Soluble glucocorticoid-induced TNF receptor (sGITR) induces inflammation in mice.
- Author:
Hyun Hee SHIN
1
;
Suk Gi KIM
;
Moo Hyung LEE
;
Jae Hee SUH
;
Byoung S KWON
;
Hye Seon CHOI
Author Information
1. Department of Biological Sciences and the Immunomodulation Research Center, University of Ulsan, Ulsan 680-749, Korea.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- MeSH:
Animals;
Carrier Proteins/metabolism;
Flow Cytometry;
Inflammation/*chemically induced/pathology;
Injections;
Male;
Mice;
Mice, Inbred C57BL;
Receptors, Nerve Growth Factor/*metabolism;
Receptors, Tumor Necrosis Factor/*metabolism;
Solubility;
Spleen/metabolism/pathology;
Support, Non-U.S. Gov't
- From:Experimental & Molecular Medicine
2003;35(5):358-364
- CountryRepublic of Korea
- Language:English
-
Abstract:
Glucocorticoid-induced TNF receptor (GITR) was a new member of the TNF/nerve growth factor receptor (TNFR/ NGFR) family and induced in murine T cells by dexamathasone. Recombinant soluble GITR (sGITR) induced an inflammation in peritoneal membrane and changes in spleen after i.p. injection of 3 mg/kg in C57BL/6 mice. Spleen was enlarged and percentage of neutrophils and monocytes were increased. The area of red pulp in spleen was increased, while that of white pulp was decreased after GITR injection. The thickening of membrane and neutrophil infiltration was observed in peritoneal membrane with increased myeloperoxidase activity. At later time, neutrophil infiltration moved to inside the tissue with tissue damage. GITR ligand and GITR were expressed constitutively on the surface of spleen cells and cells from peritoneal fluid. In contrast, no significant change in the spleen and in peritoneal membrane was observed in mice treated with LPS. GITR may play a role in body's inflammatory processes.
