Lymphocyte polarization: Pathophysiological relevance of Th9 and Th17
DOI:
https://doi.org/10.5902/2236583432689Keywords:
T-Lymphocytes, Interleukins, Transcription factors, Regulatory T LymphocytesAbstract
The polarization of TCD4+ cells is one of the most important mechanisms of the immune response. Each of the subtypes or cell patterns are derived from the polarization due to the interaction of TCD4+ naive cells as antigens presented by antigen-presenting cells. The expression of certain transcription factors and the production of specific interleukins constitute the identity of each one of them. In addition to the Th1 and Th2 already described, the role of the Th17 and Th9 polarizations are increasingly present in the initiation of several pathologies and are a promising way to outline possible therapeutic strategies. For the bibliographic review of the descriptive exploratory type, the databases Scielo, PubMed, Lilacs and Bireme.Downloads
References
Yamane H, Paul WE. Early signaling events that underlie fate decisions of naive CD4+ T cells towards distinct T-helper cell subsets. Immunol Rev. 2013;252(1):12-23.
Hoe E, Anderson J, Nathanielsz J, Toh ZQ, Marimla R, Balloch A, Licciardi PV. The contrasting roles of Th17 immunity in human health and disease. Microbiol Immunol. 2017;61(2):49-56. Mini-Review
Maddur MS, Miossec P, Kaveri SV, Bayry J. Th17 cells: biology, pathogenesis of autoimmune and inflammatory diseases, and therapeutic strategies. Am J Pathol. 2012 Jul;181(1):8-18. doi: 10.1016/j.ajpath.2012.03.044.
Chen X, Oppenheim JJ. Th17 cells and Tregs: unlikely allies. Journal of Leukocyte Biology. 2014 2;95(5):723 – 731.
Rojas-Zuleta WG, Sanchez E. IL-9: Function, Sources, and Detection. Methods Mol Biol. 2017;1585:21-35. doi: 10.1007/978-1-4939-6877-0_2.
Goswami R, Jabeen R, Yagi R, Pham D, Zhu J, Goenka S, et al. STAT6-dependent regulation of Th9 development. J Immunol 2012;188(3):968–75.
Dardalhon V, Awasthi A, Kwon H, Galileos G, Gao W, Sobel RA, et al. IL-4 inhibits TGF-beta-induced Foxp3+ T cells and, together with TGF-beta, generates IL-9+ IL-10+ Foxp3(−) effector T cells. Nat Immunol 2008;9(12):1347–55.
Xiao X, Balasubramanian S, Liu W, Chu X,Wang H, Taparowsky EJ, et al. OX40 signaling favors the induction of T(H)9 cells and airway inflammation. Nat Immunol 2012; 13(10):981–90.
A. Jash, A. Sahoo, G.C. Kim, C.S. Chae, J.S. Hwang, J.E. Kim, et al., Nuclear factor of activated T cells 1 (NFAT1)-induced permissive chromatin modification facilitates nuclear factor-kappaB (NF-kappaB)-mediated interleukin-9 (IL-9) transactivation, J. Biol. Chem. 287 (2012) 15445–15457.
R.J. Noelle, E.C. Nowak, Cellular sources and immune functions of interleukin- 9, Nat. Rev. Immunol. 10 (2010) 683–687.
Wiener, Z., A. Falus, & S. Toth. 2004. IL-9 increases the expression of several cytokines in activated mast cells, while the IL-9-induced IL-9 production is inhibited in mast cells of histamine-free transgenic mice. Cytokine 26: 122–130.
Dugas,B., J.C.Renauld, J. Pene, et al. 1993. Interleukin-9 potentiates the interleukin-4-induced immunoglobulin (IgG, IgMand IgE) production by normal human B lymphocytes. Eur. J. Immunol. 23: 1687–1692.
Louahed, J., M. Toda, J. Jen, et al. 2000. Interleukin-9 upregulates mucus expression in the airways [see comments]. Am. J. Respir. Cell. Mol. Biol. 22: 649–656.
Louahed, J. 2001. Interleukin 9 promotes influx and local maturation of eosinophils. Blood 97: 1035–1042.
Korn T, Bettelli E, Oukka M, Kuchroo VK. IL-17 and Th17 Cells. Annu Rev Immunol. 2009;27:485-517. doi: 10.1146/annurev.immunol.021908.132710. Review.
Muranski P, Restifo NP. Essentials of Th17 cell commitment and plasticity. Blood. 2013 Mar 28;121(13):2402-14. doi: 10.1182/blood-2012-09-378653. Epub 2013 Jan 16. Review.
Guéry L, Hugues S. Th17 Cell Plasticity and Functions in Cancer Immunity. BioMed Research International. 2015;2015:1 – 11.
Sakaguchi S., Yamaguchi T., Nomura T., Ono M. (2008) Regulatory T cells and immune tolerance. Cell133, 775–787.
Staudt V, Bothur E, Klein M et al (2010) Interferon-regulatory factor 4 is essential for the developmental program of T helper 9 cells. Immunity 33:192–202. doi:10.1016/j.immuni.2010.07.014
Shimbara, A., P. Christodoulopoulos, A. Soussi-Gounni, et al. 2000. IL-9 and its receptor in allergic and nonallergic lung disease: increased expression in asthma. J. Allergy Clin. Immunol. 105: 108–115.
S.T. Holgate, Innate and adaptive immune responses in asthma, Nat. Med. 18 (2012) 673–683.
Busse, W.W., Holgate, S., Kerwin, E., Chon, Y., Feng, J., Lin, J., Lin, S.L., 2013. Randomized, double-blind, placebo-controlled study of brodalumab, a human anti-IL-17 receptor monoclonal antibody, in moderate to severe asthma. Am. J. Respir. Crit. Care Med. 188, 1294–1302.2013.
Gong F, Pan YH, Huang X, Zhu HY, Jiang DL. From bench to bedside: Therapeutic potential of interleukin-9 in the treatment of asthma. Exp Ther Med. 2017 Feb;13(2):389-394. doi: 10.3892/etm.2017.4024.
Patel D. D., Lee D. M., Kolbinger F., Antoni C. (2013) Effect of IL-17A blockade with secukinumab in autoimmune diseases. Ann. Rheum. Dis. 72 (Suppl. 2), ii116–ii123.
Yuan A, Yang H, Qi H, Cui J, Hua W, Li C, Pang Z, Zheng W, Cui G. IL-9 antibody injection suppresses the inflammation in colitis mice. Biochem Biophys Res Commun. 2015 Dec 25;468(4):921-6. doi: 10.1016/j.bbrc.2015.11.057. Epub 2015 Nov 19.
Neurath MF, Finotto S. IL-9 signaling as key driver of chronic inflammation in mucosal immunity. Cytokine & Growth Factor Reviews. 2016 06;29(8):93 – 99.
Lu Y, Hong S, Li H, Park J, Hong B, Wang L, et al. Th9 cells promote antitumor immune responses in vivo. J Clin Invest 2012;122:4160–71.
Végran F, Apetoh L, Ghiringhelli F. Th9 Cells: A Novel CD4 T-cell Subset in the Immune War against Cancer. Cancer Research. 2016 08;76(19):5628 – 5633.
Vargas TR, Humblin E, Végran F, Ghiringhelli F, Apetoh L. TH9 cells in anti-tumor immunity. Seminars in Immunopathology. 2016 11;39(1):39 – 46.
R. Purwar, C. Schlapbach, S. Xiao, H.S. Kang, W. Elyaman, X. Jiang, et al., Robust tumor immunity to melanoma mediated by interleukin-9-producing T cells, Nat. Med. 18 (2012) 1248–1253.
