinocyte-deri
181 okine interleukin-6 and the chemokine MIP-2 (macrophage inflammatory protein 2) but impair levels of
182 a], tumor necrosis factor alpha), chemokine (macrophage inflammatory protein 2), Th1/Th2 indicator (I
183 1beta, a major proinflammatory cytokine, and macrophage inflammatory protein 2, a chemokine involved
184 TNFalpha, macrophage inflammatory protein 1, macrophage inflammatory protein 2, and IFNgamma upon sti
186 stimulated gamma interferon, interleukin 6, macrophage inflammatory protein 2, and monocyte chemoatt
188 including keratinocyte-derived chemokine and macrophage inflammatory protein 2, and severe lung neutr
189 genes encoding interleukin-1beta [IL-1beta], macrophage inflammatory protein 2, IL-12, and gamma inte
190 showed that keratinocyte-derived chemokine, macrophage inflammatory protein 2, RANTES, tumor necrosi
191 the keratinocyte-derived chemokine, RANTES, macrophage inflammatory protein 2, tumor necrosis factor
192 utrophil influx, cytokine and chemokine (KC, macrophage inflammatory protein 2, tumor necrosis factor
193 olecule 1, keratinocyte chemoattractant, and macrophage inflammatory protein 2, which favored neutrop
196 red for 10 days increased neutrophil counts, macrophage inflammatory protein-2 (MIP-2) and chemokine
197 sma levels of the neutrophil chemoattractant macrophage inflammatory protein-2 (MIP-2) and pulmonary
198 ages with increasing amounts of NaCl induced macrophage inflammatory protein-2 (MIP-2) and tumor necr
200 s in keratinocyte-derived chemokine (KC) and macrophage inflammatory protein-2 (MIP-2) production as
201 in mice, keratinocyte-derived cytokine (KC), macrophage inflammatory protein-2 (MIP-2), and TNF-alpha
202 uced production of several cytokines such as macrophage inflammatory protein-2 (MIP-2), ILs, TNFalpha
203 ulation of proinflammatory cytokines such as macrophage inflammatory protein-2 (MIP-2), upregulation
206 y cytokines tumor necrosis factor- alpha and macrophage inflammatory protein-2 and with a decrease in
207 ne-induced neutrophil chemoattractant-1, and macrophage inflammatory protein-2 contents were increase
208 eater monocyte chemoattractant protein-1 and macrophage inflammatory protein-2 expression; (2) more m
209 hemoattractant protein-1, interleukin-6, and macrophage inflammatory protein-2 following stimulation
210 less tumor necrosis factor-alpha, IL-6, and macrophage inflammatory protein-2 in bronchial alveolar
211 l production of KC and the related chemokine macrophage inflammatory protein-2 is decreased in both B
212 erleukin-1beta, neutrophil chemokine KC, and macrophage inflammatory protein-2 messenger RNA by polym
213 erleukin-1beta, neutrophil chemokine KC, and macrophage inflammatory protein-2 messenger RNA expressi
214 r the tumor necrosis factor-alpha, IL-6, and macrophage inflammatory protein-2 production in LPS-stim
215 ificantly increased neutrophil infiltration, macrophage inflammatory protein-2 production, and lung m
216 atment of primary wild-type hepatocytes with macrophage inflammatory protein-2 revealed that low conc
217 of airway keratinocyte-derived chemokine and macrophage inflammatory protein-2 significantly improves
218 hemokines keratinocyte-derived chemokine and macrophage inflammatory protein-2 were significantly low
219 t cytokines such as interleukin-1a, MIG, and macrophage inflammatory protein-2 within the tumor and t
220 ut it reduced levels of bacteremia and serum macrophage inflammatory protein-2) (MIP-2), interleukin-
221 macrophages, both alarmins increased MIP-2 (macrophage inflammatory protein-2) chemokine expression,
223 ediators, including TNF-alpha, IL-1beta, and macrophage inflammatory protein-2, and decreases interst
224 s, such as interleukin-1beta, interleukin-6, macrophage inflammatory protein-2, and keratinocyte chem
225 C chemokine, monocyte chemotactic protein-1, macrophage inflammatory protein-2, granulocyte colony-st
226 hemoattractant protein-1, interleukin-6, and macrophage inflammatory protein-2, important for neutrop
227 lung, and decreased levels of blood amylase, macrophage inflammatory protein-2, interleukin 6, and hi
229 mortalized murine melanocytes overexpressing macrophage inflammatory protein-2, was inhibited or enha
230 e synthase, tumor necrosis factor alpha, and macrophage inflammatory protein-2, was significantly att
236 ha; IFN-inducible protein-10; interleukin-6; macrophage inflammatory protein-2; monocyte chemotactic
237 ating factor (G-CSF) and chemokines, such as macrophage-inflammatory protein-2 (MIP-2; CXCL2), can in
238 mulating factor (mGM-CSF), human CCL20/human macrophage inflammatory protein 3alpha (hCCL20/hMIP-3alp
239 s selectively express CCR6, the receptor for macrophage inflammatory protein 3alpha (MIP-3alpha), and
240 inflammatory Th17-like phenotype and express macrophage inflammatory protein 3alpha and alpha4beta7 i
241 hrough the action of their chemoattractants, macrophage inflammatory protein 3alpha and chemerin.
