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

Abstract

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.

• Authors: Eva Szomolanyi-Tsuda, Mina O Seedhom, Michael C Carroll, Robert L Garcea
• Journal: Virology (Virology) Vol. 352 Issue 1 Pg. 52-60 (Aug 15 2006) ISSN: 0042-6822 [Print] United States
• PMID: 16733062 (Publication Type: Journal Article, Research Support, N.I.H., Extramural)

Chemical References

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

Topics

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