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1 inactivating CXC chemokines and inactivating CC chemokines.
2 se of infectious viral particles and CXC and CC chemokines.
3 s and destroys many of these proinflammatory CC chemokines.
4 in the zebrafish genome that encode putative CC chemokines.
5 served synteny between teleost and mammalian CC chemokines.
6 at sequestering and scavenging inflammatory CC chemokines.
7 ner that now engages functional responses to CC chemokines.
8 th high affinity to multiple proinflammatory CC chemokines.
9 ytoid DC subsets and their responsiveness to CC chemokines.
10 ding conventional receptors for inflammatory CC chemokines.
11 e binding affinity between vCCI and multiple CC chemokines.
12 s so by facilitating removal of inflammatory CC chemokines.
13 ternalizes and degrades most proinflammatory CC-chemokines.
14 argeting CCL2 and CCL13 in addition to other CC-chemokines.
15 ine milieu and caused significant release of CC-chemokines.
16 racting with up to 14 different inflammatory CC-chemokines.
17 g, internalizing, and degrading inflammatory CC-chemokines.
18 ted protein-2, CCL15/MIP-1delta/hemofiltrate CC chemokine-2/leukotactin-1, and CCL23/CKbeta8/myeloid
20 dothelia venules, and production of IL-6 and CC chemokines, all characteristics of mucosal lymphoid t
21 rat cytomegalovirus (RCMV) encodes multiple CC chemokine-analogous proteins, including r129 (HCMV UL
22 d considerably less TNF-alpha, IL-6, and CXC/CC chemokine and soluble ICAM-1 proteins in bronchoalveo
23 ox infection and is able to selectively bind CC chemokines and inhibit their interactions with host r
24 ophage populations in response to a range of CC chemokines and other chemoattractant signalling molec
25 and scavenger receptor for most inflammatory CC chemokines and prevents the development of exacerbate
26 cine induced the significant upregulation of CC chemokines and the downmodulation of CCR5 expression
29 onocyte chemoattractant protein-1 (MCP-1), a CC chemokine, and interleukin-8 (IL-8), a CXC chemokine,
30 hatic endothelium, internalizes and degrades CC chemokines, and D6(-/-) mice demonstrated increased c
31 y secretory IgA antibodies, up-regulation of CC chemokines, and the first demonstration of protective
32 ncept that an innate mechanism consisting of CC chemokines, APOBEC3G, and adaptive immunity by CD4 an
36 blood group Ag (dfy) binds selective CXC and CC chemokines at high affinity and is expressed on eryth
38 R, transforming growth factor-beta1, IL-17A, CC chemokine attractant ligand-20) and Th-1-associated c
39 , and use it to identify 10 novel polyvalent CC-chemokine binding evasin-like peptides from salivary
41 nt negative Toll/IL-1 signaling adapter, and CC-chemokine binding protein (MVADelta4-HIV); (ii) harbo
42 elucidate the ligand-binding surface of the CC chemokine-binding proteins Evasin-1 and Evasin-4, pro
44 to the inserted domain, producing a typical CC chemokine "body" containing even further-increased CC
47 and it remains controversial whether dimeric CC chemokines can bind and activate their receptors.
48 ression of metalloproteases (MMP-9, ADAM-8), CC chemokines (CCL-20), CXC chemokines (IL-8, CXCL-10, C
49 7) (Cys + 4), are crucial for binding of the CC chemokines CCL1 (agonist) and MC148 (antagonist), res
50 Although recent studies have suggested that CC chemokine CCL2 may directly affect the angiogenesis,
52 y of the CXCL1 dimer is novel: dimers of the CC chemokines CCL2 and CCL4 are inactive, and the dimer
53 icated that macrophages and the inflammatory CC-chemokine CCL2, which is scavenged by ACKR2, are asso
54 n-8) were found to be the most abundant, but CC chemokines (CCL2/monocyte chemotactic protein 1 and C
56 ial cells, cause excessive production of the CC chemokine CCL3 (also known as MIP-1alpha), which recr
60 show that syndecan-1 ectodomains bind to the CC chemokines (CCL7, CCL11, and CCL17) implicated in all
61 s cancer-related inflammation genes (CXC and CC chemokines, chemokine receptors, cytokines and Cox-2)
62 etion of IL-8, a CXC chemokine, and MCP-1, a CC chemokine, confirmed the inhibitory effect of a proge
63 onflicting results and indicate that dimeric CC chemokines do not bind to their receptors with affini
64 an atypical viral chemokine consisting of a CC chemokine domain and a unique non-chemokine domain, b
69 ecreted (RANTES, or CCL5) is a member of the CC chemokine family of proteins, strongly chemoattractan
70 essed and secreted; CCL5) is a member of the CC chemokine family of proteins, which is strongly chemo
71 Results are discussed in terms of CXC and CC chemokine function and have significant biological im
74 n can be protumorigenic, and proinflammatory CC chemokines have been linked with various aspects of c
