International Immunology, Vol. 13, No. 12, 1471-1478,
December 2001
© 2001 Japanese Society for Immunology
IL-1
, but not IL-1ß, is required for contact-allergen-specific T cell activation during the sensitization phase in contact hypersensitivity
Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan
1 Present address: Institute for Experimental Animals, School of Medicine, Kanazawa University, 13-1 Takaramachi, Kanazawa 920-8640, Japan
Correspondence to: Y. Iwakura
Contact hypersensitivity (CHS) is a T cell-mediated cellular immune response caused by epicutaneous exposure to contact allergens. In this reaction, after the first epicutaneous allergen sensitization, Langerhans cells (LC) catch allergens and migrate from the skin to draining lymph nodes (LN) and activate naive T cells. Although IL-1 is suggested to be involved in these processes, the mechanisms have not been elucidated completely. In this report, to elucidate roles of IL-1
and IL-1ß in CHS, we analyzed ear swelling in 2,4,6-trinitrochlorobenzene (TNCB)-induced CHS using gene-targeted mice. We found that ear swelling was suppressed in IL-1
-deficient (IL-1
/) mice but not in IL-1ß/ mice. LC migration from the skin into LN was delayed in both IL-1
/ and IL-1ß/ mice, suggesting that this defect was not the direct cause for the reduced CHS in these mice. However, we found that the proliferative response of trinitrophenyl (TNP)-specific T cells after sensitization with TNCB was specifically reduced in IL-1
/ mice. Furthermore, adoptive transfer of TNP-conjugated IL-1-deficient epidermal cells (EC) into wild-type mice indicated that only IL-1
, but not IL-1ß, produced by antigen-presenting cells in EC could prime allergen-specific T cells. These observations indicate that IL-1
, but not IL-1ß, plays a crucial role in TNCB-induced CHS by sensitizing TNP-specific T cells.
Keywords: contact hypersensitivity, IL-1, knockout mice, Langerhans cell
Transmitting editor: K.Sugamura
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
M. Elkabets, Y. Krelin, S. Dotan, A. Cerwenka, A. Porgador, R. G. Lichtenstein, M. R. White, M. Zoller, Y. Iwakura, C. A. Dinarello, et al. Host-Derived Interleukin-1{alpha} Is Important in Determining the Immunogenicity of 3-Methylcholantrene Tumor Cells J. Immunol., April 15, 2009; 182(8): 4874 - 4881. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. S. Miller, E. M. Pietras, L. H. Uricchio, K. Hirano, S. Rao, H. Lin, R. M. O'Connell, Y. Iwakura, A. L. Cheung, G. Cheng, et al. Inflammasome-Mediated Production of IL-1beta Is Required for Neutrophil Recruitment against Staphylococcus aureus In Vivo J. Immunol., November 15, 2007; 179(10): 6933 - 6942. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Kakurai, R. Monteforte, H. Suto, M. Tsai, S. Nakae, and S. J. Galli Mast Cell-Derived Tumor Necrosis Factor Can Promote Nerve Fiber Elongation in the Skin during Contact Hypersensitivity in Mice Am. J. Pathol., November 1, 2006; 169(5): 1713 - 1721. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Suto, S. Nakae, M. Kakurai, J. D. Sedgwick, M. Tsai, and S. J. Galli Mast Cell-Associated TNF Promotes Dendritic Cell Migration J. Immunol., April 1, 2006; 176(7): 4102 - 4112. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. Matsuki, S. Nakae, K. Sudo, R. Horai, and Y. Iwakura Abnormal T cell activation caused by the imbalance of the IL-1/IL-1R antagonist system is responsible for the development of experimental autoimmune encephalomyelitis Int. Immunol., February 1, 2006; 18(2): 399 - 407. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. R. Timoshanko, A. R. Kitching, Y. Iwakura, S. R. Holdsworth, and P. G. Tipping Contributions of IL-1{beta} and IL-1{alpha} to Crescentic Glomerulonephritis in Mice J. Am. Soc. Nephrol., April 1, 2004; 15(4): 910 - 918. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Mori, T. Kondo, T. Nishie, T. Ohshima, and M. Asano Impairment of Skin Wound Healing in {beta}-1,4-Galactosyltransferase-Deficient Mice with Reduced Leukocyte Recruitment Am. J. Pathol., April 1, 2004; 164(4): 1303 - 1314. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Werman, R. Werman-Venkert, R. White, J.-K. Lee, B. Werman, Y. Krelin, E. Voronov, C. A. Dinarello, and R. N. Apte The precursor form of IL-1{alpha} is an intracrine proinflammatory activator of transcription PNAS, February 24, 2004; 101(8): 2434 - 2439. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Nakae, Y. Komiyama, S. Narumi, K. Sudo, R. Horai, Y.-i. Tagawa, K. Sekikawa, K. Matsushima, M. Asano, and Y. Iwakura IL-1-induced tumor necrosis factor-{alpha} elicits inflammatory cell infiltration in the skin by inducing IFN-{gamma}-inducible protein 10 in the elicitation phase of the contact hypersensitivity response Int. Immunol., February 1, 2003; 15(2): 251 - 260. [Abstract] [Full Text] [PDF] |
||||




