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Gene Review

IL5  -  interleukin 5

Homo sapiens

Synonyms: B-cell differentiation factor I, EDF, Eosinophil differentiation factor, IL-5, Interleukin-5, ...
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Disease relevance of IL5


Psychiatry related information on IL5

  • These results may suggest that activated eosinophils by IL-5 play an important role in host defense mechanisms, releasing their toxic granule proteins on adjoining tumor cells [6].
  • BACKGROUND: Psychometric properties of the Chinese version of CBCL, TRF, and YSR were understudied [7].

High impact information on IL5

  • Through the release of cytokines such as IL-4, IL-13, and IL-5, these cells orchestrate the recruitment and activation of the primary effector cells of the allergic response, the mast cell and the eosinophil [8].
  • The data suggest that ancestral telomeres, like those of vertebrates, contained a TRF-like protein as well as Rap1 [9].
  • A first class codes for an IL5-specific chain (hIL5R alpha) [10].
  • A human high affinity interleukin-5 receptor (IL5R) is composed of an IL5-specific alpha chain and a beta chain shared with the receptor for GM-CSF [10].
  • Interleukin-5 (IL-5) specifically induces the differentiation of eosinophils, which are important in host defence and the pathogenesis of allergies and asthma [11].

Chemical compound and disease context of IL5


Biological context of IL5

  • OBJECTIVE: We sought to determine whether the related palindromic elements from IL4, IL5, and IL13 also act as enhancers of gene transcription [17].
  • These data indicate that the PER-117 cell line is a model to study signal transduction and transcriptional activation of the human IL5 gene in human T-cells [18].
  • Interestingly in BOS, the number of IL5- and IL10-producing cells was significantly lower than in stable patients (P < or = .05), suggesting a possible role of these Th2 cytokines in the modulation of graft tolerance [19].
  • Messenger RNA expression of the cytokine gene cluster, interleukin 3 (IL-3), IL-4, IL-5, and granulocyte/macrophage colony-stimulating factor, in allergen-induced late-phase cutaneous reactions in atopic subjects [20].
  • These observations suggest a potentially autocrine effect of IL-5 on hMC for amplification of allergic immune responses, in addition to its recognized paracrine effects on eosinophils, and implicate both IL-4 and IL-5 in the modulation of the hMC phenotype [21].

Anatomical context of IL5

  • The finding that IL5 and GM-CSF share a receptor subunit provides a molecular basis for the observation that these cytokines can partially interfere with each other's binding and have highly overlapping biological activities on eosinophils [10].
  • We also provide experimental data to show that the binding of NFAT to the nucleotides GAA at positions -113 to -111 of the human IL5 promoter is associated with functional activity in human T cells [22].
  • IL5 production in the PER-117 cell line can be activated by phorbol 12-myristate 13-acetate alone and further enhanced by calcium ionophore A23187, cyclic adenosine 3', 5'-monophosphate or anti-CD28 antibodies [18].
  • Human Jurkat cells express IL4 but one of the main factors restricting studies of human IL5 expression has been the lack of human T-cell lines which express significant levels of IL5 in an inducible fashion [18].
  • The asthmatic population demonstrated an increased amount of Th2-mediated serum IgE anti-Hep B antibody, as compared to nonasthmatic children; but comparable amounts of IgG1, IgG2, IgG3, IgA, and IgM anti-Hep B antibody and lymphocyte IFNgamma, IL4, and IL5 [23].

Associations of IL5 with chemical compounds

  • The conditions used to stimulate the PER-117 cells determined whether IL5 production was inhibited by cyclosporin A or dexamethasone [18].
  • The inhibition of binding IL5 to its receptor by the isothiazolone derivatives is abrogated by free-sulfhydryl-containing compounds such as dithiothreitol, indicating that the isothiazolones react with the sulfhydryl group of free cysteine residues in the hIL5R alpha [24].
  • By contrast, others observed no significant loss of bcl-2 protein expression in steroid-, alpha-APO-1 - and IL5-treated cells when compared with untreated or fresh cells [25].
  • In contrast, after prednisone treatment, SR asthmatics had no significant change in either the number of BAL cells expressing mRNA for IL-4 or IL-5 [26].
  • Unlike IL-4, IL-5 priming did not enhance FcvarepsilonRI-dependent histamine release [21].

