A histological study on experimental autoimmune myocarditis with special reference to initiation of the disease and cardiac dendritic cells

1995 ◽  
Vol 426 (5) ◽  
Author(s):  
K. Suzuki
Keyword(s):  
Dendritic Cells ◽  
Special Reference ◽  
Histological Study ◽  
Autoimmune Myocarditis ◽  
Experimental Autoimmune Myocarditis ◽  
Experimental Autoimmune

Abstract 129: Suppressor of Cytokine Signaling 1 in Dendritic Cells Inhibits Myocardial Inflammation in Experimental Autoimmune Myocarditis

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Kazuko Tajiri ◽  
Kyoko Imanaka-Yoshida ◽  
Michiaki Hiroe ◽  
Nobutake Shimojo ◽  
Satoshi Sakai ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
T Cell ◽  
Cd4 T Cells ◽  
Cytokine Signaling ◽  
Autoimmune Myocarditis ◽  
Dc Function ◽  
Autoreactive T Cell ◽  
Experimental Autoimmune Myocarditis ◽  
Experimental Autoimmune

Introduction: Autoimmunity is considered to play an important role in the development of myocarditis and dilated cardiomyopathy. Recent reports have indicated that a subgroup of myocarditis patients may benefit from immune-targeted therapies. Suppressor of cytokine signaling1 (SOCS1) is an intracellular, cytokine-inducible protein that regulates the responses of immune cells to cytokines. We therefore hypothesized that overexpression of SOCS1 may inhibit the inflammation of myocarditis and cardiomyopathy. Methods and Results: Myocarditis was induced by subcutaneous immunization with cardiac specific peptides derived from α-myosin heavy chain in BALB/c mice on days 0 and 7. Plasmid DNA encoding SOCS1 (pSOCS1) was injected intraperitoneally into mice on days 0, 5 and 10. pSOCS1 treatment significantly decreased heart-to-body weight ratios and the number of infiltrating cells in the heart. Echocardiography showed preserved contractile function in pSOCS1-treated mice. Although autoimmune myocarditis is a CD4+ T cell-mediated disease, pSOCS1 treatment does not have a direct suppressive effect on autoreactive T-cell activation. The introduced pSOCS1 suppressed proinflammatory cytokine production and STAT1 phosphorylation in dendritic cells (DCs). In addition, the proliferative responses of autoreactive CD4+ T cells co-cultured with DCs from pSOCS1-treated mice were much weaker than those of cells cultured with DCs from control plasmid-injected mice. These results suggested that the inoculated pSOCS1 may have been transfected into DCs and impaired DC function in vivo. Conclusion: The administration of pSOCS1 protected mice from the development of experimental autoimmune myocarditis, which was mediated by the inhibition of DC function that in turn reduced the activation of autoreactive CD4+ T cells.

scholarly journals Innate Signaling Promotes Formation of Regulatory Nitric Oxide–Producing Dendritic Cells Limiting T-Cell Expansion in Experimental Autoimmune Myocarditis

Circulation ◽  
2013 ◽  
Vol 127 (23) ◽  
pp. 2285-2294 ◽  
Author(s):  
Gabriela Kania ◽  
Stefanie Siegert ◽  
Silvia Behnke ◽  
Rafael Prados-Rosales ◽  
Arturo Casadevall ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Dendritic Cells ◽  
T Cell ◽  
Cell Expansion ◽  
Autoimmune Myocarditis ◽  
Experimental Autoimmune Myocarditis ◽  
T Cell Expansion ◽  
Experimental Autoimmune

scholarly journals Myosin-primed tolerogenic dendritic cells ameliorate experimental autoimmune myocarditis

2013 ◽  
Vol 101 (2) ◽  
pp. 203-210 ◽  
Author(s):  
Jun-Ho Lee ◽  
Tae-Hoon Kim ◽  
Hyo Eun Park ◽  
Eun Gae Lee ◽  
Nam-Chul Jung ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Autoimmune Myocarditis ◽  
Tolerogenic Dendritic Cells ◽  
Experimental Autoimmune Myocarditis ◽  
Experimental Autoimmune
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