Abstract
The effect of the Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1) on the activation and differentiation of normal B cells was investigated. B cells of transgenic mice expressing LMP1 under the control of immunoglobulin promoter/enhancer displayed enhanced expression of activation antigens and spontaneously proliferated and produced antibody. Humoral immune responses of LMP1 transgenic mice in CD40-deficient or normal backgrounds revealed that LMP1 mimics CD40 signals to induce extrafollicular B cell differentiation but, unlike CD40, blocks germinal center formation. Thus, these specific properties of LMP1 may determine the site of primary B cell infection and the state of infection in the natural course of EBV infection, whereas subsequent loss of LMP1 expression may affect the site of persistent latent infection.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Antibody Affinity
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B-Lymphocytes / immunology*
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B-Lymphocytes / metabolism
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B-Lymphocytes / virology
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CD40 Antigens / genetics
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CD40 Antigens / metabolism*
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Cell Differentiation
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Female
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Germinal Center / immunology
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Germinal Center / metabolism
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Herpesvirus 4, Human / metabolism*
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Herpesvirus 4, Human / physiology
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Immunization
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Immunoglobulin Class Switching
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Immunoglobulins / biosynthesis
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Interleukin-4 / pharmacology
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Lymphocyte Activation*
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Male
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Mice
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Mice, Inbred C57BL
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Mice, Transgenic
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Molecular Mimicry*
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NF-kappa B / metabolism
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Signal Transduction
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Spleen / immunology
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Viral Matrix Proteins / genetics
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Viral Matrix Proteins / metabolism*
Substances
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CD40 Antigens
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EBV-associated membrane antigen, Epstein-Barr virus
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Immunoglobulins
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NF-kappa B
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Viral Matrix Proteins
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Interleukin-4