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Gene Review

IL9  -  interleukin 9

Homo sapiens

Synonyms: Cytokine P40, HP40, IL-9, Interleukin-9, P40, ...
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Disease relevance of IL9


Psychiatry related information on IL9

  • Despite this normal B-1 lymphocyte number, IL-9 failed to restore classical functions of B-1 cells, namely, the production of natural IgM Abs, the T15 Id Ab response to phosphorylcholine immunization, and the antipolysaccharide humoral response against Streptococcus pneumoniae [6].
  • 5. The reaction time of the subject was on average 19% shorter in the trials in which a P40 was present, thus suggesting that P40 can influence subsequent perceptual processing by the brain in the same trial [7].
  • Adult thalamocortical terminals visualized by anterograde tract-tracing display significantly larger cross-section areas than terminals at postnatal day (P) 35, P40, and P49 critical period ages [8].
  • METHODS: Behavioral measures, including prepulse inhibition (PPI) and total locomotor activity, after amphetamine exposure were assessed at postnatal day 20 (P20) (prepuberty), P40 (puberty), P60 (postpuberty), and P80 (adulthood) in animals previously exposed to allopregnanolone (10 mg/kg) on P2 and P5 [9].
  • The most striking finding in patients with Huntington's disease was a drastic diminution of the amplitude of the early cortical components, especially N20/P25 for the median nerve and N33/P40 for the tibial nerve [10].

High impact information on IL9

  • The interleukin-2 receptor (IL-2R) consists of three subunits: the IL-2R alpha, IL-2R beta, and IL-2R gamma chains, the last of which is also used in the receptors for IL-4, IL-7, and IL-9 [11].
  • While a hexapeptide sequence NH2 terminus of fibrillarin is shared with an Epstein-Barr virus-encoded nuclear antigen, the COOH-terminal region shares sequence homology with P40, the capsid protein encoded by herpes virus type 1 [12].
  • By contrast, a large number of cytokines examined, including the mast cell growth factors/agonists in rodents, interleukin 3 (IL-3), IL-4, IL-9, and nerve growth factor, were ineffective in this respect [13].
  • Transgene induction resulted in lymphocytic and eosinophilic infiltration of the lung, airway epithelial cell hypertrophy with mucus production, and mast cell hyperplasia, similar to that seen in mice that constitutively expressed IL-9 in their lungs [14].
  • The constitutive overexpression of IL-9 in the lungs of transgenic mice resulted in an asthma-like phenotype [14].

Chemical compound and disease context of IL9

  • To define the contribution of IL-9 to lung inflammation we generated transgenic mice in which lung-specific expression of the IL-9 transgene is inducible by doxycycline [14].
  • CITED2 is inducible by varying stimuli including lipopolysaccharide, hypoxia, and cytokines such as interleukin 9 and interferon gamma [15].
  • A striking feature of these animals is a robust peribronchial and perivascular eosinophilia after allergen challenge, suggesting that IL-9 is a potent factor in regulating this process [16].
  • In earlier studies, using a newborn mouse model of excitotoxic lesions mimicking those described in human cerebral palsy, we found that IL-9 pretreatment exacerbated brain damage produced by intracerebral injections of the glutamatergic analog ibotenate [17].
  • Propofol-treated patients had shorter stays in the post-anesthesia care unit (PACU; P-20, 131+/-35 min [mean +/- SD]; P-40, 141+/-34 min; placebo, 191+/-92 min; P = 0.005) and higher satisfaction with their control of PONV than placebo (P < 0.01) [18].

Biological context of IL9

  • Transfection of this cDNA in a murine T-cell clone conferred responsiveness to human IL-9 [19].
  • Transient expression of this cDNA produced high-affinity binding sites for IL-9 [19].
  • In addition, the terminal deoxynucleotidyl transferase assay (TDTA) and standard analysis of DNA cleavage by gel electrophoresis were used to evaluate induction of prevention of apoptosis by IL-9 [20].
  • Previous studies suggested that protein tyrosine phosphorylation may be involved in IL-9 signaling pathways [2].
  • These results will now allow us to study the regulatory mechanism of IL-9 gene expression in normal and leukemic human T cells [21].

