Th1 and Th2 cytokine production is suppressed at the level of transcriptional regulation in Kawasaki disease
Authors: J. KIMURA1; H. TAKADA; A. NOMURA1; T. OHNO1; Y. MIZUNO2; M. SAITO1; K. KUSUHARA1; T. HARA1
Source: Clinical & Experimental Immunology, Volume 137, Number 2, August 2004 , pp. 444-449(6)
Publisher: Wiley-Blackwell
Abstract:
SUMMARY To clarify the functional state of T cells in Kawasaki disease, we analysed mRNA expression levels of Th1/Th2 cytokines (IFN-
and IL-4) along with Th1/Th2-inducing transcription factors, T-bet and GATA-3, which play pivotal roles in the development of Th1 and Th2 cells, respectively. By real-time PCR, IFN-
mRNA levels in peripheral blood mononuclear cells (PBMNC) were significantly decreased in Kawasaki disease patients compared with those with measles, and tended to be lower than those in healthy controls. T-bet mRNA levels were significantly decreased in patients with Kawasaki disease compared with healthy controls. In addition, IL-4 and GATA-3 mRNA levels were significantly decreased in Kawasaki disease compared with healthy controls. Regulatory cytokine mRNA levels (TGF-
and IL-10) were also decreased in Kawasaki disease. The mRNA levels of IFN-
showed a significant positive correlation with those of T-bet in Kawasaki disease. These results suggest that the suppressed function of Th1 and Th2, associated with the suppression of both T-bet and GATA-3 gene expression, may be one of the immunological characteristics of Kawasaki disease.
Keywords:
Kawasaki disease;
T-bet;
GATA-3;
IFN-
;
IL-4
Document Type: Research article
DOI: http://dx.doi.org/10.1111/j.1365-2249.2004.02506.x
Affiliations: 1: Department of Paediatrics, Graduate School of Medical Sciences, Kyushu University and 2: Fukuoka Children's Hospital and Medical Centre for Infectious Diseases, Fukuoka, Japan
Publication date: 2004-08-01
- In this: publication
- By this: publisher
- In this Subject: Microbiology , Allergy & Immunology
- By this author: J. KIMURA ; H. TAKADA ; A. NOMURA ; T. OHNO ; Y. MIZUNO ; M. SAITO ; K. KUSUHARA ; T. HARA

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