Th1 and Th17 cells: Adversaries and collaborators

Annals of the New York Academy of Sciences

Volumn 1183, Issue , 2010, Pages 211-221

  Damsker, Jesse M ^a   Hansen, Anna M ^a   Caspi, Rachel R ^a  

^a NATIONAL EYE INSTITUTE   (United States)

Author keywords

Autoimmune disease; Inflammation; Th1; Th17

Indexed keywords

CXCL1 CHEMOKINE; CXCL11 CHEMOKINE; CXCL2 CHEMOKINE; CXCL9 CHEMOKINE; EPITHELIAL DERIVED NEUTROPHIL ACTIVATING FACTOR 78; GAMMA INTERFERON; GAMMA INTERFERON INDUCIBLE PROTEIN 10; INTERLEUKIN 12P35; INTERLEUKIN 12P40; INTERLEUKIN 17; INTERLEUKIN 17F; INTERLEUKIN 21; INTERLEUKIN 22; INTERLEUKIN 4; INTERLEUKIN 6; TUMOR NECROSIS FACTOR ALPHA;

AUTOIMMUNE DISEASE; CD4+ T LYMPHOCYTE; EFFECTOR CELL; NONHUMAN; PATHOGENESIS; REVIEW; TH1 CELL; TH17 CELL;

MUS;

EID: 75749097320     PISSN: 00778923     EISSN: 17496632     Source Type: Book Series    
DOI: 10.1111/j.1749-6632.2009.05133.x     Document Type: Review

References (87)