Anatomical context of IL9

  • This variant could be permanently expressed in a cytokine-dependent murine T-cell line but lacked the ability to induce proliferation in response to human IL9 [22].
  • The mechanism by which IL-9 affects eosinophils (eos) is not known [23].
  • IL-9 and interferon gamma (IFN-gamma) mRNAs were also expressed at high levels in chronically infected cell lines [24].
  • As a single agent IL-9 supported, in a concentration-dependent fashion, maturation of burst-forming units-erythroid (BFU-E) of adult and fetal origin [25].
  • IL-9 had a wider spectrum of action on progenitors of fetal origin than on progenitors of adult origin, supporting the generation of fetal multipotent colony-forming unit (CFU)-Mix and CFU-GM colonies [25].

Associations of IL9 with chemical compounds

  • However, tyrosine kinases activated by IL-9 have not been identified [2].
  • To investigate whether this cytokine has a direct activity on the development of eos and eosinophilic inflammation, a model of thioglycolate-induced peritoneal inflammation was used in IL-9 transgenic (TG5) and background strain (FVB) mice [23].
  • The colony-forming ability of HL60, K562, and KG1 cells and fresh AML cell populations upon IL-9 stimulation was assessed by a clonogenic assay in methylcellulose, whereas the cell-cycle characteristics of leukemic samples were determined by the acridine-orange flow cytometric technique and the bromodeoxyuridine (BRDU) incorporation assay [20].
  • The induction of IL-9 was allergen specific, reflecting donor RAST profile [3].
  • Oxidative burst in lipopolysaccharide-activated human alveolar macrophages is inhibited by interleukin-9 [26].

Physical interactions of IL9

  • Sharing of IL-9R/IL-2R components was furthermore suggested by inhibition of 125I-IL-2 binding to primary AML cells with excess of unlabeled IL-9 [27].
  • Analysis of mixing experiments and of the morphology of the BFU-E in culture indicated that IL-9 interacts preferentially with a relatively early population of IL-3-responsive BFU-E [28].

Enzymatic interactions of IL9

  • However, costimulation with SLF plus IL-9 in MO7e cells resulted in the nuclear translocation of serine-hyperphosphorylated Stat3 [29].

Regulatory relationships of IL9

  • The kinetic studies indicate that tyrosine phosphorylation and activation of JAK kinases induced by IL-9 occurred within 1 minute, peaked by 5 to 10 minutes, and persisted at least for 45 minutes [2].
  • The effect of these three proteins on IL-9 signal transduction was assessed by transient transfection in HEK-293 cells expressing the components of the IL-9 signalling pathway and a STAT-responsive reporter construct [30].
  • In summary, the data showed that IL-9 can rescue only a small subset of Th2 cells from apoptosis induced by growth factor withdrawal and that expression of IL-9R alpha is required for the antiapoptotic signals mediated by this cytokine [31].
  • Therefore, the responsiveness of human Th1 and Th2 cell clones to IL-9 was measured by examining the ability of this cytokine to prevent apoptosis induced by IL-2 deprivation [31].
  • IL-9 also up-regulated the IL-5R-alpha chain cell surface expression during terminal eosinophil differentiation of the HL-60 cell line [1].

Other interactions of IL9

  • Tyrosine phosphorylation and activation of JAK family tyrosine kinases by interleukin-9 in MO7E cells [2].
  • Furthermore, we show that signal transducers and activators of transcription (Stat) 91 or related protein and an 88-kD Stat 91-associated protein are rapidly tyrosine phosphorylated following IL-9 treatment [2].
  • Also at lower grades of rejection, mRNA for IL-6 and IL-9 was present [32].
  • In Der p-triggered reactions of non-atopic and atopic subjects, IL-9 showed the highest selectivity for atopics, IL-5 and IL-13 being produced more frequently in non-atopic donors [3].
  • Analysis of IL-9R alpha subunit expression on 18 T cell clones revealed that IL-9 responsiveness was directly proportional to the expression of the high-affinity receptor [31].

