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1 nophilia was dependent on eotaxin-1 (but not eotaxin-2).
2 ion of CCL7/MCP-3, CC11/eotaxin-1, and CCL24/eotaxin-2.
3 t role for individually ablated eotaxin-1 or eotaxin-2.
4 te a cooperative mechanism between IL-13 and eotaxin-2.
5 apid proteolysis of eotaxin, but not IL-8 or eotaxin-2.
6 tion epitope on eosinophils was decreased by eotaxin-2.
7 due to a reduction in the levels of IL-5 and Eotaxin-2.
8 mice had a fivefold increased production of eotaxin-2 (534 pg/mL) and a sevenfold increase in bronch
9 93 amino acids, is most homologous to human eotaxin-2 (59.1% identity), but is only 38.9% identical
11 ion regulated chemokine (TARC), eotaxin, and eotaxin-2 acted specifically on in vitro derived Th2 lym
12 and 11/eotaxin-1, and CC chemokine ligand 24/eotaxin-2 all reduced CNV area and lesion number in thes
13 quences of genetically ablating eotaxin-1 or eotaxin-2 alone, eotaxin-1 and eotaxin-2 together, and C
14 l) eosinophilia revealed a dominant role for eotaxin-2 and a synergistic reduction in eotaxin-1/2 dou
17 nophil chemoattractant molecules (eotaxin-1, eotaxin-2, and their receptor CCR3) and with mice geneti
18 responses to the known ligands, eotaxin and eotaxin-2, because the DC response to these chemokines i
19 al CC chemokines including eotaxin (CCL-11), eotaxin-2 (CCL-24), RANTES (CCL-5), and monocyte chemota
20 infection results in enhanced expression of eotaxin-2 (CCL24), thymus and activation-regulated chemo
22 mplete abrogation of allergen-induced airway eotaxin-2/CCL24 and periostin levels in miR-155 KO mice.
24 ve chemokines, eotaxins (eotaxin-1/CCL11 and eotaxin-2/CCL24), eosinophils, and the inflammatory bowe
26 the receptor CCR3 including eotaxin-1/CCL11, eotaxin-2/CCL24, eotaxin-3/CCL26, RANTES/CCL5, and MEC/C
29 servations made in eotaxin-1-deficient mice, eotaxin-2-deficient mice had normal base-line eosinophil
30 ollowing intratracheal IL-13 administration, eotaxin-2-deficient mice showed a profound reduction in
31 ial lung tissue eosinophils in IL-13-treated eotaxin-2-deficient mice was indistinguishable from wild
34 ut) and mice deficient in both eotaxin-1 and eotaxin-2 (eotaxin-1/2 double knockout)] were subjected
37 Mechanistic analysis identified IL13-induced eotaxin-2 expression by macrophages in a distinct lung c
38 particular, IL-13 mediates allergen-induced eotaxin-2 expression, and eotaxin-2 mediates IL-13-induc
39 induced pulmonary eosinophilia, we generated eotaxin-2 gene-deficient mice by homologous recombinatio
41 ce genetically engineered to be deficient in eotaxin-2 had a marked reduction of luminal eosinophils.
42 m revealed a TH2-dominated microenvironment (eotaxin-2, IL-5, IL-18, and IL-13) and increased signall
43 tic analysis revealed distinct expression of eotaxin-2 in bronchoalveolar lavage fluid cells consiste
44 nd, in order to address the specific role of eotaxin-2 in IL-13-induced pulmonary eosinophilia, we ge
45 ng to the N-terminal region of CCR3 binds to eotaxin-2, inducing concentration-dependent chemical shi
48 IL-12), and chemokine (CXCL13, CCL20, CCL21, eotaxin-2, KC, and MCP-1) production as well as inflamma
50 mokine, thymus-expressed chemokine, eotaxin, eotaxin 2, macrophage-derived chemokines, and C10 were a
51 ce of CCR3 ligands other than eotaxin (e.g., eotaxin-2) may reflect the evolution of host counter mea
53 s allergen-induced eotaxin-2 expression, and eotaxin-2 mediates IL-13-induced airway eosinophilia.
54 CCR3, which recognizes the ligands eotaxin, eotaxin-2, monocyte chemotactic protein (MCP) 3, MCP4, a
57 albumin-induced expressions of eotaxin-1 and eotaxin-2 mRNA in the lungs were almost completely depen
62 e with the CCR3 ligands CCL11/eotaxin, CCL24/eotaxin-2, or CCL26/eotaxin-3 on 1) wound repair, using
63 ormal increases in IL-5, IL-13, eotaxin, and eotaxin-2 production are abrogated in the RAGE knockouts
67 inflammatory protein (MIP) 1alpha and 1beta, eotaxin-2, serum amyloid A3 (Saa3), and insulin-like gro
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