ライフサイエンスコーパス: eotaxin-2

1 nophilia was dependent on eotaxin-1 (but not eotaxin-2).

2 due to a reduction in the levels of IL-5 and Eotaxin-2.

3 ion of CCL7/MCP-3, CC11/eotaxin-1, and CCL24/eotaxin-2.

4 t role for individually ablated eotaxin-1 or eotaxin-2.

5 te a cooperative mechanism between IL-13 and eotaxin-2.

6 apid proteolysis of eotaxin, but not IL-8 or eotaxin-2.

7 tion epitope on eosinophils was decreased by 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

10 The structure of eotaxin-2 (73 amino acid residues) consists of a helical

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

15 protein-1 (MBP-1), galectin-10 (CLC/GAL-10), Eotaxin-2 and Eotaxin-3, and urine osteopontin (OPN) and

16 We found that eotaxin-2 and I-309 were induced by LPS; in addition, ma

17 DSS treatment of eotaxin-2(-/-) and eotaxin-1/2(-/-) mice demonstrated th

18 nophil chemoattractant molecules (eotaxin-1, eotaxin-2, and their receptor CCR3) and with mice geneti

19 responses to the known ligands, eotaxin and eotaxin-2, because the DC response to these chemokines i

20 al CC chemokines including eotaxin (CCL-11), eotaxin-2 (CCL-24), RANTES (CCL-5), and monocyte chemota

21 Nasal eotaxin-2, CCL22/MDC, and monocyte chemoattactant protei

22 infection results in enhanced expression of eotaxin-2 (CCL24), thymus and activation-regulated chemo

23 Chemokines, eotaxin-1 (CCL11) and eotaxin-2 (CCL24), which are known to attract eosinophil

24 mplete abrogation of allergen-induced airway eotaxin-2/CCL24 and periostin levels in miR-155 KO mice.

25 Intranasal instillation of eotaxin-2/CCL24 before allergen challenge partially rest

26 ve chemokines, eotaxins (eotaxin-1/CCL11 and eotaxin-2/CCL24), eosinophils, and the inflammatory bowe

27 ophil-recruiting chemokines eotaxin-1/CCL11, eotaxin-2/CCL24, and eotaxin-3/CCL26 are expressed.

28 the receptor CCR3 including eotaxin-1/CCL11, eotaxin-2/CCL24, eotaxin-3/CCL26, RANTES/CCL5, and MEC/C

29 The eotaxin-2 cDNA contains an open reading frame that encod

30 ow report the characterization of the murine eotaxin-2 cDNA, gene and protein.

31 13/MCP-4, CCL18/PARC, CCL26/eotaxin-3, CCL24/Eotaxin-2), coupled with significant upregulation in the

32 servations made in eotaxin-1-deficient mice, eotaxin-2-deficient mice had normal base-line eosinophil

33 ollowing intratracheal IL-13 administration, eotaxin-2-deficient mice showed a profound reduction in

34 ial lung tissue eosinophils in IL-13-treated eotaxin-2-deficient mice was indistinguishable from wild

35 We report the solution structure of eotaxin-2 determined using heteronuclear and triple reso

36 Simultaneously, eotaxin-2 enhanced eosinophil adhesion to BSA.

37 ut) and mice deficient in both eotaxin-1 and eotaxin-2 (eotaxin-1/2 double knockout)] were subjected

38 The maximal response induced by eotaxin or eotaxin-2 exceeded that of RANTES or MCP-4.

39 mice strongly induced colonic eotaxin-1 and eotaxin-2 expression and eosinophil levels.

40 Mechanistic analysis identified IL13-induced eotaxin-2 expression by macrophages in a distinct lung c

41 particular, IL-13 mediates allergen-induced eotaxin-2 expression, and eotaxin-2 mediates IL-13-induc

42 Type 2 inflammation (eosinophilia, eotaxin-2 expression, IL-4/IL-5/IL-13 production, mucus

43 induced pulmonary eosinophilia, we generated eotaxin-2 gene-deficient mice by homologous recombinatio

44 rank order of potency: eotaxin approximately eotaxin-2 > MCP-4 approximately RANTES.