Analytical, diagnostic and therapeutic context of IL9

  • METHODS: Peripheral blood mononuclear cell (PBMC) from control adults and from atopic patients were cultured with various allergens or phytohaemagglutinin (PHA) and secreted IL-5, IL-9 and IL-13 were measured by ELISA [3].
  • The inhibitory effect of IL-9 was abolished by anti-hIL-9R alpha monoclonal antibody, and presence of IL-9 receptors on AM was demonstrated by immunofluorescence [26].
  • Furthermore, in this study, reverse transcriptase-polymerase chain reaction amplification (RT-PCR) did not show the constitutive expression of IL-9 mRNA in the cell lines and the AML samples studied at diagnosis [4].
  • The receptor for human interleukin-9 (hIL-9) might be a target for selective immunotherapy [33].
  • Under these experimental conditions, the slight but significant (p < 0.01, Student's t test) production of IgG (50 ng/mL) was also potentiated when the cell cultures were performed in the presence of 300 U/mL of IL-9/P40 [34].


  1. Interleukin-9 enhances interleukin-5 receptor expression, differentiation, and survival of human eosinophils. Gounni, A.S., Gregory, B., Nutku, E., Aris, F., Latifa, K., Minshall, E., North, J., Tavernier, J., Levit, R., Nicolaides, N., Robinson, D., Hamid, Q. Blood (2000) [Pubmed]
  2. Tyrosine phosphorylation and activation of JAK family tyrosine kinases by interleukin-9 in MO7E cells. Yin, T., Yang, L., Yang, Y.C. Blood (1995) [Pubmed]
  3. Allergen-induced interleukin-9 production in vitro: correlation with atopy in human adults and comparison with interleukin-5 and interleukin-13. Devos, S., Cormont, F., Vrtala, S., Hooghe-Peters, E., Pirson, F., Snick, J. Clin. Exp. Allergy (2006) [Pubmed]
  4. Interleukin-9 in human myeloid leukemia cells. Lemoli, R.M., Fortuna, A., Tafuri, A., Grande, A., Amabile, M., Martinelli, G., Ferrari, S., Tura, S. Leuk. Lymphoma (1997) [Pubmed]
  5. Increased expression of interleukin-9, interleukin-9 receptor, and the calcium-activated chloride channel hCLCA1 in the upper airways of patients with cystic fibrosis. Hauber, H.P., Manoukian, J.J., Nguyen, L.H., Sobol, S.E., Levitt, R.C., Holroyd, K.J., McElvaney, N.G., Griffin, S., Hamid, Q. Laryngoscope (2003) [Pubmed]
  6. IL-9-induced expansion of B-1b cells restores numbers but not function of B-1 lymphocytes in xid mice. Knoops, L., Louahed, J., Renauld, J.C. J. Immunol. (2004) [Pubmed]
  7. Non-averaged human brain potentials in somatic attention: the short-latency cognition-related P40 component. Tomberg, C., Desmedt, J.E. J. Physiol. (Lond.) (1996) [Pubmed]
  8. Quantitative morphology and postsynaptic targets of thalamocortical axons in critical period and adult ferret visual cortex. Erisir, A., Dreusicke, M. J. Comp. Neurol. (2005) [Pubmed]
  9. Neonatal neurosteroid administration results in development-specific alterations in prepulse inhibition and locomotor activity: neurosteroids alter prepulse inhibition and locomotor activity. Gizerian, S.S., Moy, S.S., Lieberman, J.A., Grobin, A.C. Psychopharmacology (Berl.) (2006) [Pubmed]
