| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
*
Division of Immunobiology, Research Institute for Biological Sciences, and
Department of Applied Biological Science, Science University of Tokyo, Noda City, Chiba, Japan; and
New Product Research Laboratories III, Daiichi Pharmaceutical Co., Kitakasai, Edogawa, Tokyo, Japan
Atopic dermatitis (AD) is a pruritic inflammatory skin disease
characterized by elevation of plasma levels of total IgE, infiltration
of mast cells and eosinophils, and the expression of cytokines by Th2 T
cells. However, the role of Th2 cells in the pathogenesis of AD is not
fully understood. In this study we examined the NC/Nga (NC) mouse model
of AD and established STAT6-deficient (SATA6-/-) NC mice
to investigate the relevance of IL-4-mediated immune responses.
Surprisingly, these mice elicited AD-like skin lesions at equivalent
frequency and time of onset compared with normal NC littermates.
Histological features of the lesion in STAT6-/- NC mice
fulfilled the criteria for the pathogenesis of AD, although these mice
fail to produce IgE and Th2 cytokines. The lymph nodes proximal to the
regions of skin that developed lesions exhibited massive enlargement
elicited by the accumulation of activated IFN-
-secreting T cells.
Moreover, caspase I, IL-18, IL-12, and IFN- are found to be highly
expressed at the skin lesion, occurring simultaneously with elevation
of eotaxin 2 and CCR3 expression. Therefore, the Th2-mediated immune
response is not necessary for the development of AD-like skin disease
in NC mice. The skin microenvironment that favored IFN- production
tightly correlates with the skin disease in NC mice through the
infiltration of eosinophils.
This article has been cited by other articles:
|
|
 |
|
  D. Voskas, Y. Babichev, L. S. Ling, J. Alami, Y. Shaked, R. S. Kerbel, B. Ciruna, and D. J. Dumont An eosinophil immune response characterizes the inflammatory skin disease observed in Tie-2 transgenic mice J. Leukoc. Biol., July 1, 2008; 84(1): 59 - 67. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Inoue and Y. Aramaki Suppression of Skin Lesions by Transdermal Application of CpG-Oligodeoxynucleotides in NC/Nga Mice, a Model of Human Atopic Dermatitis J. Immunol., January 1, 2007; 178(1): 584 - 591. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Terada, H. Tsutsui, Y. Imai, K. Yasuda, H. Mizutani, K. Yamanishi, M. Kubo, K. Matsui, H. Sano, and K. Nakanishi Contribution of IL-18 to atopic-dermatitis-like skin inflammation induced by Staphylococcus aureus product in mice PNAS, June 6, 2006; 103(23): 8816 - 8821. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Ozaki, Y.-i. Seki, A. Fukushima, and M. Kubo The Control of Allergic Conjunctivitis by Suppressor of Cytokine Signaling (SOCS)3 and SOCS5 in a Murine Model J. Immunol., October 15, 2005; 175(8): 5489 - 5497. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. M. Zmolik and M. E. Mummert Pep-1 as a Novel Probe for the In Situ Detection of Hyaluronan J. Histochem. Cytochem., June 1, 2005; 53(6): 745 - 751. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Tanaka, S. Kanaji, A. Hirano, K. Arima, A. Shinagawa, C. Goda, S. Yasunaga, K. Ikizawa, Y. Yanagihara, M. Kubo, et al. Induction and activation of the aryl hydrocarbon receptor by IL-4 in B cells Int. Immunol., June 1, 2005; 17(6): 797 - 805. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Tsukuba, K. Okamoto, Y. Okamoto, M. Yanagawa, K. Kohmura, Y. Yasuda, H. Uchi, T. Nakahara, M. Furue, K. Nakayama, et al. Association of Cathepsin E Deficiency with Development of Atopic Dermatitis J. Biochem., December 1, 2003; 134(6): 893 - 902. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