1. Mosmann, T.R. & R.L. Coffman. 1989. TH1 and TH2 cells: different patterns of lymphokine secretion lead to different functional properties. Annu. Rev. Immunol. 7: 145-173.
2. Ferber, I.A. et al. 1996. Mice with a disrupted IFNgamma gene are susceptible to the induction of experimental autoimmune encephalomyelitis (EAE). J. Immunol. 156: 5-7.
3. Jones, L.S. et al. 1997. IFN-gamma-deficient mice develop experimental autoimmune uveitis in the context of a deviant effector response. J. Immunol. 158: 5997-6005.
4. Matthys, P. et al. 1998. Anti-IL-12 antibody prevents the development and progression of collagen-induced arthritis in IFN-gamma receptor-deficient mice. Eur. J. Immunol. 28: 2143-2151.
5. Luger, D. et al. 2008. Either a Th17 or a Th1 effector response can drive autoimmunity: conditions of disease induction affect dominant effector category. J. Exp.Med. 205: 799-810.
6. Haak, S. et al. 2009. IL-17A and IL-17F do not contribute vitally to autoimmune neuro-inflammation in mice. J. Clin. Invest. 119: 61-69.
7. Saoudi, A. et al. 1993. TH2 activated cells prevent experimental autoimmune uveoretinitis, a TH1-dependent autoimmune disease. Eur. J. Immunol. 23: 3096-3103.
8. Cua, D.J., D.R. Hinton & S.A. Stohlman. 1995. Selfantigen-induced Th2 responses in experimental allergic encephalomyelitis (EAE)-resistant mice. Th2-mediated suppression of autoimmune disease. J. Immunol. 155: 4052-4059.
9. Merrill, J.E. et al. 1992. Inflammatory leukocytes and cytokines in the peptide-induced disease of experimental allergic encephalomyelitis in SJL and B10.PL mice. Proc. Natl. Acad. Sci. USA 89: 574-578.
10. Renno, T. et al. 1995. TNF-alpha expression by resident microglia and infiltrating leukocytes in the central nervous system of mice with experimental allergic encephalomyelitis. Regulation by Th1 cytokines. J. Immunol. 154: 944-953.
11. Pettinelli, C.B. & D.E.McFarlin. 1981. Adoptive transfer of experimental allergic encephalomyelitis in SJL/J mice after in vitro activation of lymph node cells by myelin basic protein: requirement for Lyt 1+ 2-T lymphocytes. J. Immunol. 127: 1420-1423.
12. Panitch, H.S. 1992. Interferons in multiple sclerosis. A review of the evidence. Drugs 44: 946-962.
13. Chitnis, T. et al. 2001. Effect of targeted disruption of STAT4 and STAT6 on the induction of experimental autoimmune encephalomyelitis. J. Clin. Invest. 108: 739-747.
14. Becher, B., B.G. Durell & R.J. Noelle. 2002. Experimental autoimmune encephalitis and inflammation in the absence of interleukin-12. J. Clin. Invest. 110: 493-497.
15. Cua, D.J. et al. 2003. Interleukin-23 rather than interleukin-12 is the critical cytokine for autoimmune inflammation of the brain. Nature 421: 744-748.
16. Langrish, C.L. et al. 2005. IL-23 drives a pathogenic T cell population that induces autoimmune inflammation. J. Exp. Med. 201: 233-240.
17. Caspi, R.R. et al. 1996. Genetic susceptibility to experimental autoimmune uveoretinitis in the rat is associated with an elevated Th1 response. J. Immunol. 157: 2668-2675.
18. Tarrant, T.K. et al. 1998. Endogenous IL-12 is required for induction and expression of experimental autoimmune uveitis. J. Immunol. 161: 122-127.
19. Germann, T., H. Hess, J. Szeliga & E. Rude. 1996. Characterization of the adjuvant effect of IL-12 and efficacy of IL-12 inhibitors in type II collagen-induced arthritis. Ann. N. Y. Acad. Sci. 795: 227-240.
20. Billiau, A. et al. 1988. Enhancement of experimental allergic encephalomyelitis in mice by antibodies against IFN-gamma. J. Immunol. 140: 1506-1510.
21. Caspi, R.R. et al. 1994. Endogenous systemic IFNgamma has a protective role against ocular autoimmunity in mice. J. Immunol. 152: 890-899.
22. Gran, B. et al. 2002. IL-12p35-deficient mice are susceptible to experimental autoimmune encephalomyelitis: evidence for redundancy in the IL-12 system in the induction of central nervous system autoimmune demyelination. J. Immunol. 169: 7104-7110.
23. Gutcher, I. et al. 2006. Interleukin 18-independent engagement of interleukin 18 receptor-alpha is required for autoimmune inflammation. Nat. Immunol. 7: 946-953.
24. Moseley, T.A.,D.R.Haudenschild, L. Rose&A.H. Reddi. 2003. Interleukin-17 family and IL-17 receptors. Cytokine Growth Factor Rev. 14: 155-174.
25. Kolls, J.K. & A. Linden. 2004. Interleukin-17 family members and inflammation. Immunity 21: 467-476.
26. Veldhoen,M., R.J.Hocking, R.A. Flavell & B. Stockinger. 2006. Signals mediated by transforming growth factorbeta initiate autoimmune encephalomyelitis, but chronic inflammation is needed to sustain disease. Nat. Immunol. 7: 1151-1156.
27. Sutton,C. et al. 2006. A crucial role for interleukin (IL)-1 in the induction of IL-17-producing T cells thatmediate autoimmune encephalomyelitis. J. Exp.Med. 203: 1685-1691.
28. Kotake, S. et al. 1999. IL-17 in synovial fluids from patients with rheumatoid arthritis is a potent stimulator of osteoclastogenesis. J. Clin. Invest. 103: 1345-1352.
