T cell-independent and T cell-dependent immunoglobulin G responses to polyomavirus infection are impaired in complement receptor 2-deficient mice.
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.
Szomolanyi-Tsuda
Eva
E
Department of Pathology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA. Eva.Szomolanyi-Tsuda@umassmed.edu
Seedhom
Mina O
MO
Carroll
Michael C
MC
Garcea
Robert L
RL
D019264:Adoptive Transfer; D000818:Animals; D000956:Antigens, Viral / Q000276:immunology; D036022:Capsid Proteins / Q000276:immunology; D007074:Immunoglobulin G / Q000097:blood*; D051379:Mice; D018345:Mice, Knockout; D016513:Mice, SCID; D011120:Polyomavirus / Q000276:immunology; D027601:Polyomavirus Infections / Q000276:immunology / Q000821:virology; D017464:Receptors, Complement 3d / Q000172:deficiency* / Q000235:genetics; D013601:T-Lymphocytes / Q000276:immunology*
D000956:Antigens, Viral; D036022:Capsid Proteins; D007074:Immunoglobulin G; D017464:Receptors, Complement 3d; C062481:VP1 protein, polyomavirus