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Gene Review

Il5  -  interleukin 5

Rattus norvegicus

Synonyms: B-cell growth factor II, BCGF-II, Cytotoxic T-lymphocyte inducer, Eosinophil differentiation factor, IL-5, ...
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Disease relevance of Il5


High impact information on Il5

  • By immunofluorescence staining and flow fluorocytometry, the R52.120 and R52.625 antibodies bound to all 12 IL-5-sensitive cell lines tested [6].
  • Taken together from these results, we conclude that the R52.120 and R52.625 mAbs recognize epitopes on the IL-5-R complex very close or identical to the IL-5 binding sites [6].
  • Blockade of IL-4 or IL-5 following IL-9 induction reduced airway eosinophilia without affecting mucus production [7].
  • Murine interleukin-5 (IL-5) is known to play an essential role in Ig production of B cells and proliferation and differentiation of eosinophils [8].
  • Homology search for the amino acid sequence of the IL-5 receptor reveals that the IL-5 receptor contains a common motif of a cytokine receptor family that is recently identified [8].

Chemical compound and disease context of Il5


Biological context of Il5


Anatomical context of Il5


Associations of Il5 with chemical compounds

  • IL-4 and IL-5 mRNAs were induced by an antigen that is used to cross-link receptor bound IgE, by calcium ionophore, or by ionophore with phorbol ester and were markedly inhibited by dexamethasone [2].
  • Hydrocortisone at 10(-6) and 10(-7) M almost completely inhibited IL-4 and IL-5 mRNA production [2].
  • Here we examined the role of IL-5 and CS/2 in the expression of germline gamma1 transcripts and the generation of reciprocal products forming DNA circles as byproducts of mu-gamma1 switch recombination [17].
  • The cells were then washed and their capacity to produce IL-4, IL-5 and IFN-gamma determined following stimulation with phorbol 12-myristate 13-acetate (PMA) and ionomycin [18].
  • Draining LNC from OX-treated rats expressed elevated IFN-gamma mRNA, whereas those from TMA-treated rats expressed elevated IL-5 mRNA compared to controls [19].

Regulatory relationships of Il5

  • Results from PCR showed that prior to antigen challenge, BN rats expressed in their lungs mRNA for IL-4 and -5 and SD rats expressed very little mRNA for IL-5 only [20].

Other interactions of Il5

  • Our results showed that the mean values for IL-4 and IL-5 mRNA were increased significantly in sensitized rats compared with control rats [3].
  • The level of IL-4, IL-5, and IL-10 expression declined rapidly after 12 days [21].
  • There was no marked change in IL-5, IL-13 or transforming growth factor-beta (TGF-beta) in either strain [22].
  • In the inguinal LN, there were early mRNA elevations of IL-6 (a 2.5-fold increase by 6 hours, which correlated positively with the joint swelling) and IL-2 (4-fold by 6 hours), as well as later rises of IL-4 and IL-5 (2.5- and 4-fold, respectively, by day 3) [23].
  • We found that instillation of galectin-3 gene in these rats led to normalization of the eosinophil and T cell count in bronchoalveolar lavage fluid and that there was a strong concomitant inhibition of IL-5 mRNA in the lungs [14].

Analytical, diagnostic and therapeutic context of Il5

  • Bronchoalveolar lavage fluid from OVA-challenged rats showed eosinophilia and an increase in the number of cells expressing IL-4 and IL-5 mRNA [24].
  • Semiquantitative RT-PCR analysis of BAL cells showed that the cells from aged rats preferentially expressed Th1 type cytokine (IFN-gamma) mRNA, whereas cells from young animals expressed more Th2 type cytokine mRNAs including those for IL-4 and IL-5 [25].
  • These results demonstrate that CD38 ligation induces only germline gamma1 transcription and that IL-5 promotes both mu-gamma1 switch recombination and lgG1 secretion in an IL-4-independent manner [17].
  • Cytospin preparations from BAL cells were assessed for the presence of eosinophils by immunocytochemistry for major basic protein and for IL-4, IL-5, and IFN-gamma expression [26].
  • This effect was related to the inhibition of IL-5 (from 70.9 +/- 25.2 to 12.05 +/- 7.165 pg/mL) and CCL11/eotaxin levels (from 60.4 +/- 8.54 to 32.8 +/- 8.4 ng/mL) in pleural lavage fluid, using ELISA [27].