  10. Evoked potentials in patients with Huntington's disease and their offspring. I. Somatosensory evoked potentials. Noth, J., Engel, L., Friedemann, H.H., Lange, H.W. Electroencephalography and clinical neurophysiology. (1984) [Pubmed]
  11. Functional activation of Jak1 and Jak3 by selective association with IL-2 receptor subunits. Miyazaki, T., Kawahara, A., Fujii, H., Nakagawa, Y., Minami, Y., Liu, Z.J., Oishi, I., Silvennoinen, O., Witthuhn, B.A., Ihle, J.N. Science (1994) [Pubmed]
  12. Antifibrillarin autoantibodies present in systemic sclerosis and other connective tissue diseases interact with similar epitopes. Kasturi, K.N., Hatakeyama, A., Spiera, H., Bona, C.A. J. Exp. Med. (1995) [Pubmed]
  13. c-kit ligand: a unique potentiator of mediator release by human lung mast cells. Bischoff, S.C., Dahinden, C.A. J. Exp. Med. (1992) [Pubmed]
  14. 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]
  15. CITED2-mediated regulation of MMP-1 and MMP-13 in human chondrocytes under flow shear. Yokota, H., Goldring, M.B., Sun, H.B. J. Biol. Chem. (2003) [Pubmed]
  16. IL-9 induces chemokine expression in lung epithelial cells and baseline airway eosinophilia in transgenic mice. Dong, Q., Louahed, J., Vink, A., Sullivan, C.D., Messler, C.J., Zhou, Y., Haczku, A., Huaux, F., Arras, M., Holroyd, K.J., Renauld, J.C., Levitt, R.C., Nicolaides, N.C. Eur. J. Immunol. (1999) [Pubmed]
  17. Deleterious effects of IL-9-activated mast cells and neuroprotection by antihistamine drugs in the developing mouse brain. Patkai, J., Mesples, B., Dommergues, M.A., Fromont, G., Thornton, E.M., Renauld, J.C., Evrard, P., Gressens, P. Pediatr. Res. (2001) [Pubmed]
  18. Patient-controlled antiemesis: a randomized, double-blind comparison of two doses of propofol versus placebo. Gan, T.J., El-Molem, H., Ray, J., Glass, P.S. Anesthesiology (1999) [Pubmed]
  19. Expression cloning of the murine and human interleukin 9 receptor cDNAs. Renauld, J.C., Druez, C., Kermouni, A., Houssiau, F., Uyttenhove, C., Van Roost, E., Van Snick, J. Proc. Natl. Acad. Sci. U.S.A. (1992) [Pubmed]
  20. Interleukin-9 stimulates the proliferation of human myeloid leukemic cells. Lemoli, R.M., Fortuna, A., Tafuri, A., Fogli, M., Amabile, M., Grande, A., Ricciardi, M.R., Petrucci, M.T., Bonsi, L., Bagnara, G., Visani, G., Martinelli, G., Ferrari, S., Tura, S. Blood (1996) [Pubmed]
  21. Human interleukin-9: genomic sequence, chromosomal location, and sequences essential for its expression in human T-cell leukemia virus (HTLV)-I-transformed human T cells. Kelleher, K., Bean, K., Clark, S.C., Leung, W.Y., Yang-Feng, T.L., Chen, J.W., Lin, P.F., Luo, W., Yang, Y.C. Blood (1991) [Pubmed]
  22. Molecular analysis of human interleukin-9 receptor transcripts in peripheral blood mononuclear cells. Identification of a splice variant encoding for a nonfunctional cell surface receptor. Grasso, L., Huang, M., Sullivan, C.D., Messler, C.J., Kiser, M.B., Dragwa, C.R., Holroyd, K.J., Renauld, J.C., Levitt, R.C., Nicolaides, N.C. J. Biol. Chem. (1998) [Pubmed]
