RGD Reference Report - Treatment and prevention of experimental autoimmune myocarditis with CD28 superagonists. - Chinchilla Research Resource Database
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Treatment and prevention of experimental autoimmune myocarditis with CD28 superagonists.

Authors: Wang, Shu  Liu, Jing  Wang, Min  Zhang, Jinghui  Wang, Zhaohui 
Citation: Wang S, etal., Cardiology. 2010;115(2):107-13. doi: 10.1159/000256660. Epub 2009 Nov 10.
CRRD ID: 13702882
Pubmed: (View Article at PubMed) PMID:19907173
DOI: Full-text: DOI:10.1159/000256660


OBJECTIVES: Experimental autoimmune myocarditis (EAM), a rodent model of human dilated cardiomyopathy (DCM), is mediated by an autoimmune mechanism. We investigated whether a CD28 superagonistic antibody selectively targeting CD4+CD25+ regulatory T cells (T(regs)) provides effective therapy for EAM.
METHODS: Four groups of 5 rats were used. The normal control group was immunized with PBS. The EAM group was immunized with porcine myosin. The experimental group was immunized with myosin and superagonistic CD28 antibody JJ316. The final group was immunized with myosin and an unrelated rat IgG. Autoantibody and IL-10 production, CD4+CD25+ cell levels, Foxp3 expression and cardiac histology were analyzed.
RESULTS: Anti-myosin autoantibody levels were higher in the EAM and isotype control groups than the normal control group (p < 0.05), and reduced in the CD28-JJ316 group (p < 0.05). The levels of CD25+CD4+ cells, IL-10 and splenocyte Foxp3 expression were significantly lower in the EAM and isotype control groups versus the CD28-JJ316 group (p < 0.05). Infiltration of inflammatory cells was observed in the EAM and isotype control groups, whereas CD28-JJ316 ameliorated myocarditis.
CONCLUSION: CD28 superagonists could be effective in EAM treatment by up-regulating Foxp3 expression and contributing to CD4+CD25+ T(reg) activation and expansion. The enhancement in IL-10 by CD28 superagonists also ameliorated the disease.

Annotation

Disease Annotations    

Objects Annotated

Genes (Homo sapiens)
CD28  (CD28 molecule)
FOXP3  (forkhead box P3)
IL10  (interleukin 10)


Additional Information

 



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.