  1. Roles of TH1 and TH2 cytokines in a murine model of allergic dermatitis. Spergel, J.M., Mizoguchi, E., Oettgen, H., Bhan, A.K., Geha, R.S. J. Clin. Invest. (1999) [Pubmed]
  2. Induction of interleukin-4 and interleukin-5 expression in mast cells is inhibited by glucocorticoids. Sewell, W.A., Scurr, L.L., Orphanides, H., Kinder, S., Ludowyke, R.I. Clin. Diagn. Lab. Immunol. (1998) [Pubmed]
  3. Expression of interferon-gamma, interleukin-4 and interleukin-5 mRNA in the nasal mucosal membrane of rats with allergic rhinitis. El-Naggar, M.M., Ukai, K., Takeuchi, K., Sakakura, Y. Scand. J. Immunol. (1998) [Pubmed]
  4. The rat interleukin-5 gene: characterization and expression by retroviral gene transfer and polymerase chain reaction. Uberla, K., Li, W.Q., Qin, Z.H., Richter, G., Raabe, T., Diamantstein, T., Blankenstein, T. Cytokine (1991) [Pubmed]
  5. Critical role for T cells in Sephadex-induced airway inflammation: pharmacological and immunological characterization and molecular biomarker identification. Haddad, e.l.-.B., Underwood, S.L., Dabrowski, D., Birrell, M.A., McCluskie, K., Battram, C.H., Pecoraro, M., Foster, M.L., Belvisi, M.G. J. Immunol. (2002) [Pubmed]
  6. Monoclonal antibodies reactive with the mouse interleukin 5 receptor. Rolink, A.G., Melchers, F., Palacios, R. J. Exp. Med. (1989) [Pubmed]
  7. Pulmonary overexpression of IL-9 induces Th2 cytokine expression, leading to immune pathology. Temann, U.A., Ray, P., Flavell, R.A. J. Clin. Invest. (2002) [Pubmed]
  8. Molecular cloning and expression of the murine interleukin-5 receptor. Takaki, S., Tominaga, A., Hitoshi, Y., Mita, S., Sonoda, E., Yamaguchi, N., Takatsu, K. EMBO J. (1990) [Pubmed]
  9. Effect of allergen-specific immunotherapy on interleukin-4, interleukin-5 and interferon-gamma mRNA expression in the nasal mucosa of rats with allergic rhinitis. El-Naggar, M.M., Ukai, K., Takeuchi, K., Sakakura, Y. Scand. J. Immunol. (1998) [Pubmed]
  10. Systemic mycobacterial infection inhibits antigen-specific immunoglobulin E production, bronchial mucus production and eosinophilic inflammation induced by allergen. Yang, X., Wang, S., Fan, Y., Zhu, L. Immunology (1999) [Pubmed]
  11. Cutting edge: lipoxin (LX) A4 and aspirin-triggered 15-epi-LXA4 block allergen-induced eosinophil trafficking. Bandeira-Melo, C., Bozza, P.T., Diaz, B.L., Cordeiro, R.S., Jose, P.J., Martins, M.A., Serhan, C.N. J. Immunol. (2000) [Pubmed]
  12. Montelukast, a leukotriene receptor antagonist, inhibits the late airway response to antigen, airway eosinophilia, and IL-5-expressing cells in Brown Norway rats. Ihaku, D., Cameron, L., Suzuki, M., Molet, S., Martin, J., Hamid, Q. J. Allergy Clin. Immunol. (1999) [Pubmed]
  13. Corticotropin-releasing factor: actions on the sympathetic nervous system and metabolism. Brown, M.R., Fisher, L.A., Spiess, J., Rivier, C., Rivier, J., Vale, W. Endocrinology (1982) [Pubmed]
  14. Gene therapy with galectin-3 inhibits bronchial obstruction and inflammation in antigen-challenged rats through interleukin-5 gene downregulation. del Pozo, V., Rojo, M., Rubio, M.L., Cortegano, I., Cárdaba, B., Gallardo, S., Ortega, M., Civantos, E., López, E., Martín-Mosquero, C., Peces-Barba, G., Palomino, P., González-Mangado, N., Lahoz, C. Am. J. Respir. Crit. Care Med. (2002) [Pubmed]
