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Gene Review

Ccl24  -  chemokine (C-C motif) ligand 24

Mus musculus

Synonyms: C-C motif chemokine 24, CKb-6, Eosinophil chemotactic protein 2, Eotaxin-2, MPIF-2, ...
 
 
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Disease relevance of Ccl24

  • However, following intratracheal IL-13 administration, eotaxin-2-deficient mice showed a profound reduction in airway eosinophilia compared with wild type mice [1].
  • OBJECTIVE: We sought to determine whether eotaxin-2 was a cofactor with IL-5 for the regulation of pulmonary eosinophilia and to identify the combined role of these molecules in the induction of phenotypic characteristics of allergic lung disease [2].
 

High impact information on Ccl24

  • In particular, mice with defects in eosinophil development (Deltadbl-GATA) and eosinophil recruitment [mice deficient in CCR3 (CCR3 knockout) and mice deficient in both eotaxin-1 and eotaxin-2 (eotaxin-1/2 double knockout)] were subjected to Aspergillus fumigatus-induced allergic airway inflammation [3].
  • Dramatic increases in the expression of IL-5 and -13 and Eotaxin 2 were detected in LPS-treated BMMCs after costimulation with LPS and IgE/Ag [4].
  • Mechanistic analysis identified IL13-induced eotaxin-2 expression by macrophages in a distinct lung compartment (luminal inflammatory cells) compared with eotaxin-1, which was expressed solely in the tissue [1].
  • Notably, in contrast to observations made in eotaxin-1-deficient mice, eotaxin-2-deficient mice had normal base-line eosinophil levels in the hematopoietic tissues and gastrointestinal tract [1].
  • We aimed to examine the consequences of genetically ablating eotaxin-1 or eotaxin-2 alone, eotaxin-1 and eotaxin-2 together, and CCR3 [5].
 

Chemical compound and disease context of Ccl24

  • Analysis of airway (luminal) eosinophilia revealed a dominant role for eotaxin-2 and a synergistic reduction in eotaxin-1/2 double-deficient (DKO) and CCR3-deficient mice [5].
 

Biological context of Ccl24

 

Anatomical context of Ccl24

 

Associations of Ccl24 with chemical compounds

 

Other interactions of Ccl24

  • CONCLUSION: These investigations demonstrate important cooperativity between eotaxin-2, IL-5, and IL-13 signaling systems and eosinophils for the development of hallmark features of allergic disease of the lung [2].
  • Neither eotaxin-2 nor IL-5 alone induced these features of allergic disease [2].
 

Analytical, diagnostic and therapeutic context of Ccl24

References

  1. Identification of a cooperative mechanism involving interleukin-13 and eotaxin-2 in experimental allergic lung inflammation. Pope, S.M., Fulkerson, P.C., Blanchard, C., Akei, H.S., Nikolaidis, N.M., Zimmermann, N., Molkentin, J.D., Rothenberg, M.E. J. Biol. Chem. (2005) [Pubmed]
  2. Eotaxin-2 and IL-5 cooperate in the lung to regulate IL-13 production and airway eosinophilia and hyperreactivity. Yang, M., Hogan, S.P., Mahalingam, S., Pope, S.M., Zimmermann, N., Fulkerson, P., Dent, L.A., Young, I.G., Matthaei, K.I., Rothenberg, M.E., Foster, P.S. J. Allergy Clin. Immunol. (2003) [Pubmed]
  3. A central regulatory role for eosinophils and the eotaxin/CCR3 axis in chronic experimental allergic airway inflammation. Fulkerson, P.C., Fischetti, C.A., McBride, M.L., Hassman, L.M., Hogan, S.P., Rothenberg, M.E. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  4. Regulation of allergic airway inflammation through Toll-like receptor 4-mediated modification of mast cell function. Nigo, Y.I., Yamashita, M., Hirahara, K., Shinnakasu, R., Inami, M., Kimura, M., Hasegawa, A., Kohno, Y., Nakayama, T. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  5. The eotaxin chemokines and CCR3 are fundamental regulators of allergen-induced pulmonary eosinophilia. Pope, S.M., Zimmermann, N., Stringer, K.F., Karow, M.L., Rothenberg, M.E. J. Immunol. (2005) [Pubmed]
  6. Alanine scanning mutagenesis of the chemokine receptor CCR3 reveals distinct extracellular residues involved in recognition of the eotaxin family of chemokines. Duchesnes, C.E., Murphy, P.M., Williams, T.J., Pease, J.E. Mol. Immunol. (2006) [Pubmed]
  7. Murine eotaxin-2: a constitutive eosinophil chemokine induced by allergen challenge and IL-4 overexpression. Zimmermann, N., Hogan, S.P., Mishra, A., Brandt, E.B., Bodette, T.R., Pope, S.M., Finkelman, F.D., Rothenberg, M.E. J. Immunol. (2000) [Pubmed]
 
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