77 genin (ANG), growth factors, and the CXC and CC chemokines IFN-gamma inducible protein (IP)-10, growt
78 without the availability of similar sets of CC chemokines in closely related species or a sequenced
79 emonstrate the importance of proinflammatory CC chemokines in de novo tumorigenesis and reveal chemok
82 lysis provides insight into the mechanism of CC-chemokine inhibition employed by the poxvirus family
84 The soluble poxvirus-encoded protein viral CC chemokine inhibitor (vCCI), a CC chemokine inhibitor,
85 ation of CC chemokines by the broad-spectrum CC chemokine inhibitor 35k efficiently reduced hepatic f
86 otein viral CC chemokine inhibitor (vCCI), a CC chemokine inhibitor, can bind to human CC chemokines
87 In turn, this NKp30-induced secretion of cc-chemokines is able to significantly suppress the repl
88 receptor ACKR2, which scavenges inflammatory CC-chemokines, is differentially expressed during mammar
89 -alpha) markedly increased the expression of CC chemokine ligand (CCL) 20, a CC chemokine receptor (C
90 N-formyl methionyl leucyl phenylalanine and CC chemokine ligand (CCL) 3 (neutrophils), or upon stimu
91 ar cells (FRCs), through their expression of CC chemokine ligand (CCL)19 and CCL21, attract and retai
92 d can reduce CXC chemokine ligand (CXCL)12-, CC chemokine ligand (CCL)19-, or CCL21-induced cell migr
94 e show that a latency-associated increase in CC chemokine ligand (CCL)8 results in the recruitment of
95 tor 9 (CCR9), which is a unique receptor for CC chemokine ligand (CCL25), is mainly expressed on lymp
98 endothelial growth factor receptor 2, CCR3, CC chemokine ligand 11/eotaxin-1, and CC chemokine ligan
100 C5aR-targeted mice produced large amounts of CC chemokine ligand 17 (CCL17) and CCL22 ex vivo, sugges
101 e thymus- and activation-regulated chemokine/CC chemokine ligand 17 (TARC/CCL17) and macrophage-deriv
105 rete immunosuppressive (interleukin [IL] 10, CC chemokine ligand 18) and tumor-promoting (IL-6, IL-8)
107 kine ligand 9 (CXCL9) and CXCL10, as well as CC chemokine ligand 2 (CCL2) and CCL5, were prominently
108 mice that lack the monocyte chemoattractant CC chemokine ligand 2 (CCL2) and found that biomaterials
109 evels of monocyte chemoattractant protein 1 [CC chemokine ligand 2 (CCL2) in the systematic nomenclat
114 of murine PD, several chemokines, including CC chemokine ligand 2 (CCL2, Monocyte Chemoattractant Pr
115 Obese adipose tissue exhibits increases in CC chemokine ligand 2 (CCL2, or monocyte chemoattractant
116 ession of monocyte chemoattractant protein-1/CC chemokine ligand 2 (MCP-1/CCL2), a chemokine required
117 k inflammatory cytokines TNF-alpha, IL-6, or CC chemokine ligand 2 succumb to infection with A/Vietna
121 x with C chemokine ligand 1/lymphotactin and CC chemokine ligand 2/monocyte chemoattractant protein 1
122 d the macrophage inflammatory protein 3alpha/CC chemokine ligand 20 (CCL20) produced by epithelial ce
123 d Piasy inhibits, keratinocyte production of CC chemokine ligand 20 (CCL20), a psoriatic chemokine es
128 to secondary lymphoid tissue chemokine (SLC)/CC chemokine ligand 21 (CCL21) were significantly lower
131 CCR3, CC chemokine ligand 11/eotaxin-1, and CC chemokine ligand 24/eotaxin-2 all reduced CNV area an
132 toxin-sensitive chemoattractant signaling by CC chemokine ligand 25 through CC chemokine receptor 9,
138 Interestingly, plasma levels of chemokines CC chemokine ligand 5 and CXC-chemokine ligand 4 were in
140 d in Trim32-deficient keratinocytes, whereas CC chemokine ligand 5 induction by tumor necrosis factor
142 ndritic cells and chemokine mRNA expression (CC chemokine ligand [CCL]5, CCL2, and CC chemokine recep
143 n a significant up-regulation of E-selectin, CC chemokine ligand-2, and interleukin-6 promoter activi
145 ugh induction of expression of the chemokine CC-chemokine ligand 28 (CCL28), which, in turn, promotes
149 We have produced a covalent dimer of the CC chemokine macrophage inflammatory protein-1beta (MIP-
150 ng enzyme catalytic polypeptide 3 G/F/H) and CC chemokines (macrophage inflammatory protein 1-alpha,
151 esses by demonstrating that IL-13 stimulates CC chemokines, matrix metalloproteinases, mucin genes, a
153 port that the murine cytomegalovirus-encoded CC chemokine, MCK2, enhanced CCR2-dependent recruitment
154 by the murine cytomegalovirus (MCMV)-encoded CC chemokine, MCK2, which promotes recruitment of CX3CR1
155 ng affinity between vCCI and other wild type CC chemokines, MCP-1 (monocyte chemoattractant protein-1
156 study, we describe the interactions of three CC chemokines, MCP-1/CCL2, MCP-2/CCL8, and MCP-3/CCL7, w
157 17) implicated in allergic diseases, inhibit CC chemokine-mediated T cell migration, and suppress all
158 llergic lung inflammation via suppression of CC chemokine-mediated Th2 cell recruitment to the lung.
