IFN-γ and TNF-α are involved in urushiol-induced contact hypersensitivity in mice

Immunology and Cell Biology

Volumn 83, Issue 1, 2005, Pages 18-24

  Wakabayashi, Toshiteru ^a   Hu, Dong Liang ^a   Tagawa, Yoh Ichi ^b   Sekikawa, Kenji ^c   Iwakura, Yoichiro ^d   Hanada, Katsumi ^a   Nakane, Akio ^a  

^a HIROSAKI UNIVERSITY   (Japan)

^b SHINSHU UNIVERSITY SCHOOL OF MEDICINE   (Japan)

^c NATIONAL INSTITUTE OF AGROBIOLOGICAL SCIENCES   (Japan)

^d UNIVERSITY OF TOKYO   (Japan)

Author keywords

Contact hypersensitivity; IFN ; IFN inducible protein 10; TNF ; Urushiol

Indexed keywords

CD4 ANTIGEN; CD8 ANTIGEN; CHEMOKINE; CYTOKINE; GAMMA INTERFERON; GAMMA INTERFERON INDUCIBLE PROTEIN 10; MESSENGER RNA; TUMOR NECROSIS FACTOR ALPHA; URUSHIOL;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ANTIGEN SPECIFICITY; ARTICLE; CONTACT ALLERGY; CONTACT SENSITIZATION; CONTROLLED STUDY; CYTOKINE RELEASE; EAR; EDEMA; FEMALE; GENE EXPRESSION; INFLAMMATORY CELL; KNOCKOUT MOUSE; MALE; MOUSE; NONHUMAN; PROVOCATION TEST; SKIN DEFECT; T LYMPHOCYTE;

ANIMALS; CATECHOLS; CD4-POSITIVE T-LYMPHOCYTES; CD8-POSITIVE T-LYMPHOCYTES; CHEMOKINES, CXC; DERMATITIS, CONTACT; FEMALE; INTERFERON TYPE II; MALE; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; RNA, MESSENGER; TUMOR NECROSIS FACTOR-ALPHA;

ANIMALIA;

EID: 13144266710     PISSN: 08189641     EISSN: None     Source Type: Journal    
DOI: 10.1111/j.1440-1711.2005.01310.x     Document Type: Article

References (36)