29. Nurieva, R. et al. 2007. Essential autocrine regulation by IL-21 in the generation of inflammatory T cells. Nature 448: 480-483.
30. Liang, S.C. et al. 2006. Interleukin (IL)-22 and IL-17 are coexpressed by Th17 cells and cooperatively enhance expression of antimicrobial peptides. J. Exp. Med. 203: 2271-2279.
31. Chung, Y. et al. 2006. Expression and regulation of IL-22 in the IL-17-producing CD4+ T lymphocytes. Cell Res. 16: 902-907.
32. Aujla, S.J. et al. 2008. IL-22 mediates mucosal host defense against Gram-negative bacterial pneumonia. Nat. Med. 14: 275-281.
33. Zheng, Y. et al. 2008. Interleukin-22 mediates early host defense against attaching and effacing bacterial pathogens. Nat. Med. 14: 282-289.
34. Aggarwal, S. et al. 2003. Interleukin-23 promotes a distinct CD4 T cell activation state characterized by the production of interleukin-17. J. Biol. Chem. 278: 1910-1914.
35. Oppmann, B. et al. 2000. Novel p19 protein engages IL-12p40 to forma cytokine, IL-23,with biological activities similar as well as distinct from IL-12. Immunity 13: 715-725.
36. Bettelli, E. et al. 2006. Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells. Nature 441: 235-238.
37. Mangan, P.R. et al. 2006. Transforming growth factorbeta induces development of the T(H)17 lineage. Nature 441: 231-234.
38. Korn, T. et al. 2008. IL-6 controls Th17 immunity in vivo by inhibiting the conversion of conventional T cells into Foxp3+ regulatory T cells. Proc.Natl. Acad. Sci.USA 105: 18460-18465.
39. Liu, R. et al. 2008. IL-21 receptor expression determines the temporal phases of experimental autoimmune encephalomyelitis. Exp. Neurol. 211: 14-24.
40. Piao, W.H. et al. 2008. IL-21 modulates CD4+ CD25+ regulatory T-cell homeostasis in experimental autoimmune encephalomyelitis. Scand. J. Immunol. 67: 37-46.
41. Harrington, L.E. et al. 2005. Interleukin 17-producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages. Nat. Immunol. 6: 1123-1132.
42. Ivanov, I.I. et al. 2006. The orphan nuclear receptor RORgammat directs the differentiation program of proinflammatory IL-17+ T helper cells. Cell 126: 1121-1133.
43. Yang, X.O. et al. 2007. STAT3 regulates cytokinemediated generation of inflammatory helper T cells. J. Biol. Chem. 282: 9358-9363.
44. Bauquet, A.T. et al. 2009. The costimulatory molecule ICOS regulates the expression of c-Maf and IL-21 in the development of follicular T helper cells and TH-17 cells. Nat. Immunol. 10: 167-175.
45. Lock,C. et al. 2002. Gene-microarray analysis ofmultiple sclerosis lesions yields new targets validated in autoimmune encephalomyelitis. Nat. Med. 8: 500-508.
46. Matusevicius, D. et al. 1999. Interleukin-17 mRNA expression in blood and CSF mononuclear cells is augmented in multiple sclerosis. Mult. Scler. 5: 101-104.
47. Teunissen, M.B. et al. 1998. Interleukin-17 and interferon-gamma synergize in the enhancement of proinflammatory cytokine production by human keratinocytes. J. Invest. Dermatol. 111: 645-649.
48. Aarvak, T., M. Chabaud, P. Miossec & J.B. Natvig. 1999. IL-17 is produced by some proinflammatory Th1/Th0 cells but not by Th2 cells. J. Immunol. 162: 1246-1251.
49. Amadi-Obi, A. et al. 2007. TH17 cells contribute to uveitis and scleritis and are expanded by IL-2 and inhibited by IL-27/STAT1. Nat. Med. 13: 711-718.
50. Chi, W. et al. 2008. Upregulated IL-23 and IL-17 in Behcet patients with active uveitis. Invest. Ophthalmol. Vis. Sci. 49: 3058-3064.
51. Nakae, S., A. Nambu, K. Sudo & Y. Iwakura. 2003. Suppression of immune induction of collagen-induced arthritis in IL-17-deficient mice. J. Immunol. 171: 6173-6177.
52. Hofstetter, H.H. et al. 2005. Therapeutic efficacy of IL-17 neutralization in murine experimental autoimmune encephalomyelitis. Cell. Immunol. 237: 123-130.
53. Murphy, C.A. et al. 2003. Divergent pro-and antiinflammatory roles for IL-23 and IL-12 in joint autoimmune inflammation. J. Exp. Med. 198: 1951-1957.
54. Korn, T. et al. 2007. Myelin-specific regulatory T cells accumulate in the CNS but fail to control autoimmune inflammation. Nat. Med. 13: 423-431.
55. Gocke, A.R. et al. 2007. T-bet regulates the fate of Th1 and Th17 lymphocytes in autoimmunity. J. Immunol. 178: 1341-1348.
56. Bettelli, E. et al. 2004. Loss of T-bet, but not STAT1, prevents the development of experimental autoimmune encephalomyelitis. J. Exp. Med. 200: 79-87.
57. Lovett-Racke, A.E. et al. 2004. Silencing T-bet defines a critical role in the differentiation of autoreactive T lymphocytes. Immunity 21: 719-731.
58. Park, H. et al. 2005. A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17. Nat. Immunol. 6: 1133-1141.
59. Tang, J. et al. 2007. Autoimmune uveitis elicited with antigen-pulsed dendritic cells has a distinct clinical signature and is driven by unique effector mechanisms: initial encounter with autoantigen defines disease phenotype. J. Immunol. 178: 5578-5587.