242 tion contributed to increased mRNA levels of macrophage inflammatory protein 3alpha and more fluid ac
243 lation of monocyte chemotactic protein 1 and macrophage inflammatory protein 3alpha in the skin.
244 ory cytokine (keratinocyte-derived cytokine, macrophage inflammatory protein 3alpha, and IL-6) expres
245 n of neutrophils across the endothelium, and macrophage inflammatory protein 3alpha, which is a chemo
247 asthmatic patients increased sputum IL-6 and macrophage inflammatory protein 3alpha/CCL20 levels were
248 m neutrophil numbers and IL-1beta, IL-6, and macrophage inflammatory protein 3alpha/CCL20 levels were
249 The TH17-associated mediators IL-23 and macrophage inflammatory protein 3alpha/CCL20 were highly
250 upregulation of homeostatic chemokine CCL19/macrophage inflammatory protein 3beta and proinflammator
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 Cs) from explanted mouse skin in response to macrophage inflammatory protein-3beta (MIP-3beta)/CCL19
255 hemokine, monocyte chemotactic protein 1, or macrophage inflammatory protein alpha, compared with the
256 ll-derived neutrophil-activating peptide-78, macrophage-inflammatory protein alpha, and interleukin-8
257 M-CSF, macrophage chemoattractant protein-1, macrophage inflammatory protein-alpha and -beta, and TNF
258 y, MRL/MpJ mice had lower gene expression of macrophage inflammatory proteins and macrophage-derived
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 ntly higher concentrations of interleukin-8, macrophage inflammatory protein (MIP)-1alpha , MIP-1beta
273 and produce very low levels of CCR5 ligands 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 okines [keratinocyte cell-derived chemokine, macrophage inflammatory protein (MIP)-1alpha, and MIP-1b
278 rmal T-cell expressed and secreted (RANTES), macrophage inflammatory protein (MIP)-1alpha, and MIP-1b
279 10, macrophage migration inhibitory factor, macrophage inflammatory protein (MIP)-1alpha, and MIP-1b
280 rmal T-cell expressed and secreted (RANTES), 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 ed vascular inflammatory repair occurs via a macrophage inflammatory protein (MIP)-1alpha- and MIP-2-
285 IP-10/CXCL10 (P<0.05), MCP-1/CCL2 (P<0.05), macrophage inflammatory protein (MIP)-1alpha/CCL3 (P<0.0
286 nocyte chemoattractant protein (MCP)-1/CCL2, macrophage inflammatory protein (MIP)-1alpha/CCL3, inter
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
296 ines/chemokines in injured muscles: mRNAs of macrophage-inflammatory protein (MIP)-1alpha, MIP-1beta,
297 ase (monocyte chemotactic protein-1 [MCP-1], macrophage inflammatory protein [MIP] 1alpha, RANTES, tu
298 [IP-10], monocyte chemoattractant protein-1, macrophage inflammatory protein [MIP]-1alpha, MIP-1beta)
299 cell-derived factor [SDF]-1alpha) and CCL19 (macrophage inflammatory protein [MIP]-3beta), as well as
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