Physical interactions of IL5

  • Human IL5 was shown by analytical ultracentrifugation to form a 1:1 complex with the soluble domain of the hIL5 receptor alpha subunit (shIL5R alpha) [27].
  • This region contains two potential GATA-3-binding sites and increases expression from the hIL-5 promoter by up to ninefold [28].
  • Cross-linking experiments on HL-60 cells demonstrated two IL-5-containing complexes of Mr 150,000 and Mr 80,000 both of which were inhibited by GM-CSF [29].
  • The resulting CrkL.STAT5 complexes translocated to the nucleus and bound STAT5 consensus DNA-binding sites present in the promoters of IL-5-regulated genes, as shown in gel mobility and antibody supershift assays [30].
  • In conclusion, these data suggests that the composite NFAT/AP-1 binding element (- 115 to - 100) plays a crucial role in IL-5 synthesis by peripheral T cells of asthmatic patients [31].

Enzymatic interactions of IL5

  • We propose that the unique regulatory mechanism of IL-5 gene transcription involves the reversible histone modification catalysed by HDAC4 and p300, which are recruited by the transcription factors [32].
  • STAT-1 was tyrosine phosphorylated within 15 min of IL-5 stimulation [33].

Regulatory relationships of IL5

  • As the same beta c subunit also forms high-affinity receptors for IL-5 and granulocyte-macrophage colony-stimulating factor (GM-CSF) with the respective cytokine-specific alpha subunit, the expression of the alpha subunits is responsible for specificity of cytokines [34].
  • These results suggest that IL-2 induces IL-5 leading to marked peripheral eosinophilia and extravascular eosinophil degranulation [35].
  • Release of IL-8 protein and storage of IL-4 and IL-10 proteins were enhanced by exogenous IL-5 and inhibited by a transcription inhibitor, actinomycin D [36].
  • Only PAF and eotaxin induced transmigration of eosinophils through Matrigel in the presence of IL-5; PAF was more potent than eotaxin at the optimal concentration [37].
  • In the asthmatics, the percentages of CD4 T-LC expressing IL-5 mRNA correlated with disease severity and the numbers of peripheral blood eosinophils (P < 0.01) [38].
  • Mutation of reporter gene plasmids showed the Ets/NFAT site was of equal importance to the AP-1 and GATA-3 sites in regulating IL-5 transcription [39].

Other interactions of IL5

  • Additionally, pretreatment of hMCs with MK571 or with the cys-LT biosynthetic inhibitor MK886 decreased IL-5 and TNF-alpha production in response to IgE receptor cross-linkage, implying a positive feedback by endogenously produced cys-LTs [40].
  • The aim of this study was to examine the pattern of Th1- and Th2-type (IL-4, IL-5, and IL-13) cytokines in the early ileal lesions occurring in patients with CD 3 months after ileal resection and ileocolonic anastomosis [41].
  • Humanized monoclonal antibodies (hMAbs) against IL-5, and a recombinant soluble human IL-4 receptor have been developed as possible treatments for this disorder [42].
  • The induction of detectable levels of IL-5 and GM-CSF in the circulation may explain the eosinophilia and neutrophilia observed in these patients [43].
  • T helper 1 (Th1)/Th2 ([IL-2 + IFN-gamma]/[IL-4 + IL-5]) cytokine mRNA ratios, thought to reflect the Th deviation of the pathogenic disease-specific T cells, and type-1/type-2 mRNA ratios, thought to reflect the overall immune response polarization, were significantly increased in ITP patients [44].

Analytical, diagnostic and therapeutic context of IL5

  • By contrast, steroid-sensitive (SS) asthmatics respond well to glucocorticoids, and this is accompanied by a decrease in the numbers of bronchoalveolar lavage (BAL) messenger RNA+ (mRNA+) cells expressing IL-4 and IL-5, and an increase in interferon gamma (IFN-gamma) transcripts [26].
  • These data further demonstrate that CDE maturing in the continued presence of IL-5 adhere to HUVEC predominantly through VLA-4 ligation [45].
  • Studies using cellular autoradiography showed that IL-5 receptors were evenly distributed on eosinophils but that receptor distribution on HL-60 cells was noticeably heterogeneous [3].
  • Kinetic analysis using surface plasmon resonance yielded data consistent with the Kd values from calorimetry and also with the possibility of conformational isomerization in the interaction of hIL5 with the receptor alpha subunit [27].
  • Titration microcalorimetry yielded equilibrium dissociation constants of 3.1 and 2.0 nM, respectively, for the binding of hIL5 to shIL5R alpha and to a chimeric form of the receptor containing shIL5R alpha fused to the immunoglobulin Fc domain (shIL5R alpha-Fc) [27].


