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mediates coordinate expression of
antigen-processing genes in RSV-infected pulmonary
epithelial cells
Departments of 1 Medicine, 2 Pediatrics, and 3 Microbiology and Immunology and 4 Sealy Center for Molecular Science, The University of Texas Medical Branch, Galveston, Texas 77555-1060
Major
histocompatibility complex (MHC) class I-restricted cytotoxic T
lymphocytes (CTLs) clear respiratory tract infections caused by the
pneumovirus respiratory syncytial virus (RSV) and also mediate
vaccine-induced pulmonary injury. Herein we examined the mechanism for
RSV-induced MHC class I presentation. Like infectious viruses,
conditioned medium from RSV-infected cells (RSV-CM) induces naive cells
to coordinately express a gene cluster encoding the transporter
associated with antigen presentation 1 (TAP1) and low molecular mass
protein (LMP) 2 and LMP7. Neutralization of RSV-CM with antibodies to
interferon (IFN)-
largely blocked TAP1/LMP2/LMP7 expression, whereas anti-interleukin-1 antibodies were without effect,
and recombinant IFN- increased TAP1/LMP2/LMP7 expression to levels produced by RSV-CM. LMP2, LMP7, and TAP1 expression were
required for MHC class I upregulation because the irreversible proteasome inhibitor lactacystin or transfection with a competitive TAP1 inhibitor blocked inducible class I expression. We conclude that
RSV infection coordinately increases MHC class I expression and
proteasome activity through the paracrine action of IFN- to induce
expression of the TAP1/LMP2/LMP7 locus, an event that may be
important in the initiation of CTL-mediated lung injury.
respiratory syncytial virus; pulmonary inflammation; major
histocompatibility complex class II locus; ABC transporter; 26S
proteasome; interferon-
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