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Gene Review

Il17a  -  interleukin 17A

Mus musculus

Synonyms: CTLA-8, Ctla-8, Ctla8, Cytotoxic T-lymphocyte-associated antigen 8, IL-17, ...
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Disease relevance of Il17a


Psychiatry related information on Il17a

  • The effects of alcohol consumption on pulmonary release of IL-17 are unknown [7].
  • CONCLUSIONS: The results of these experiments strongly implicate IL-17 as an important pathway for the immunosuppression associated with alcohol abuse and support gene therapeutic approaches to augment immune function in the alcoholic host or to treat infections associated with alcoholism [7].

High impact information on Il17a

  • Intestinal inflammation was associated with IL-23 (p19) mRNA-producing intestinal dendritic cells and IL-17A mRNA within the intestine [8].
  • TGFbeta in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-producing T cells [9].
  • Treg can be substituted by TGFbeta1, which, together with the proinflammatory cytokine IL-6, supports the differentiation of IL-17-producing T cells, a process that is amplified by IL-1beta and TNFalpha [9].
  • Our data indicate that, in the presence of IL-6, TGFbeta1 subverts Th1 and Th2 differentiation for the generation of IL-17-producing T cells [9].
  • The range of identified effector CD4 T cell lineages has recently expanded with description of an IL-17-producing subset, called Th17, which develops via cytokine signals distinct from, and antagonized by, products of the Th1 and Th2 lineages [10].

Chemical compound and disease context of Il17a


Biological context of Il17a

  • STAT3 and NF-{kappa}B Signal Pathway Is Required for IL-23-Mediated IL-17 Production in Spontaneous Arthritis Animal Model IL-1 Receptor Antagonist-Deficient Mice [12].
  • Phagocytosis of apoptotic neutrophils regulates granulopoiesis via IL-23 and IL-17 [13].
  • Collectively, these data show that severe IL-17-mediated EAM can develop in the absence of T-bet, and that T-bet can regulate autoimmunity via the control of nonspecific CD8+ T cell bystander functions in the inflamed target organ [14].
  • We also show that IL-23 is required for the induction of an IL-17-producing Ag-specific phenotype in naive CD4 T cells in vitro and that absence of IL-12p70 promotes an increase in the number of IL-17-producing Ag-specific CD4 T cells both in vitro and in vivo [15].
  • Neutralization of IL-17 significantly prevented joint swelling at day 1 of flare and significantly suppressed joint inflammation and cartilage proteoglycan depletion at day 4, as assessed by histology [16].

Anatomical context of Il17a

  • IL-23 has proinflammatory activity, inducing IL-17 secretion from activated CD4(+) T cells and stimulating the proliferation of memory CD4(+) T cells [12].
  • We found that the culture supernatant of mouse resident peritoneal exudate cells (PEC) cocultured with FasL-expressing tumor (FFL) cells induced IL-17 production in freshly isolated resident PEC [17].
  • In these analyses, as little as 20 pg of peritoneal IL-17 induced neutrophil infiltration [18].
  • This curbs phagocyte secretion of IL-23, a cytokine controlling IL-17 production by Tn cells [13].
  • In embryonic fibroblasts (EFs) derived from TRAF6 knockout mice, IL-17 failed to activate the IkappaB kinases (IKKs) and JNK [19].

Associations of Il17a with chemical compounds

  • Local IL-17 promoted osteoclastic bone destruction, which was accompanied with marked tartrate-resistant acid phosphatase activity at sites of bone erosion in cortical, subchondral, and trabecular bone [20].
  • Our findings indicate that IL-17 plays an important role in activating T cells in allergen-specific T cell-mediated immune responses [3].
  • Induction of G-CSF expression in 3T3 cells by IL-17 did not appear to require tyrosine kinase activation or de novo protein synthesis [21].
  • Antibody-independent, interleukin-17A-mediated, cross-serotype immunity to pneumococci in mice immunized intranasally with the cell wall polysaccharide [22].
  • A similar pattern was observed for IL-17, supporting a contribution of T cells to the neutrophilic inflammation only at high-dose exposure to LPS [23].
  • The synergy between TNF-alpha and IL-17 reflects their independent actions on KC gene expression; TNF-alpha serves as a stimulus to initiate transcription through activation of NF-kappaB, whereas IL-17 drives mRNA stabilization through an Act1-dependent pathway [24].
  • Airway neutrophilia was abolished by a single treatment with neutralizing monoclonal antibody against IL-17 before alpha-GalCer administration [25].