  15. The role of interleukin-5 (IL-5) in allergic airway hyperresponsiveness in mice. Nagai, H., Yamaguchi, S., Tanaka, H. Ann. N. Y. Acad. Sci. (1996) [Pubmed]
  16. Rat models of asthma and chronic obstructive lung disease. Martin, J.G., Tamaoka, M. Pulmonary pharmacology & therapeutics. (2006) [Pubmed]
  17. IL-5 induces IgG1 isotype switch recombination in mouse CD38-activated sIgD-positive B lymphocytes. Mizoguchi, C., Uehara, S., Akira, S., Takatsu, K. J. Immunol. (1999) [Pubmed]
  18. Generation of rat Th2-like cells in vitro is interleukin-4-dependent and inhibited by interferon-gamma. Noble, A., Staynov, D.Z., Kemeny, D.M. Immunology (1993) [Pubmed]
  19. Selectivity of IgE responses, mast cell sensitization, and cytokine expression in the immune response of Brown Norway rats to chemical allergens. Vento, K.L., Dearman, R.J., Kimber, I., Basketter, D.A., Coleman, J.W. Cell. Immunol. (1996) [Pubmed]
  20. Cytokine expression in the presence or absence of late airway responses after antigen challenge of sensitized rats. Renzi, P.M., al Assaad, A.S., Yang, J., Yasruel, Z., Hamid, Q. Am. J. Respir. Cell Mol. Biol. (1996) [Pubmed]
  21. Elimination of IgE regulatory rat CD8+ T cells in vivo increases the co-ordinate expression of Th2 cytokines IL-4, IL-5 and IL-10. Noble, A., Staynov, D.Z., Diaz-Sanchez, D., Lee, T.H., Kemeny, D.M. Immunology (1993) [Pubmed]
  22. Th1/Th2 cytokine gene expression after mercuric chloride in susceptible and resistant rat strains. Gillespie, K.M., Saoudi, A., Kuhn, J., Whittle, C.J., Druet, P., Bellon, B., Mathieson, P.W. Eur. J. Immunol. (1996) [Pubmed]
  23. Expression of cytokine mRNA and protein in joints and lymphoid organs during the course of rat antigen-induced arthritis. Pohlers, D., Siegling, A., Buchner, E., Schmidt-Weber, C.B., Palombo-Kinne, E., Emmrich, F., Bräuer, R., Kinne, R.W. Arthritis Res. Ther. (2005) [Pubmed]
  24. The immunomodulatory actions of prostaglandin E2 on allergic airway responses in the rat. Martin, J.G., Suzuki, M., Maghni, K., Pantano, R., Ramos-Barbón, D., Ihaku, D., Nantel, F., Denis, D., Hamid, Q., Powell, W.S. J. Immunol. (2002) [Pubmed]
  25. Decreased expression of Th2 type cytokine mRNA contributes to the lack of allergic bronchial inflammation in aged rats. Ide, K., Hayakawa, H., Yagi, T., Sato, A., Koide, Y., Yoshida, A., Uchijima, M., Suda, T., Chida, K., Nakamura, H. J. Immunol. (1999) [Pubmed]
  26. Adoptively transferred late allergic response is inhibited by IL-4, but not IL-5, antisense oligonucleotide. Molet, S., Ramos-Barbón, D., Martin, J.G., Hamid, Q. J. Allergy Clin. Immunol. (1999) [Pubmed]
  27. Pharmacological study of anti-allergic activity of Syzygium cumini (L.) Skeels. Brito, F.A., Lima, L.A., Ramos, M.F., Nakamura, M.J., Cavalher-Machado, S.C., Siani, A.C., Henriques, M.G., Sampaio, A.L. Braz. J. Med. Biol. Res. (2007) [Pubmed]
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