159 vides the first definitive evidence that the CC chemokine MIP-1beta dimer is not able to bind or acti
161 CD8(+) T cells produced abundant amounts of CC chemokines (MIP-1beta, MIP-1alpha, and RANTES) but no
162 n orthopoxvirus vCCI in complex with a human CC chemokine, MIP-1beta (macrophage inflammatory protein
163 nverse correlation between the proportion of CC chemokine-modulated CCR5-expressing CD4(+) T cells an
165 ded by marked and selective induction of the CC chemokine monocyte chemoattractant protein-1 (MCP-1).
166 or activate its receptor and implicates the CC chemokine monomer as the sole receptor-interacting un
167 Bronchial epithelial cells (BECs) produce CC chemokines, notably CCL26 (eotaxin-3), which recruits
170 homology among monomer folds of all CXC and CC chemokines permits heterodimer assembly, our calculat
172 ization of late memory CD8(+) T cells toward CC chemokine production and away from IL-2 production su
173 n coinfected tissues by up-regulation of the CC chemokine RANTES, a well-known inhibitor of R5 HIV-1
174 similar experiments were conducted with the CC chemokine RANTES, and it was demonstrated that the pr
175 icular, the content of T lymphocytes bearing CC chemokine receptor (CCR) 1, CCR3, and CCR5 receptors
176 nophil signaling molecules [eg, eotaxins and CC chemokine receptor (CCR) 3] in IL-13-mediated airway
179 points to cross-talk between FcepsilonRI and CC chemokine receptor (CCR)-mediated signaling pathways
180 sted naloxone-induced down-regulation of the CC chemokine receptor (CCR)5 in NY1DD mice but not in co
181 xpression of CC chemokine ligand (CCL) 20, a CC chemokine receptor (CCR)6 ligand, in human keratinocy
183 Among 11 surveyed chemokine receptors, only CC chemokine receptor (CCR5), CXC chemokine receptor (CX
186 m of vitamin D3, signaled T cells to express CC chemokine receptor 10, which enabled them to migrate
188 ing restrictions to a linear aminobutyramide CC chemokine receptor 2 (CCR2) antagonist lead (2) led t
193 with relatively high numbers of parasites in CC chemokine receptor 2 (CCR2) KO mice, indicating that
194 dels that the expression of the inflammatory CC chemokine receptor 2 (CCR2) on donor-derived CD8+ T c
198 CC chemokine ligand 2 (CCL2), a ligand of CC chemokine receptor 2 (CCR2), is essential to mount an
200 ssion (CC chemokine ligand [CCL]5, CCL2, and CC chemokine receptor 2 [CCR2]) remained unchanged.
201 ice was reduced by 67%, but was unaltered in CC chemokine receptor 2(-/-) (CCR2(-/-)), CCR3(-/-), or
202 ory chemokine/receptor and cytokines (MCP-1, CC chemokine receptor 2, and interleukins 1beta and 6),
204 This study demonstrates that expression of CC chemokine receptor 4 (CCR4) by DCs is required for EA
205 ive of this study was to examine the role of CC chemokine receptor 4 (CCR4) in macrophage polarizatio
208 amulizumab, a defucosylated, humanized, anti-CC chemokine receptor 4 monoclonal antibody, in 41 pretr
219 eptor, CD4, and through a coreceptor, either CC chemokine receptor 5 (CCR5) or CXC chemokine receptor
220 We demonstrate that signaling through the CC chemokine receptor 5 (CCR5) prevents uncontrolled pos
221 globulin (Ig) G4 monoclonal antibody against CC chemokine receptor 5 (CCR5) with robust in vitro acti
222 a32, a complete loss-of-function mutation in CC chemokine receptor 5 (CCR5), has been previously asso
226 SIV hosts from AIDS and the discovery of low CC chemokine receptor 5 expression on CD4+ T cells as a
228 r gut homing, as indicated by high levels of CC chemokine receptor 6 and integrin beta7 expression.