1. Friedmann PS. Contact hypersensitivity. Curr. Opin. Immunol. 1989; 1: 690-3.
2. Cavani A, Albanesi C, Traidl C, Sebastiani S, Girolomoni G, Effector and regulatory T cells in allergic contact dermatitis. Trends Immunol. 2001; 22: 118-20.
3. Wang B, Feliciani C, Freed I, Cai Q, Sauder DN. Insights into molecular mechanisms of contact hypersensitivity gained from gene knockout studies. J. Leukoc. Biol 2001; 70: 185-91.
4. Kehren J, Desvignes C, Krasteva M et al. Cytotoxicity is mandatory for CD8(+) T cell-mediated contact hypersensitivity. J. Exp. Med. 1999; 189: 779-86.
5. + T cells are the dominant effector cells in trinitrophenyl- specific contact hypersensitivity. J. Invest. Dermatol. 2000; 115: 260-6.
6. + cells secreting TH1 or TH2 cytokines. Immunity 1995; 2: 271-9.
7. Abbas AK, Murphy KM, Sher A. Functional diversity of helper T lymphocytes. Nature 1996; 383: 789-93.
8. Lu B, Ebensperger C, Dembic Z et al. Targeted disruption of the interferon-γ receptor 2 gene results in severe immune defects in mice. Proc. Natl. Acad. Sci. USA 1998; 95: 8233-8.
9. Reeve VE, Bosnic M, Nishimura N. Interferon-γ is involved in photoimmunoprotection by UVA (320-400 nm) radiation in mice. J. Invest. Dermatol. 1999; 112: 945-50.
10. Piguet PF, Grau GE, Hauser C, Vassalli P. Tumor necrosis factor is a critical mediator in hapten induced irritant and contact hypersensitivity reactions. J. Exp. Med. 1991; 173: 673-9.
11. Biedermann T, Kneilling M, Mailhammer R et al. Mast cells control neutrophil recruitment during T cell-mediated delayed-type hypersensitivity reactions through tumor necrosis factor and macrophage inflammatory protein 2. J. Exp. Med. 2000; 192: 1441-52.
12. Kigman AM. Poison ivy (Rhus) dermatitis. Arch. Dermatol. 1958; 77: 149-80.
13. Symes WF, Dawson CR. Poison ivy 'urushio'. J. Am. Chem. Soc. 1975; 76: 2959-63.
14. Billets SJ, Craig JC, Corbett MD, Vickery JF. Component analysis of the urushiol content of poison ivy and poison oak. Phytochemistry 1976; 15: 533-5.
15. Kalish RS, Wood JA, LaPorte A. Processing of urushiol (poison ivy) hapten by both endogenous and exogenous pathways for presentation to T cells in vitro. J. Clin. Invest. 1994; 93: 2039-47.
16. + T cells. Int. Arch. Allergy Immunol. 1998; 117: 194-201.
17. Taniguchi T, Takata M, Ikeda A, Momotani E, Sekikawa K. Failure of germinal center formation and impairment of response to endotoxin in tumor necrosis factor alpha-deficient mice. Lab. Invest. 1997; 77: 647-58.
18. -/- mice: role for IFN-γ in activating apoptosis of hepatocytes. J. Immunol. 1997; 159: 1418-28.
19. Nakane A, Yamada K, Hasegawa S et al. Endogenous cytokines during a lethal infection with Listeria monocytogenes in mice. FEMS Microbiol. Lett. 1999; 175: 133-42.
20. + cell-depleted mice. Infect. Immun. 1991; 59: 3439-45.
21. Ishida Y, Kondo T, Ohshima T, Fujiwara H, Iwakura Y, Mukaida N. A pivotal involvement of IFN-γ in the pathogenesis of acetaminophen-induced acute liver injury. FASEB J. 2002; 16: 1227-36.
22. Nakae S, Komiyama Y, Narumi S et al. IL-1-induced tumor necrosis factor-α elicits inflammatory cell infiltration in the skin by inducing IFN-γ-inducible protein 10 in the elicitation phase of the contact hypersensitivity response. Int. Immunol. 2003; 15: 251-60.
23. Ikeda Y, Yasuno H, Sato A, Kawai K. Oral and epicutaneous desensitization in urushiol contact dermatitis in guinea pigs sensitized by 2 methods of different sensitizing potency. Contact Dermatitis 1998; 39: 286-92.
24. + urushiol (poison ivy)-reactive T lymphocytes. J. Invest. Dermatol. 1997; 108: 253-7.
25. McMillan EM, Stoneking L, Burdick S, Cowan I, Husain-Hamzavi SL. Immunophenotype of lymphoid cells in positive patch tests of allergic contact dermatitis. J. Invest. Dermatol. 1985; 84: 229-33.
26. Boehm U, Klamp T, Groot M, Howard JC. Cellular responses to interferon-γ. Annu. Rev. Immunol. 1997; 15: 749-95.
27. Goebeler M, Meinardus-Hager G, Roth J, Goerdt S, Sorg C. Nickel chloride and cobalt chloride, two common contact sensitizers, directly induce expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and endothelial leukocyte adhesion molecule (ELAM-1) by endothelial cells. J. Invest. Dermatol. 1993; 100: 759-65.
28. McHale JF, Harari OA, Marshall D, Haskard DO. Vascular endothelial cell expression of ICAM-1 and VCAM-1 at the onset of eliciting contact hypersensitivity in mice: evidence for a dominant role of TNF-α. J. Immunol. 1999; 162: 1648-55.
29. Matsuda H, Ushio H, Geba GP, Askenase PW. Human platelets can initiate T cell-dependent contact sensitivity through local serotonin release mediated by IgE antibodies. J. Immunol. 1997; 158: 2891-7.
30. Okazaki F, Kanzaki H, Fujii K et al. Initial recruitment of interferon-γ-producing CD8+ effector cells, followed by infiltration of CD4+ cells in 2,4,6-trinitro-1-chlorobenzene (TNCB)-induced murine contact hypersensitivity reactions. J. Dermatol. 2002; 29: 699-708.
31. Wang B, Fujisawa H, Zhuang L et al. CD4+ Th1 and CD8+ type 1 cytotoxic T cells both play a crucial role in the full development of contact hypersensitivity. J. Immunol. 2000; 165: 6783-90.
32. Abe M, Kondo T, Xu H, Fairchild RL. Interferon-γ inducible protein (IP-10) expression is mediated by CD8+ T cells and is regulated by CD4+ T cells during the elicitation of contact hypersensitivity. J. Invest. Dermatol. 1996; 107: 360-6.
33. Boorsma DM, de Haan P, Willemze R, Stoof TJ. Human growth factor (huGRO), interleukin-8 (IL-8) and interferon-γ-inducible protein (γ-IP-10) gene expression in cultured normal human keratinocytes. Arch. Dermatol. Res. 1994; 286: 471-5.
34. Wong P, Pamer EG. CD8 T cell responses to infectious pathogens. Annu. Rev. Immunol. 2003; 21: 29-70.
35. Ardavin C. Origin, precursors and differentiation of mouse dendritic cells. Nat. Rev. Immunol. 2003; 3: 582-90.
36. Powell SM, Barrett DK. An outbreak of contact dermatitis from Rhus verniciflua (Toxicodendron vernicifluum). Contact Dermatitis 1986; 14: 288-9.