Physical interactions of Il17a

  • Stability studies revealed that IL-17 stabilized G-CSF mRNA levels, with a t1/2 of 4 h, compared to a t1/2 of less than 2 h in medium or LPS-treated cells [21].

Regulatory relationships of Il17a


Other interactions of Il17a

  • Interestingly, bacillus Calmette-Gu??rin immune T cells generated in the absence of IL-12 or IL-23 were deficient in IFN-gamma production, but exhibited a robust IL-17 secretion associated with a degree of protection against pulmonary infection [29].
  • IL-1beta further increased the production of IL-23, which induced IL-17 production and OX40 expression in splenic CD4(+) T cells of IL-1Ra(-/-) mice [12].
  • Involvement of IL-17 in Fas ligand-induced inflammation [18].
  • Antibodies neutralising interleukin (IL)-1alpha, IL-1beta, soluble IL-6 receptor, IL-17, or tumour necrosis factor-alpha, when added to individual SFs, only occasionally decreased the bone-resorbing activity [30].
  • Messenger RNA levels of IL-17, IL-12, and cathepsin K in the synovial tissue were suppressed, as were IL-6 and IL-12 protein production [31].
  • The results apply to initial generation of the IL-17 phenotype because naive CD62L(high) Daf1(-/-) T cells produce 3-fold more IL-17 in response to TGF-beta and IL-6, whereas CD62L(high) Daf1(-/-)C5aR(-/-)C3aR(-/-) T cells produce 4-fold less [32].