45 ce genetically engineered to be deficient in eotaxin-2 had a marked reduction of luminal eosinophils.

46 m revealed a TH2-dominated microenvironment (eotaxin-2, IL-5, IL-18, and IL-13) and increased signall

47 tic analysis revealed distinct expression of eotaxin-2 in bronchoalveolar lavage fluid cells consiste

48 nd, in order to address the specific role of eotaxin-2 in IL-13-induced pulmonary eosinophilia, we ge

49 ng to the N-terminal region of CCR3 binds to eotaxin-2, inducing concentration-dependent chemical shi

50 Thus, murine eotaxin-2 is a constitutively expressed eosinophil chemo

51 The human CC chemokine eotaxin-2 is a specific agonist for the chemokine recept

52 IL-12), and chemokine (CXCL13, CCL20, CCL21, eotaxin-2, KC, and MCP-1) production as well as inflamma

53 Greater eosinophilia and eotaxin 2 levels were observed in MWCNT-treated females

54 es IL-5 systemically from mature T cells and eotaxin-2 locally from lung epithelial cells.

55 mokine, thymus-expressed chemokine, eotaxin, eotaxin 2, macrophage-derived chemokines, and C10 were a

56 ce of CCR3 ligands other than eotaxin (e.g., eotaxin-2) may reflect the evolution of host counter mea

57 Our data suggest that eotaxin, eotaxin-2, MCP-4, and RANTES induce eosinophil TEM via C

58 s allergen-induced eotaxin-2 expression, and eotaxin-2 mediates IL-13-induced airway eosinophilia.

59 CCR3, which recognizes the ligands eotaxin, eotaxin-2, monocyte chemotactic protein (MCP) 3, MCP4, a

60 Eotaxin, eotaxin-2, monocyte chemotactic protein (MCP)-4, and RAN

61 Analysis of eotaxin-2 mRNA expression in mice transgenic for IL-4 bu

62 albumin-induced expressions of eotaxin-1 and eotaxin-2 mRNA in the lungs were almost completely depen

63 Furthermore, eotaxin-2 mRNA was strongly induced by both transgenic o

64 umigatus or OVA revealed marked induction of eotaxin-2 mRNA.

65 We report that in the absence of eotaxin-2 or CCR3, there was a profound reduction in IL-

66 When eotaxin-2 or other CCR3-active chemokines were added to

67 e with the CCR3 ligands CCL11/eotaxin, CCL24/eotaxin-2, or CCL26/eotaxin-3 on 1) wound repair, using

68 r eosinophilic cationic protein (P = 0.008), eotaxin-2 (P = 0.008), eotaxin-3 (P = 0.031), pulmonary

69 ormal increases in IL-5, IL-13, eotaxin, and eotaxin-2 production are abrogated in the RAGE knockouts

70 Recombinant eotaxin-2 protein induced dose-dependent chemotactic res

71 These results show that eotaxin-2 rapidly reduced alpha4 integrin function while

72 In a flow-based adhesion assay, eotaxin-2 reduced eosinophil accumulation and the streng

73 inflammatory protein (MIP) 1alpha and 1beta, eotaxin-2, serum amyloid A3 (Saa3), and insulin-like gro

74 Comparison of the eotaxin-2 structure with those of related chemokines ind

75 RV-C induced higher expression of CCL24 (eotaxin-2) than RV-A in the responses of children with a

76 eotaxin-1 or eotaxin-2 alone, eotaxin-1 and eotaxin-2 together, and CCR3.

77 LF, the levels of IL-5, IL-13, eotaxin-1 and eotaxin-2 were significantly lower in FHL2-KO mice.