IK induced by coxsackievirus B3 infection transiently downregulates expression of MHC class II through increasing cAMP

Hye Lim Park, Yeon Jung Kim, Ha Na Na, Mi Young Park, Joo Young Kim, Cheol Won Yun, Jae Hwan Nam

Research output: Contribution to journalArticle

3 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)13-24
Number of pages12
JournalViral Immunology
Volume26
Issue number1
DOIs
Publication statusPublished - 2013 Feb 1

ASJC Scopus subject areas

  • Immunology
  • Molecular Medicine
  • Virology

Fingerprint Dive into the research topics of 'IK induced by coxsackievirus B3 infection transiently downregulates expression of MHC class II through increasing cAMP'. Together they form a unique fingerprint.

  • Cite this