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Overexpression of CIITA in T cells aggravates Th2-mediated colitis in mice
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- Authors
- Issue Date
- 2006-10-18
- Publisher
- Korean Academy of Medical Science
- Citation
- J Korean Med Sci. 2006 Oct;21(5):877-82.
- Keywords
- Animals ; Colitis/*etiology ; Interleukin-4/biosynthesis ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Nuclear Proteins/*physiology ; Oxazolone/pharmacology ; T-Lymphocytes/*metabolism ; Th2 Cells/*immunology ; Trans-Activators/*physiology
- 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.
- ISSN
- 1011-8934 (Print)
- Language
- English
- URI
- http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17043423
https://hdl.handle.net/10371/22581
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