T cell-independent and T cell-dependent immunoglobulin G responses to polyomavirus infection are impaired in complement receptor 2-deficient mice

Virology. 2006 Aug 15;352(1):52-60. doi: 10.1016/j.virol.2006.04.018. Epub 2006 Jun 2.


Polyomavirus (PyV) infection induces protective T cell-independent (TI) IgM and IgG antibody responses in T cell-deficient mice, but these responses are not generated by immunization with viral proteins or virus like particles. We hypothesized that innate signals contribute to the generation of isotype-switched antiviral antibody responses. We studied the role of complement receptor (CR2) engagement in TI and T cell-dependent (TD) antibody responses to PyV using CR2-deficient mice. Antiviral IgG responses were reduced by 80-40% in CR2-/- mice compared to wild type. Adoptive transfer experiments demonstrated the need for CR2 not only in TD, but also in TI IgG responses to PyV. Transfer of CR2-/- B lymphocytes to SCID mice resulted in TI antiviral IgG responses that corresponded to 10% of that seen in wild-type B cell-reconstituted mice. Thus, our studies revealed a profound dependence of TI and TD antiviral antibody responses on CR2-mediated signals in PyV-infected mice, where the viral antigen is abundant and persistent.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Adoptive Transfer
  • Animals
  • Antigens, Viral / immunology
  • Capsid Proteins / immunology
  • Immunoglobulin G / blood*
  • Mice
  • Mice, Knockout
  • Mice, SCID
  • Polyomavirus / immunology
  • Polyomavirus Infections / immunology
  • Polyomavirus Infections / virology
  • Receptors, Complement 3d / deficiency*
  • Receptors, Complement 3d / genetics
  • T-Lymphocytes / immunology*


  • Antigens, Viral
  • Capsid Proteins
  • Immunoglobulin G
  • Receptors, Complement 3d
  • VP1 protein, polyomavirus