  23. Interleukin 9 promotes influx and local maturation of eosinophils. Louahed, J., Zhou, Y., Maloy, W.L., Rani, P.U., Weiss, C., Tomer, Y., Vink, A., Renauld, J., Van Snick, J., Nicolaides, N.C., Levitt, R.C., Haczku, A. Blood (2001) [Pubmed]
  24. Activation of interleukin-13 expression in T cells from HTLV-1-infected individuals and in chronically infected cell lines. Chung, H.K., Young, H.A., Goon, P.K., Heidecker, G., Princler, G.L., Shimozato, O., Taylor, G.P., Bangham, C.R., Derse, D. Blood (2003) [Pubmed]
  25. Effect of interleukin-9 on clonogenic maturation and cell-cycle status of fetal and adult hematopoietic progenitors. Holbrook, S.T., Ohls, R.K., Schibler, K.R., Yang, Y.C., Christensen, R.D. Blood (1991) [Pubmed]
  26. Oxidative burst in lipopolysaccharide-activated human alveolar macrophages is inhibited by interleukin-9. Pilette, C., Ouadrhiri, Y., Van Snick, J., Renauld, J.C., Staquet, P., Vaerman, J.P., Sibille, Y. Eur. Respir. J. (2002) [Pubmed]
  27. Transcript synthesis and surface expression of the interleukin-2 receptor (alpha-, beta-, and gamma-chain) by normal and malignant myeloid cells. Schumann, R.R., Nakarai, T., Gruss, H.J., Brach, M.A., von Arnim, U., Kirschning, C., Karawajew, L., Ludwig, W.D., Renauld, J.C., Ritz, J., Herrmann, F. Blood (1996) [Pubmed]
  28. Human P40 T-cell growth factor (interleukin-9) supports erythroid colony formation. Donahue, R.E., Yang, Y.C., Clark, S.C. Blood (1990) [Pubmed]
  29. Steel factor induces serine phosphorylation of Stat3 in human growth factor-dependent myeloid cell lines. Gotoh, A., Takahira, H., Mantel, C., Litz-Jackson, S., Boswell, H.S., Broxmeyer, H.E. Blood (1996) [Pubmed]
  30. Interleukin 9 induces expression of three cytokine signal inhibitors: cytokine-inducible SH2-containing protein, suppressor of cytokine signalling (SOCS)-2 and SOCS-3, but only SOCS-3 overexpression suppresses interleukin 9 signalling. Lejeune, D., Demoulin, J.B., Renauld, J.C. Biochem. J. (2001) [Pubmed]
  31. Rescue of human T cells by interleukin-9 (IL-9) from IL-2 deprivation-induced apoptosis: correlation with alpha subunit expression of the IL-9 receptor. Perdow-Hickman, S., Salgame, P. J. Interferon Cytokine Res. (2000) [Pubmed]
  32. In situ expression of cytokines in human heart allografts. Van Hoffen, E., Van Wichen, D., Stuij, I., De Jonge, N., Klöpping, C., Lahpor, J., Van Den Tweel, J., Gmelig-Meyling, F., De Weger, R. Am. J. Pathol. (1996) [Pubmed]
  33. A deletion mutant of Pseudomonas exotoxin-A fused to recombinant human interleukin-9 (rhIL-9-ETA') shows specific cytotoxicity against IL-9-receptor-expressing cell lines. Klimka, A., Barth, S., Drillich, S., Wels, W., van Snick, J., Renauld, J.C., Tesch, H., Bohlen, H., Diehl, V., Engert, A. Cytokines and molecular therapy. (1996) [Pubmed]
  34. Functional interaction between interleukin-9/P40 and interleukin-4 in the induction of IgE production by normal human B lymphocytes. Dugas, B., Van Snick, J., Renauld, J.C., Braquet, P., Mencia-Huerta, J.M. Biotechnology therapeutics. (1993) [Pubmed]
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