Analytical, diagnostic and therapeutic context of Il17a


  1. IL-17 Receptor Knockout Mice Have Enhanced Myelotoxicity and Impaired Hemopoietic Recovery Following Gamma Irradiation. Tan, W., Huang, W., Zhong, Q., Schwarzenberger, P. J. Immunol. (2006) [Pubmed]
  2. Herpesvirus Saimiri encodes a new cytokine, IL-17, which binds to a novel cytokine receptor. Yao, Z., Fanslow, W.C., Seldin, M.F., Rousseau, A.M., Painter, S.L., Comeau, M.R., Cohen, J.I., Spriggs, M.K. Immunity (1995) [Pubmed]
  3. Antigen-specific T cell sensitization is impaired in IL-17-deficient mice, causing suppression of allergic cellular and humoral responses. Nakae, S., Komiyama, Y., Nambu, A., Sudo, K., Iwase, M., Homma, I., Sekikawa, K., Asano, M., Iwakura, Y. Immunity (2002) [Pubmed]
  4. Interleukin 27 limits autoimmune encephalomyelitis by suppressing the development of interleukin 17-producing T cells. Batten, M., Li, J., Yi, S., Kljavin, N.M., Danilenko, D.M., Lucas, S., Lee, J., de Sauvage, F.J., Ghilardi, N. Nat. Immunol. (2006) [Pubmed]
  5. A crucial role for interleukin (IL)-1 in the induction of IL-17-producing T cells that mediate autoimmune encephalomyelitis. Sutton, C., Brereton, C., Keogh, B., Mills, K.H., Lavelle, E.C. J. Exp. Med. (2006) [Pubmed]
  6. IL-17-mediated regulation of innate and acquired immune response against pulmonary Mycobacterium bovis bacille Calmette-Guerin infection. Umemura, M., Yahagi, A., Hamada, S., Begum, M.D., Watanabe, H., Kawakami, K., Suda, T., Sudo, K., Nakae, S., Iwakura, Y., Matsuzaki, G. J. Immunol. (2007) [Pubmed]
  7. Effect of alcohol consumption on host release of interleukin-17 during pulmonary infection with Klebsiella pneumoniae. Shellito, J.E., quan Zheng, M., Ye, P., Ruan, S., Shean, M.K., Kolls, J. Alcohol. Clin. Exp. Res. (2001) [Pubmed]
  8. Differential activity of IL-12 and IL-23 in mucosal and systemic innate immune pathology. Uhlig, H.H., McKenzie, B.S., Hue, S., Thompson, C., Joyce-Shaikh, B., Stepankova, R., Robinson, N., Buonocore, S., Tlaskalova-Hogenova, H., Cua, D.J., Powrie, F. Immunity (2006) [Pubmed]
  9. TGFbeta in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-producing T cells. Veldhoen, M., Hocking, R.J., Atkins, C.J., Locksley, R.M., Stockinger, B. Immunity (2006) [Pubmed]
  10. Th17: an effector CD4 T cell lineage with regulatory T cell ties. Weaver, C.T., Harrington, L.E., Mangan, P.R., Gavrieli, M., Murphy, K.M. Immunity (2006) [Pubmed]
  11. Resident V{delta}1+ {gamma}{delta} T Cells Control Early Infiltration of Neutrophils after Escherichia coli Infection via IL-17 Production. Shibata, K., Yamada, H., Hara, H., Kishihara, K., Yoshikai, Y. J. Immunol. (2007) [Pubmed]
  12. STAT3 and NF-{kappa}B Signal Pathway Is Required for IL-23-Mediated IL-17 Production in Spontaneous Arthritis Animal Model IL-1 Receptor Antagonist-Deficient Mice. Cho, M.L., Kang, J.W., Moon, Y.M., Nam, H.J., Jhun, J.Y., Heo, S.B., Jin, H.T., Min, S.Y., Ju, J.H., Park, K.S., Cho, Y.G., Yoon, C.H., Park, S.H., Sung, Y.C., Kim, H.Y. J. Immunol. (2006) [Pubmed]
  13. Phagocytosis of apoptotic neutrophils regulates granulopoiesis via IL-23 and IL-17. Stark, M.A., Huo, Y., Burcin, T.L., Morris, M.A., Olson, T.S., Ley, K. Immunity (2005) [Pubmed]
  14. T-bet negatively regulates autoimmune myocarditis by suppressing local production of interleukin 17. Rangachari, M., Mauermann, N., Marty, R.R., Dirnhofer, S., Kurrer, M.O., Komnenovic, V., Penninger, J.M., Eriksson, U. J. Exp. Med. (2006) [Pubmed]
  15. IL-23 compensates for the absence of IL-12p70 and is essential for the IL-17 response during tuberculosis but is dispensable for protection and antigen-specific IFN-gamma responses if IL-12p70 is available. Khader, S.A., Pearl, J.E., Sakamoto, K., Gilmartin, L., Bell, G.K., Jelley-Gibbs, D.M., Ghilardi, N., deSauvage, F., Cooper, A.M. J. Immunol. (2005) [Pubmed]
  16. Blocking of interleukin-17 during reactivation of experimental arthritis prevents joint inflammation and bone erosion by decreasing RANKL and interleukin-1. Koenders, M.I., Lubberts, E., Oppers-Walgreen, B., van den Bersselaar, L., Helsen, M.M., Di Padova, F.E., Boots, A.M., Gram, H., Joosten, L.A., van den Berg, W.B. Am. J. Pathol. (2005) [Pubmed]
  17. Fas ligand induces cell-autonomous IL-23 production in dendritic cells, a mechanism for Fas ligand-induced IL-17 production. Kidoya, H., Umemura, M., Kawabe, T., Matsuzaki, G., Yahagi, A., Imamura, R., Suda, T. J. Immunol. (2005) [Pubmed]