60. Da Silva, C.A. et al. 2008. TLR-2 and IL-17A in chitininducedmacrophage activation and acute inflammation. J. Immunol. 181: 4279-4286.
61. Boniface, K. et al. 2009. Prostaglandin E2 regulates Th17 cell differentiation and function through cyclic AMP and EP2/EP4 receptor signaling. J. Exp. Med. 206: 535-548.
62. Bafica, A. et al. 2005. TLR9 regulates Th1 responses and cooperates with TLR2 in mediating optimal resistance to Mycobacterium tuberculosis. J. Exp. Med. 202: 1715-1724.
63. Deshpande, P., I.L. King & B.M. Segal. 2007. Cutting edge:CNSCD11c+ cells frommicewith encephalomyelitis polarize Th17 cells and support CD25+CD4+ T cell-mediated immunosuppression, suggesting dual roles in the disease process. J. Immunol. 178: 6695-6699.
64. Happel, K.I. et al. 2003. Cutting edge: roles of Toll-like receptor 4 and IL-23 in IL-17 expression in response to Klebsiella pneumoniae infection. J. Immunol. 170: 4432-4436.
65. Su, S.B. et al. 2007. Altered chemokine profile associated with exacerbated autoimmune pathology under conditions of genetic interferon-gamma deficiency. Invest. Ophthalmol. Vis. Sci. 48: 4616-4625.
66. Kortylewski, M. et al. 2009. Regulation of the IL-23 and IL-12 balance by Stat3 signaling in the tumor microenvironment. Cancer Cell 15: 114-123.
67. Grajewski, R.S. et al. 2008. Activation of invariant NKT cells ameliorates experimental ocular autoimmunity by a mechanism involving innate IFN-gamma production and dampening of the adaptive Th1 and Th17 responses. J. Immunol. 181: 4791-4797.
68. Avichezer, D. et al. 2000. Residues 1-20 of IRBP and whole IRBP elicit different uveitogenic and immunological responses in interferon gamma deficient mice. Exp. Eye Res. 71: 111-118.
69. Kroenke, M.A., T.J. Carlson, A.V. Andjelkovic & B.M. Segal. 2008. IL-12-and IL-23-modulated T cells induce distinct types ofEAEbased onhistology,CNSchemokine profile, and response to cytokine inhibition. J. Exp.Med. 205: 1535-1541.
70. Kelchtermans, H., A. Billiau & P. Matthys. 2008. How interferon-gamma keeps autoimmune diseases in check. Trends Immunol. 29: 479-486.
71. Stromnes, I.M. et al. 2008. Differential regulation of central nervous systemautoimmunity byT(H)1 and T(H)17 cells. Nat. Med. 14: 337-342.
72. Lees, J.R. et al. 2008. Regional CNS responses to IFNgamma determine lesion localization patterns during EAE pathogenesis. J. Exp. Med. 205: 2633-2642.
73. O'Connor, R.A. et al. 2008. Cutting edge: Th1 cells facilitate the entry of Th17 cells to the central nervous system during experimental autoimmune encephalomyelitis. J. Immunol. 181: 3750-3754.
74. Khader, S.A. et al. 2007. IL-23 and IL-17 in the establishment of protective pulmonary CD4+ T cell responses after vaccination and duringMycobacterium tuberculosis challenge. Nat. Immunol. 8: 369-377.
75. Thorley, A.J., P. Goldstraw, A. Young & T.D. Tetley. 2005. Primary human alveolar type II epithelial cellCCL20 (macrophage inflammatory protein-3alpha)-induced dendritic cell migration. Am. J. Respir. CellMol. Biol. 32: 262-267.
76. Hirota, K. et al. 2007. Preferential recruitment of CCR6-expressing Th17 cells to inflamed joints via CCL20 in rheumatoid arthritis and its animal model. J. Exp. Med. 204: 2803-2812.
77. Kutsch, O., J. Oh, A. Nath & E.N. Benveniste. 2000. Induction of the chemokines interleukin-8 and IP-10 by human immunodeficiency virus type 1 tat in astrocytes. J. Virol. 74: 9214-9221.
78. Liu, L. et al. 2006. Severe disease, unaltered leukocyte migration, and reduced IFN-gamma production in CXCR3-/-mice with experimental autoimmune encephalomyelitis. J. Immunol. 176: 4399-4409.
79. Dardalhon, V., T. Korn, V.K. Kuchroo & A.C. Anderson. 2008. Role of Th1 and Th17 cells in organ-specific autoimmunity. J. Autoimmun. 31: 252-256.
80. Shi, G. et al. 2008. Phenotype switching by inflammation-inducing polarized Th17 cells, but not by Th1 cells. J. Immunol. 181: 7205-7213.
81. Yang, X.O. et al. 2008. Molecular antagonism and plasticity of regulatory and inflammatory T cell programs. Immunity 29: 44-56.
82. Bending, D. et al. 2009. Highly purified Th17 cells from BDC2.5NOD mice convert into Th1-like cells in NOD/SCID recipient mice. J. Clin. Invest. 119: 565-572.
83. Lee, Y.K. et al. 2009. Late developmental plasticity in the T helper 17 lineage. Immunity 30: 92-107.
84. Wei, G. et al. 2009. Global mapping of H3K4me3 and H3K27me3 reveals specificity and plasticity in lineage fate determination of differentiating CD4+ T cells. Immunity 30: 155-167.
85. Martin-Orozco, N. et al. 2009. Th17 cells promote pancreatic inflammation but only induce diabetes efficiently in lymphopenic hosts after conversion into Th1 cells. Eur. J. Immunol. 39: 216-224.
86. Muranski, P. et al. 2008. Tumor-specific Th17-polarized cells eradicate large established melanoma. Blood 112: 362-373.
87. Muranski, P. & N.P. Restifo. 2009. Adoptive immunotherapy of cancer using CD4(+)Tcells. Curr.Opin. Immunol. 21: 200-208.