IL-18 in autoimmunity. Studies in autoimmune murine lupus and in human SLE

被引：0
|
作者：
Boraschi, D. [1 ]
Neumann, D. [2 ]
Martinelli, L. [1 ]
Lucchesi, D. [1 ]
Quattroni, P. [1 ]
Favilli, F. [1 ]
Italiani, P. [1 ]
Anzilotti, C. [3 ]
Pratesi, F. [3 ]
Dinarello, C. A. [4 ]
Migliorini, P. [4 ]
机构：
[1] CNR, Inst Biomed Technol, Pisa, Italy
[2] Hannover Med Sch, Pharmakol, Hannover, Germany
[3] Univ Hosp Pisa, Immunoallergol, Pisa, Italy
[4] Univ Colorado, Sch Med, Denver, CO USA
来源：
13TH INTERNATIONAL CONGRESS OF IMMUNOLOGY | 2007年
关键词：
D O I：
暂无
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
The chronic progressive lupus-like disease of lpr mice strongly involves Th1-dependent immune activation. Expression of the Th1-related cytokine IL-18 and of its receptors is greatly enhanced in lpr lymphoid organs early in life, well before pathology development. Hyper-expression of the Th2-activating IL-18-like cytokine IL-33 was evident in lpr mice, in parallel to increase of receptor expression. Expression of IL-17, present in normal organs, was undetectable in lpr mice. Thus, autoimmune pathogenesis in murine lupus correlates with up-regulation of Th1 and Th2 responses, with no involvement of Th17 reactions. In human lupus patients, serum and urine levels of IL-18 and its inhibitor IL-18BP were higher than in controls. However, only serum levels of IL-18BP positively correlated with disease severity (ECLAM score).
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页码：219 / +
页数：3
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