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  2. Effects of T-helper 2-type cytokines, interleukin-3 (IL-3), IL-4, IL-5, and IL-6 on the survival of cultured human mast cells. Yanagida, M., Fukamachi, H., Ohgami, K., Kuwaki, T., Ishii, H., Uzumaki, H., Amano, K., Tokiwa, T., Mitsui, H., Saito, H., Iikura, Y., Ishizaka, T., Nakahata, T. Blood (1995) [Pubmed]
  3. Characterization of a receptor for interleukin-5 on human eosinophils and the myeloid leukemia line HL-60. Ingley, E., Young, I.G. Blood (1991) [Pubmed]
  4. Interleukin-4 and interleukin-5 map to human chromosome 5 in a region encoding growth factors and receptors and are deleted in myeloid leukemias with a del(5q). Le Beau, M.M., Lemons, R.S., Espinosa, R., Larson, R.A., Arai, N., Rowley, J.D. Blood (1989) [Pubmed]
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  6. Cellular localization of interleukin-5 expression in rectal carcinoma with eosinophilia. Tajima, K., Yamakawa, M., Inaba, Y., Katagiri, T., Sasaki, H. Hum. Pathol. (1998) [Pubmed]
  7. Test-retest reliability and criterion validity of the Chinese version of CBCL, TRF, and YSR. Leung, P.W., Kwong, S.L., Tang, C.P., Ho, T.P., Hung, S.F., Lee, C.C., Hong, S.L., Chiu, C.M., Liu, W.S. Journal of child psychology and psychiatry, and allied disciplines. (2006) [Pubmed]
  8. Immunologic basis of antigen-induced airway hyperresponsiveness. Wills-Karp, M. Annu. Rev. Immunol. (1999) [Pubmed]
  9. Identification of human Rap1: implications for telomere evolution. Li, B., Oestreich, S., de Lange, T. Cell (2000) [Pubmed]
  10. A human high affinity interleukin-5 receptor (IL5R) is composed of an IL5-specific alpha chain and a beta chain shared with the receptor for GM-CSF. Tavernier, J., Devos, R., Cornelis, S., Tuypens, T., Van der Heyden, J., Fiers, W., Plaetinck, G. Cell (1991) [Pubmed]
  11. Creation of a biologically active interleukin-5 monomer. Dickason, R.R., Huston, D.P. Nature (1996) [Pubmed]
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  14. Regulation by IL-5 of expression of functional platelet-activating factor receptors on human eosinophils. Kishimoto, S., Shimadzu, W., Izumi, T., Shimizu, T., Fukuda, T., Makino, S., Sugiura, T., Waku, K. J. Immunol. (1996) [Pubmed]
  15. Nasal biomarker profiles in acute and chronic rhinosinusitis. Riechelmann, H., Deutschle, T., Rozsasi, A., Keck, T., Polzehl, D., Bürner, H. Clin. Exp. Allergy (2005) [Pubmed]
  16. IL-5 production by CD4+ T cells of asthmatic patients is suppressed by glucocorticoids and the immunosuppressants FK506 and cyclosporin A. Mori, A., Suko, M., Nishizaki, Y., Kaminuma, O., Kobayashi, S., Matsuzaki, G., Yamamoto, K., Ito, K., Tsuruoka, N., Okudaira, H. Int. Immunol. (1995) [Pubmed]
  17. Characterization of a palindromic enhancer element in the promoters of IL4, IL5, and IL13 cytokine genes. Codlin, S., Soh, C., Lee, T., Lavender, P. J. Allergy Clin. Immunol. (2003) [Pubmed]
  18. A human T-cell line with inducible production of interleukins 5 and 4. A model for studies of gene expression. Mordvinov, V.A., Peroni, S.E., De Boer, M.L., Kees, U.R., Sanderson, C.J. J. Immunol. Methods (1999) [Pubmed]
