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    T-Cell-independent immunoglobulin G responses in vivo are elicited by live-virus infection but not by immunization with viral proteins or virus-like particles

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    Authors
    Szomolanyi-Tsuda, Eva
    Le, Quang P.
    Garcea, Robert L.
    Welsh, Raymond M.
    UMass Chan Affiliations
    Department of Pathology
    Document Type
    Journal Article
    Publication Date
    1998-07-11
    Keywords
    Animals
    Antibodies, Viral
    Capsid
    *Capsid Proteins
    Germinal Center
    Immunoglobulin G
    Mice
    Mice, Inbred C57BL
    Mice, Inbred CBA
    Polyomavirus
    Polyomavirus Infections
    Receptors, Antigen, T-Cell, alpha-beta
    Receptors, Antigen, T-Cell, gamma-delta
    T-Lymphocytes
    Tumor Virus Infections
    Vaccination
    Virion
    Life Sciences
    Medicine and Health Sciences
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    Abstract
    Immunoglobulin G (IgG) responses to viruses are generally assumed to be T-cell dependent (TD). Recently, however, polyomavirus (PyV) infection of T-cell-deficient (T-cell receptor beta chain [TCR-beta] -/- or TCR-betaxdelta -/-) mice was shown to elicit a protective, T-cell-independent (TI) antiviral IgM and IgG response. A repetitive, highly organized antigenic structure common to many TI antigens is postulated to be important in the induction of antibody responses in the absence of helper T cells. To test whether the repetitive structure of viral antigens is essential and/or sufficient for the induction of TI antibodies, we compared the abilities of three forms of PyV antigens to induce IgM and IgG responses in T-cell-deficient mice: soluble capsid antigens (VP1), repetitive virus-like particles (VLPs), and live PyV. Immunization with each of the viral antigens resulted in IgM production. VLPs and PyV elicited 10-fold-higher IgM titers than VP1, indicating that the highly organized, repetitive antigens are more efficient in IgM induction. Antigen-specific TI IgG responses, however, were detected only in mice infected with live PyV, not in VP1- or VLP-immunized mice. These results suggest that the highly organized, repetitive nature of the viral antigens is insufficient to account for their ability to elicit TI IgG response and that signals generated by live-virus infection may be essential for the switch to IgG production in the absence of T cells. Germinal centers were not observed in T-cell-deficient PyV-infected mice, indicating that the germinal center pathway of B-cell differentiation is TD even in the context of a virus infection.
    Source
    J Virol. 1998 Aug;72(8):6665-70.
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/38687
    PubMed ID
    9658113
    Related Resources
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    UMass Chan Faculty and Researcher Publications

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