Th1-type immune responses by Toll-like receptor 4 signaling are required for the development of myocarditis in mice with BCG-induced myocarditis.

Th1-type immune responses by Toll-like receptor 4 signaling are required for the development of myocarditis in mice with BCG-induced myocarditis. Research Abstract Details 

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Th1-type immune responses by Toll-like receptor 4 signaling are required for the development of myocarditis in mice with BCG-induced myocarditis. Abstract Text:

Kimiaki Nishikubo,Kyoko Imanaka-Yoshida,Shigenori Tamaki,Michiaki Hiroe,Toshimichi Yoshida,Yukihiko Adachi,Yasuhiro Yasutomi,Kimiaki Nishikubo,Kyoko Imanaka-Yoshida,Shigenori Tamaki,Michiaki Hiroe,Toshimichi Yoshida,Yukihiko Adachi,Yasuhiro Yasutomi,

The immunological aspects of autoimmune myocarditis are difficult to understand because of the existence of many infectious agents and animal models suggesting different mechanisms in autoimmune myocarditis. To overcome these difficulties, two strains of mice, C3H/HeN and C3H/HeJ, showing different immune responses to mycobacteria, were immunized with myosin mixed with BCG. The C3H/HeN mice with a wild-type Toll-like receptor 4 (TLR4) showed severe myocarditis, whereas the C3H/HeJ mice with nonfunctional mutated TLR4 did not. CD4(+) cells from both strains of mice exhibited appreciable proliferative responses following myosin stimulation; however, the cytokines from these cells differed between these two strains. The C3H/HeN mice showed T helper (Th)1-type cytokine responses, whereas the expressions of mRNA in C3H/HeJ mice were Th2-type cytokine. When both of these strains of immunized mice were inoculated with a plasmid encoding cDNA of interleukin (IL)-4 or agonistic IL-4, the development of myocarditis was inhibited in C3H/HeN mice. Moreover, C3H/HeJ mice, in which development of myocarditis was not induced by immunization of myosin mixed with BCG, showed myocarditis after injection of IL-4 antagonistic mutant DNA for the induction of Th1-type immune responses. The results suggested that the induction of autoimmune myocarditis by myosin is affected by Th1-type immune responses.

Th1-type immune responses by Toll-like receptor 4 signaling are required for the development of myocarditis in mice with BCG-induced myocarditis. Publishing Authors By Initials

K Nishikubo,K Imanaka-Yoshida,S Tamaki,M Hiroe,T Yoshida,Y Adachi,Y Yasutomi,K Nishikubo,K Imanaka-Yoshida,S Tamaki,M Hiroe,T Yoshida,Y Adachi,Y Yasutomi,

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PUBMED ID PMID:

MEDLINE DATE: 2007 Sep-Nov

Th1-type immune responses by Toll-like receptor 4 signaling are required for the development of myocarditis in mice with BCG-induced myocarditis. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Journal of autoimmunity

VOLUME: 29

Page Numbers: 146-53

Journal Abbreviation: J. Autoimmun.

ISSN: 0896-8411

DAY: 15

MONTH: 08

YEAR: 2007

Th1-type immune responses by Toll-like receptor 4 signaling are required for the development of myocarditis in mice with BCG-induced myocarditis. Information

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LANGUAGE: eng

NlmUniqueID: 8812164

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Grant and Affiliation Information for Th1-type immune responses by Toll-like receptor 4 signaling are required for the development of myocarditis in mice with BCG-induced myocarditis.

AFFILIATION: Department of Rheumatology, National Hospital Organization, Mie Chuo Medical Center, Mie 514-1101, Japan.

Country: England

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MEDLINETA: J Autoimmun

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