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Involvement of Sema4A in the progression of experimental autoimmune myocarditis
Author(s) -
Makino Nobuhiko,
Toyofuku Toshihiko,
Takegahara Noriko,
Takamatsu Hyota,
Okuno Tatsusada,
Nakagawa Yukinobu,
Kang Sujin,
Nojima Satoshi,
Hori Masatsugu,
Kikutani Hitoshi,
Kumanogoh Atsushi
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.10.040
Subject(s) - myocarditis , autoimmunity , pathogenesis , immunology , dilated cardiomyopathy , medicine , adoptive cell transfer , cardiomyopathy , immune system , heart failure , t cell
Dilated cardiomyopathy often results from autoimmunity triggered by microbial infections during myocarditis. However, it remains unclear how immunological disorders are implicated in pathogenesis of autoimmune myocarditis. Here, we demonstrated that Sema4A, a class IV semaphorin, plays key roles in experimental autoimmune myocarditis (EAM). Dendritic cells pulsed with myosin heavy chain‐α peptides induced severe myocarditis in wild‐type mice, but not in Sema4A‐deficient mice. In adoptive transfer experiments, CD4 + T‐cells from wild‐type mice induced severe myocarditis, while CD4 + T‐cells from Sema4A‐deficient mice exhibited considerably attenuated myocarditis. Our results indicated that Sema4A is critically involved in EAM by regulating differentiation of T‐cells.