  19. The frequency of interleukin-10- and interleukin-5-secreting CD4+ T cells correlates to tolerance of transplanted lung. Bianco, A.M., Solari, N., Miserere, S., Pellegrini, C., Vitulo, P., Pozzi, E., Fietta, A., Meloni, F. Transplant. Proc. (2005) [Pubmed]
  20. Messenger RNA expression of the cytokine gene cluster, interleukin 3 (IL-3), IL-4, IL-5, and granulocyte/macrophage colony-stimulating factor, in allergen-induced late-phase cutaneous reactions in atopic subjects. Kay, A.B., Ying, S., Varney, V., Gaga, M., Durham, S.R., Moqbel, R., Wardlaw, A.J., Hamid, Q. J. Exp. Med. (1991) [Pubmed]
  21. IL-4 and -5 prime human mast cells for different profiles of IgE-dependent cytokine production. Ochi, H., De Jesus, N.H., Hsieh, F.H., Austen, K.F., Boyce, J.A. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  22. Role of nuclear factor of activated T cells (NFAT) in the expression of interleukin-5 and other cytokines involved in the regulation of hemopoetic cells. De Boer, M.L., Mordvinov, V.A., Thomas, M.A., Sanderson, C.J. Int. J. Biochem. Cell Biol. (1999) [Pubmed]
  23. Immune response to hepatitis B vaccine in asthmatic children. Masten, B., McWilliams, B., Lipscomb, M., Archibeque, T., Qualls, C., Kelly, H.W., Schuyler, M. Pediatr. Pulmonol. (2003) [Pubmed]
  24. Covalent modification of the interleukin-5 receptor by isothiazolones leads to inhibition of the binding of interleukin-5. Devos, R., Guisez, Y., Plaetinck, G., Cornelis, S., Tavernier, J., van der Heyden, J., Foley, L.H., Scheffler, J.E. Eur. J. Biochem. (1994) [Pubmed]
  25. Modulation of apoptosis with cytokines in B-cell chronic lymphocytic leukaemia. Mainou-Fowler, T., Prentice, A.G. Leuk. Lymphoma (1996) [Pubmed]
  26. Dysregulation of interleukin 4, interleukin 5, and interferon gamma gene expression in steroid-resistant asthma. Leung, D.Y., Martin, R.J., Szefler, S.J., Sher, E.R., Ying, S., Kay, A.B., Hamid, Q. J. Exp. Med. (1995) [Pubmed]
  27. Binding interactions of human interleukin 5 with its receptor alpha subunit. Large scale production, structural, and functional studies of Drosophila-expressed recombinant proteins. Johanson, K., Appelbaum, E., Doyle, M., Hensley, P., Zhao, B., Abdel-Meguid, S.S., Young, P., Cook, R., Carr, S., Matico, R. J. Biol. Chem. (1995) [Pubmed]
  28. Distal regulatory elements play an important role in regulation of the human IL-5 gene. Urwin, D.L., Schwenger, G.T., Groth, D.M., Sanderson, C.J. Eur. J. Immunol. (2004) [Pubmed]
  29. Interleukin-5, interleukin-3, and granulocyte-macrophage colony-stimulating factor cross-compete for binding to cell surface receptors on human eosinophils. Lopez, A.F., Vadas, M.A., Woodcock, J.M., Milton, S.E., Lewis, A., Elliott, M.J., Gillis, D., Ireland, R., Olwell, E., Park, L.S. J. Biol. Chem. (1991) [Pubmed]
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  32. Recruitment of histone deacetylase 4 by transcription factors represses interleukin-5 transcription. Han, S., Lu, J., Zhang, Y., Cheng, C., Han, L., Wang, X., Li, L., Liu, C., Huang, B. Biochem. J. (2006) [Pubmed]
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  34. Expression and factor-dependent modulation of the interleukin-3 receptor subunits on human hematopoietic cells. Sato, N., Caux, C., Kitamura, T., Watanabe, Y., Arai, K., Banchereau, J., Miyajima, A. Blood (1993) [Pubmed]
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