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MeSH Review

Eosinophilia

 
 
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Disease relevance of Eosinophilia

 

High impact information on Eosinophilia

 

Chemical compound and disease context of Eosinophilia

 

Biological context of Eosinophilia

 

Anatomical context of Eosinophilia

 

Gene context of Eosinophilia

  • The reduced IL-5 production in IL-4-/- mice correlated with reduced helminth-induced eosinophilia, which has been shown to be dependent on IL-5 in vivo [26].
  • Unexpectedly, N. brasiliensis-infected IL-4/13-deficient mice developed elevated IL-5 and eosinophilia, indicating that compensatory mechanisms exist for the expression of IL-5, although serum IgE remained undetectable [27].
  • These findings indicate that IL-9 is not obligatory for the development of eosinophilia and AHR, and imply that other Th2 cytokines can act in a compensatory fashion [28].
  • Human eosinophil peroxidase (EPO) was purified from eosinophil granules derived from the peripheral blood of patients with eosinophilia [29].
  • In contrast, Stat6 signaling only partially mediated antigen-induced eosinophilia with no role in vascular adhesion molecule 1 expression [30].
 

Analytical, diagnostic and therapeutic context of Eosinophilia

References

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  18. Peripheral blood eosinophilia in owl monkeys is associated with increased eosinophilopoiesis yet depressed recruitment kinetics to the Chemokine RANTES. Albert, D.L., Brodie, S.J., Sasseville, V.G., Ringler, D.J. Blood (1996) [Pubmed]
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  20. A comparison of treatment of canine cyclic hematopoiesis with recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF), G-CSF interleukin-3, and canine G-CSF. Hammond, W.P., Boone, T.C., Donahue, R.E., Souza, L.M., Dale, D.C. Blood (1990) [Pubmed]
  21. Human eotaxin is a specific chemoattractant for eosinophil cells and provides a new mechanism to explain tissue eosinophilia. Garcia-Zepeda, E.A., Rothenberg, M.E., Ownbey, R.T., Celestin, J., Leder, P., Luster, A.D. Nat. Med. (1996) [Pubmed]
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  23. Transgenic mice expressing a B cell growth and differentiation factor gene (interleukin 5) develop eosinophilia and autoantibody production. Tominaga, A., Takaki, S., Koyama, N., Katoh, S., Matsumoto, R., Migita, M., Hitoshi, Y., Hosoya, Y., Yamauchi, S., Kanai, Y. J. Exp. Med. (1991) [Pubmed]
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  26. Disruption of the murine IL-4 gene blocks Th2 cytokine responses. Kopf, M., Le Gros, G., Bachmann, M., Lamers, M.C., Bluethmann, H., Köhler, G. Nature (1993) [Pubmed]
  27. Simultaneous disruption of interleukin (IL)-4 and IL-13 defines individual roles in T helper cell type 2-mediated responses. McKenzie, G.J., Fallon, P.G., Emson, C.L., Grencis, R.K., McKenzie, A.N. J. Exp. Med. (1999) [Pubmed]
  28. The absence of interleukin 9 does not affect the development of allergen-induced pulmonary inflammation nor airway hyperreactivity. McMillan, S.J., Bishop, B., Townsend, M.J., McKenzie, A.N., Lloyd, C.M. J. Exp. Med. (2002) [Pubmed]
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  30. Signal transducer and activator of transcription factor 6 (Stat6)-deficient mice are protected from antigen-induced airway hyperresponsiveness and mucus production. Kuperman, D., Schofield, B., Wills-Karp, M., Grusby, M.J. J. Exp. Med. (1998) [Pubmed]
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  34. Association of ethylene-oxide-induced IgE antibodies with symptoms in dialysis patients. Rumpf, K.W., Seubert, S., Seubert, A., Lowitz, H.D., Valentin, R., Rippe, H., Ippen, H., Scheler, F. Lancet (1985) [Pubmed]
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