Overexpression of CIITA in T Cells Aggravates Th2-Mediated Colitis in Mice.
10.3346/jkms.2006.21.5.877
- Author:
Tae Woon KIM
1
;
Hyo Jin PARK
;
Eun Young CHOI
;
Kyeong Cheon JUNG
Author Information
1. Department of Pathology, Hallym University College of Medicine, Chuncheon, Korea.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
MHC class II transactivator protein;
CIITA Protein;
Inflammatory Bowel Diseases;
Interleukin-4;
Th2 Cells
- MeSH:
Trans-Activators/*physiology;
Th2 Cells/*immunology;
T-Lymphocytes/*metabolism;
Oxazolone/pharmacology;
Nuclear Proteins/*physiology;
Mice, Transgenic;
Mice, Inbred C57BL;
Mice;
Interleukin-4/biosynthesis;
Colitis/*etiology;
Animals
- From:Journal of Korean Medical Science
2006;21(5):877-882
- CountryRepublic of Korea
- Language:English
-
Abstract:
The MHC class II transactivator (CIITA) is the master transcriptional regulator of genes involved in MHC class II restricted antigen presentation. Previously we suggested another role of CIITA in Th1/Th2 balance by demonstrating that forced expression of CIITA in murine T cells repressed Th1 immunity both in vitro and in vivo. However, the results were contradictory to the report that CIITA functioned to suppress the production of Th2 cytokine by CD4+T cells in CIITA deficient mice. In this study, we investigated the influence of constitutive expression of CIITA in T cells on Th2 immune response in vivo using murine experimental colitis model. In the dextran sodium sulfate-induced acute colitis, a disease involving innate immunity, CIITA transgenic mice and wild type control mice showed similar progression of the disease. However, the development of oxazolone-induced colitis, a colitis mediated by predominantly Th2 immune response, was aggravated in CIITA-transgenic mice. And, CD4+T cells from the mesenteric lymph node of CIITA-transgenic mice treated with oxazolone exhibited a high level of IL-4 secretion. Together, these data demonstrate that constitutive expression of CIITA in T cells skews immune response to Th2, resulting in aggravation of Th2-mediated colitis in vivo.
