Role of RANTES in the development of autoimmune tissue injuries in MRL-Fas lpr mice

MRL-Fas lpr mice spontaneously develop a severe autoimmune disease closely resembling human SLE. To investigate the possible role of RANTES in autoimmune tissue injuries, we have constructed RANTES-deficient MRL-Fas lpr mice by gene targeting. In the RANTES-deficient mice, axillary lymph nodes were...

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Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 103(2002), 1 vom: 30. Apr., Seite 89-97
1. Verfasser: Tsukahara, Tsunemichi (VerfasserIn)
Weitere Verfasser: Makino, Yasuhiko, Fujii, Takayuki, Ogawa, Makoto, Saisho, Hiromitsu, Hamano, Yuki, Ueda, Shiro, Akikusa, Bunshiro, Danoff, Theodore M
Format: Aufsatz
Sprache:English
Veröffentlicht: 2002
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Autoantibodies Chemokine CCL5 DNA 9007-49-2
Beschreibung
Zusammenfassung:MRL-Fas lpr mice spontaneously develop a severe autoimmune disease closely resembling human SLE. To investigate the possible role of RANTES in autoimmune tissue injuries, we have constructed RANTES-deficient MRL-Fas lpr mice by gene targeting. In the RANTES-deficient mice, axillary lymph nodes were significantly reduced in size compared with those of RANTES-intact mice. Flow cytometric analysis revealed that double-negative (DN) T cells were significantly reduced. Image analyzer showed that cell-infiltrated areas in peribronchial lesions were decreased in the lung of RANTES-deficient MRL-Fas lpr mice. Furthermore, we detected continuous expression of RANTES mRNA in the lung of MRL-Fas lpr mice. In contrast, the degree of histological renal injuries and survival rate was similar in both genotypes. We speculate that RANTES is involved in the development of peribronchial pulmonary lesions in MRL-Fas lpr mice. Further studies using RANTES-deficient mice might contribute to the elucidation of the role of RANTES in autoimmune tissue injuries
Beschreibung:Date Completed 23.05.2002
Date Revised 15.11.2007
published: Print
Citation Status MEDLINE
ISSN:1521-7035