  18. Involvement of IL-17 in Fas ligand-induced inflammation. Umemura, M., Kawabe, T., Shudo, K., Kidoya, H., Fukui, M., Asano, M., Iwakura, Y., Matsuzaki, G., Imamura, R., Suda, T. Int. Immunol. (2004) [Pubmed]
  19. Requirement of tumor necrosis factor receptor-associated factor (TRAF)6 in interleukin 17 signal transduction. Schwandner, R., Yamaguchi, K., Cao, Z. J. Exp. Med. (2000) [Pubmed]
  20. IL-17 promotes bone erosion in murine collagen-induced arthritis through loss of the receptor activator of NF-kappa B ligand/osteoprotegerin balance. Lubberts, E., van den Bersselaar, L., Oppers-Walgreen, B., Schwarzenberger, P., Coenen-de Roo, C.J., Kolls, J.K., Joosten, L.A., van den Berg, W.B. J. Immunol. (2003) [Pubmed]
  21. Regulation of granulocyte colony-stimulating factor gene expression by interleukin-17. Cai, X.Y., Gommoll, C.P., Justice, L., Narula, S.K., Fine, J.S. Immunol. Lett. (1998) [Pubmed]
  22. Antibody-independent, interleukin-17A-mediated, cross-serotype immunity to pneumococci in mice immunized intranasally with the cell wall polysaccharide. Malley, R., Srivastava, A., Lipsitch, M., Thompson, C.M., Watkins, C., Tzianabos, A., Anderson, P.W. Infect. Immun. (2006) [Pubmed]
  23. Dose-dependent activation of lymphocytes in endotoxin-induced airway inflammation. Larsson, R., Rocksén, D., Lilliehöök, B., Jonsson, A., Bucht, A. Infect. Immun. (2000) [Pubmed]
  24. IL-17 enhances chemokine gene expression through mRNA stabilization. Hartupee, J., Liu, C., Novotny, M., Li, X., Hamilton, T. J. Immunol. (2007) [Pubmed]
  25. Identification of an IL-17-producing NK1.1(neg) iNKT cell population involved in airway neutrophilia. Michel, M.L., Keller, A.C., Paget, C., Fujio, M., Trottein, F., Savage, P.B., Wong, C.H., Schneider, E., Dy, M., Leite-de-Moraes, M.C. J. Exp. Med. (2007) [Pubmed]
  26. Effect of interleukin-17 on nitric oxide production and osteoclastic bone resorption: is there dependency on nuclear factor-kappaB and receptor activator of nuclear factor kappaB (RANK)/RANK ligand signaling? Van Bezooijen, R.L., Papapoulos, S.E., Löwik, C.W. Bone (2001) [Pubmed]
  27. IL-17, produced by lymphocytes and neutrophils, is necessary for lipopolysaccharide-induced airway neutrophilia: IL-15 as a possible trigger. Ferretti, S., Bonneau, O., Dubois, G.R., Jones, C.E., Trifilieff, A. J. Immunol. (2003) [Pubmed]
  28. Cutting edge: NKT cells constitutively express IL-23 receptor and RORgammat and rapidly produce IL-17 upon receptor ligation in an IL-6-independent fashion. Rachitskaya, A.V., Hansen, A.M., Horai, R., Li, Z., Villasmil, R., Luger, D., Nussenblatt, R.B., Caspi, R.R. J. Immunol. (2008) [Pubmed]
  29. Interleukin-23 Restores Immunity to Mycobacterium tuberculosis Infection in IL-12p40-Deficient Mice and Is Not Required for the Development of IL-17-Secreting T Cell Responses. Wozniak, T.M., Ryan, A.A., Britton, W.J. J. Immunol. (2006) [Pubmed]
  30. Effects on osteoclast and osteoblast activities in cultured mouse calvarial bones by synovial fluids from patients with a loose joint prosthesis and from osteoarthritis patients. Andersson, M.K., Lundberg, P., Ohlin, A., Perry, M.J., Lie, A., Stark, A., Lerner, U.H. Arthritis Res. Ther. (2007) [Pubmed]
  31. IL-4 gene therapy for collagen arthritis suppresses synovial IL-17 and osteoprotegerin ligand and prevents bone erosion. Lubberts, E., Joosten, L.A., Chabaud, M., van Den Bersselaar, L., Oppers, B., Coenen-De Roo, C.J., Richards, C.D., Miossec, P., van Den Berg, W.B. J. Clin. Invest. (2000) [Pubmed]
  32. IFN-gamma and IL-17 production in experimental autoimmune encephalomyelitis depends on local APC-T cell complement production. Liu, J., Lin, F., Strainic, M.G., An, F., Miller, R.H., Altuntas, C.Z., Heeger, P.S., Tuohy, V.K., Medof, M.E. J. Immunol. (2008) [Pubmed]
  33. Suppression of immune induction of collagen-induced arthritis in IL-17-deficient mice. Nakae, S., Nambu, A., Sudo, K., Iwakura, Y. J. Immunol. (2003) [Pubmed]
  34. CD4+ T cells mediate abscess formation in intra-abdominal sepsis by an IL-17-dependent mechanism. Chung, D.R., Kasper, D.L., Panzo, R.J., Chitnis, T., Grusby, M.J., Sayegh, M.H., Tzianabos, A.O., Chtinis, T. J. Immunol. (2003) [Pubmed]
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