IK Induced by Coxsackievirus B3 Infection Transiently Downregulates Expression of MHC Class II Through Increasing cAMP
- Authors
- Park, Hye-Lim; Kim, Yeon-Jung; Na, Ha-Na; Park, Mi-Young; Kim, Joo-Young; Yun, Cheol-Won; Nam, Jae-Hwan
- Issue Date
- Feb-2013
- Publisher
- MARY ANN LIEBERT, INC
- Citation
- VIRAL IMMUNOLOGY, v.26, no.1, pp.13 - 24
- Indexed
- SCIE
SCOPUS
- Journal Title
- VIRAL IMMUNOLOGY
- Volume
- 26
- Number
- 1
- Start Page
- 13
- End Page
- 24
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/104052
- DOI
- 10.1089/vim.2012.0054
- ISSN
- 0882-8245
- Abstract
- Major histocompatibility complex (MHC) class II expression is critical for the presentation of antigens in the immune response to viral infection. Consequently, some viruses regulate the MHC class II-mediated presentation of viral antigens as a mechanism of immune escape. In this study, we found that Coxsackievirus B3 (CVB3) infection transiently increased IK expression, which reduced the expression of MHC class II (I-A/I-E) on splenic B cells. Interestingly, CVB3-induced IK elevated cAMP, a downstream molecule of the G protein-coupled receptors, which inhibited MHC class II presentation on B cells. Transgenic mice expressing truncated IK showed lower expression of MHC class II on B cells than did wild-type mice after CVB3 infection. Taken together, these results imply that IK plays a role in downregulating MHC class II expression on B cells during CVB3 infection through the induction of cAMP.
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Collections - Graduate School > Department of Life Sciences > 1. Journal Articles
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