231 that, even when LN retention signals such as CC chemokine receptor 7 (CCR7) are down-regulated, T cel
233 s T helper 1 (Th1) effector memory cells and CC chemokine receptor 7 (CCR7)(+) cells resembling centr
234 that migration to lymph nodes occurred in a CC chemokine receptor 7-independent manner but, overall,
236 chemokine ligand 18 (CCL18), acting through CC chemokine receptor 8 (CCR8) on mononuclear cells, was
237 svirus (KSHV) that selectively activates the CC chemokine receptor 8 (CCR8), for which the endogenous
238 sm depended on alpha(4) beta(7) integrin and CC chemokine receptor 9 (CCR9) expression by LSEC-primed
240 re a gut-homing phenotype (alpha 4 beta 7(+) CC chemokine receptor 9(+)) and the capacity to home to
241 signaling by CC chemokine ligand 25 through CC chemokine receptor 9, and binding of the integrins al
246 did translational studies to examine CXC and CC chemokine receptor expression by flow cytometry on ne
247 etic ablation or pharmacologic inhibition of CC chemokine receptor type 2 (CCR2) reduced macrophage (
248 in rectal tissue (both P < .001), and plasma CC chemokine receptor type 5 (CCR5) ligand (macrophage-i
252 dial smooth muscle cells, express functional CC chemokine receptor-1 (CCR1) and respond to RANTES by
253 ession (IL-2, -4, -6, -10, and IFN-gamma and CC chemokine receptor-1 [CCR1]) was assayed in the lymph
254 uctures of PXR LBD with Adnectin-1 and CCR1 (CC chemokine receptor-1) antagonist Compound-1 were dete
255 g with our previously described(20) class of CC chemokine receptor-3 (CCR3) antagonist, we improved t
257 This study investigates whether cytokine and CC-chemokine receptor (CCR) production by DCs stimulated
259 are rapidly mobilized upon inflammation in a CC-chemokine receptor 2-dependent manner, and the noncla
260 6- and 2.4-fold increases in Ly6-C(high) and CC-chemokine receptor 2-positive cells in lesions of apo
264 A subset of CC chemokines, acting through CC chemokine receptors (CCRs) 1 to 5, is instrumental in
265 r appears to be present in a large number of CC chemokine receptors and thereby could play a more gen
266 uitment upon exposure to DEPs and that these CC chemokine receptors are important in the DEP-induced
267 1, MCP-2, RANTES, MIG, IP-10, I-TAC, and two CC chemokine receptors CCR2 and CCR5 were highly express
271 rotein-coupled receptors that includes other CC chemokine receptors, INCB3344 is at least 100-fold se
273 (ACKR2) binds and scavenges proinflammatory CC-chemokines, regulates cutaneous T-cell positioning, a
275 f MMP processing of all 14 monocyte-directed CC chemokines revealed that each is precisely cleaved by
276 crease in the expression of the nonsignaling CC chemokine scavenging receptor D6 in whole lung sample
277 s in models of inflammation, suggesting that CC-chemokine scavenging by D6 is an important component
280 Our data therefore support a role for the CC chemokine system in hepatic fibrogenesis and suggest
282 action between vCCI and eotaxin-1 (CCL11), a CC chemokine that is an important factor in the asthma r
283 CC chemokine ligand 14, CCL14, is a human CC chemokine that is of recent interest because of its n
285 D6 is a scavenging-receptor for inflammatory CC chemokines that are essential for resolution of infla
286 recorded with IL-15 receptors, APOBEC3G and CC chemokines, the latter downmodulating CCR5 molecules.
289 a CC chemokine inhibitor, can bind to human CC chemokines tightly to impair the host immune defense.
291 a "silent" receptor, as it can bind CXC and CC chemokines to undergo ligand-induced receptor interna
292 talurus punctatus, we identified 26 distinct CC chemokine transcripts and obtained the genomic sequen
293 13Phe) caused vMIP-II to form a pH-dependent CC chemokine-type dimer as determined by analytical ultr
295 BEC3G was significantly upregulated, as were CC chemokines which induce downregulation of CCR5 in CD4
296 l activity of inflammatory mediators such as CC chemokines, which have been implicated in a wide rang
297 gland expresses high levels of inflammatory CC-chemokines, which are essential in vivo regulators of
298 owed a significant decrease in the levels of CC chemokines, while exposure to R5-subtype HIV gp120 ha
299 CC chemokine inhibitor (vCCI) binds to many CC chemokines with high affinity, acting as a potent inh
300 and -4 use different pharmacophores to bind CC chemokines, with the principal binding occurring thro
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