Premium
The protective role of IL‐13 in Experimental Autoimmune Myocarditis
Author(s) -
Cihakova Daniela,
Barin Jobert G,
Afanasyeva Marina,
Kimura Miho,
Fairweather DeLisa,
Berg Michael,
Talor Monica V.,
Baldeviano G. Christian,
Frisancho Sylvia,
Gabrielson Kathleen,
Bedja Djahida,
McKenzie Andrew N.J.,
Rose Noel R
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a128-c
Subject(s) - myocarditis , immunology , medicine , cardiology
IL‐13 knockout (KO) BALB/c mice developed severe myosin‐induced experimental autoimmune myocarditis (EAM) and coxsackievirus B3 ‐induced myocarditis with impaired cardiac function in some of the IL‐13 KO mice. Total CD45+ leukocyte, B cell and macrophage were increased in the hearts of IL‐13 KO mice. Spleen T cells from IL‐13 KO mice were highly activated and had increased proliferation in vitro to myosin. Hearts of IL‐13 KO mice had increased levels of the proinflammatory and profibrotic cytokines IL‐1b, IL‐18, IFN‐g, TGF‐a, IL‐4 and histamine. Severe EAM in IL‐13 KO was not due to increased IL‐4, as myocarditis was mild in IL‐4 KO mice. CD4+CD25+Foxp3+ regulatory T cell numbers were not altered in the heart, but decreased in the spleen of IL‐13 KO mice. Thus, IL‐13 protects against severe myocarditis in BALB/c mice by inhibiting macrophage, T cells and B cell/antibody‐mediated damage to the heart.