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Antigen-presentation capacity of dendritic cells is impaired in ongoing enterovirus myocarditis

Item Type:Article
Title:Antigen-presentation capacity of dendritic cells is impaired in ongoing enterovirus myocarditis
Creators Name:Rahnefeld, A. and Ebstein, F. and Albrecht, N. and Opitz, E. and Kuckelkorn, U. and Stangl, K. and Rehm, A. and Kloetzel, P.M. and Voigt, A.
Abstract:Coxsackievirus B3 (CVB3)-infection is a frequent cause of acute myocarditis, which may result in chronic myocarditis and virus persistence. Investigation of the initial immune responses to CVB3 may shed light on the mechanisms that contribute to ongoing disease. DCs, as key professional APCs, were investigated in two MHC-matched hosts: while C57BL/6 mice are resistant to chronic CVB3-myocarditis, the A.BY/SnJ mouse strain exhibits susceptibility. DC maturation and activation were critically impaired in A.BY/SnJ mice, as reflected by the failure of DCs to induce co-stimulatory molecules and cytokine/chemokine responses. MHC class I-restricted antigen presentation via the cross-presentation pathway was also affected in DCs from A.BY/SnJ mice. DC maturation involves the accumulation of DC aggresome-like induced structures (DALISs) and the transient storage of defective ribosomal products (DRiPs). DCs from A.BY/SnJ mice showed permanent DALIS accumulation; the detection of poly-ubiquitinylated CVB3 proteins in these DALISs suggested a limitation in the MHC class I antigenic supply in this host. In conclusion, ongoing chronic disease in A.BY/SnJ mice due to a failure to clear the virus may be attributed to defects in DC maturation/activation and DC MHC class I antigen processing.
Keywords:Animal Models, DC, Infectious Disease, Myocarditis, Proteasome, Virology, Animals, Mice
Source:European Journal of Immunology
Publisher:Wiley (U.S.A.)
Page Range:2774-2781
Date:September 2011
Official Publication:https://doi.org/10.1002/eji.201041039
PubMed:View item in PubMed

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