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Downregulation of TAP1 in B Lymphocytes by Cellular and Epstein-Barr Virus-Encoded Interleukin-10
Reinhard Zeidler,
Günther Eissner,
Petra Meissner,
Stephan Uebel,
Robert Tampé,
Sabine Lazis, and
Wolfgang Hammerschmidt
From the GSF-National Research Center for Environment and Health, Institut für Klinische Molekularbiologie und Tumorgenetik, and the Institut für Experimentelle Hämatologie, München, Germany; and the Max-Planck-Institut für Biochemie, Martinsried, Germany.
Virally infected cells degrade intracellular viral proteins proteolytically and present the resulting peptides in association with major histocompatibility complex (MHC) class I molecules to CD8+ cytotoxic T lymphocytes (CTLs). These cells are normally prone to CTL-mediated elimination. However, several viruses have evolved strategies to avoid detection by the immune system that interfere with the pathway of antigen presentation. Epstein-Barr virus (EBV) expresses a predominantly late protein, the BCRF1 gene product vIL-10, that is similar in sequence to the human interleukin-10 (hIL-10). We show here that vIL-10 affects the expression of one of the two transporter proteins (TAPs) associated with antigen presentation. Similarly, hIL-10 showed the same activity. Expression of the LMP2 and TAP1 genes but not expression of TAP2 or LMP7 is efficiently downregulated, indicating a specific IL-10 effect on the two divergently transcribed TAP1 and LMP2 genes. Downregulation of TAP1 by IL-10 hampers the transport of peptide antigens into the endoplasmatic reticulum, as shown in the TAP-specific peptide transporter assay, their loading onto empty MHC I molecules, and the subsequent translocation to the cell surface. As a consequence, IL-10 causes a general reduction of surface MHC I molecules on B lymphocytes that might also affect the recognition of EBV-infected cells by cytotoxic T cells.
Blood, Vol. 90 No. 6 (September 15), 1997:
pp. 2390-2397
© 1997 by The American Society of Hematology.
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