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Journal of Virology, March 2005, p. 2964-2972, Vol. 79, No. 5
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.5.2964-2972.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

MyD88 Expression Is Required for Efficient Cross-Presentation of Viral Antigens from Infected Cells

Margaret Chen,1,2*,{dagger} Christina Barnfield,1,{dagger} Tanja I. Näslund,1 Marina N. Fleeton,1,{ddagger} and Peter Liljeström1,2

Microbiology and Tumor Biology Center, Karolinska Institutet, Stockholm,1 Department of Vaccine Research, Swedish Institute for Infectious Disease Control, Solna, Sweden2

Received 10 August 2004/ Accepted 15 October 2004

While virus-infected dendritic cells (DCs) in certain instances have the capacity to activate naïve T cells by direct priming, cross-priming by DCs via the uptake of antigens from infected cells has lately been recognized as another important pathway for the induction of antiviral immunity. During cross-priming, danger and stranger signals play important roles in modulating immune responses. Analogous to what has been shown for other microbial infections, virally infected cells may contain several pathogen-associated molecular patterns that are recognized by Toll-like receptors (TLRs). We analyzed whether the efficient presentation of antigens derived from infected cells requires the usage of MyD88, which is a common adaptor molecule used by all TLRs. For this study, we used murine DCs that were wild type or deficient in MyD88 expression and fibroblasts that were infected with an alphavirus replicon to answer this question. Our results show that when DCs are directly infected, they are able to activate antigen-specific CD8+ T cells in a MyD88-independent manner. In contrast, a strict requirement of MyD88 for cross-priming was observed when virally infected cells were used as a source of antigen in vitro and in vivo. This indicates that the effects of innate immunity stimulation via the MyD88 pathway control the efficiency of cross-presentation, but not direct presentation or DC maturation, and have important implications in the development of cytotoxic T lymphocyte responses against alphaviral replicon infections.

* Corresponding author. Mailing address: Department of Vaccine Research, Swedish Institute for Infectious Disease Control, 171 82 Solna, Sweden. Phone: 46-8-4572559. Fax: 46-8-310848. E-mail: Margaret.Chen{at}mtc.ki.se.

{dagger} M.C. and C.B. contributed equally to this work.

{ddagger} Present address: Virology Unit, Trinity College, Dublin, Ireland.

Journal of Virology, March 2005, p. 2964-2972, Vol. 79, No. 5
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.5.2964-2972.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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