Efficient production of complement (C3d)3 fusion proteins using the baculovirus expression vector system

Barrault, Denise V.; Steward, M. W.; Cox, Vivienne F.; Smith, Richard A.; Knight, Andrew M.

doi:10.1016/j.jim.2005.07.013

Cited by 8 publications

(5 citation statements)

References 26 publications

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“…These CR2-mediated effects at the surface of B cells and FDCs are collectively referred to as the “molecular adjuvant” effects of complement and have been shown in various experimental systems in which antigen is fused to multiple copies of C3d to lower the threshold dose of antigen required for an antibody response in the absence of other “traditional” adjuvants from two to four orders of magnitude (Barrault et al, 2005; Dempsey et al, 1996; Wang et al, 2004a; Wang et al, 2004b). However, these same CR2:C3d-mediated molecular adjuvant effects, which are beneficial in the host’s immune response to foreign antigen, can also amplify an antibody-mediated autoimmune response in the case of individuals having B cells reactive against self-antigens.…”

Section: Complement Receptor Cr2 In Humoral Immunitymentioning

confidence: 99%

Regulation of Humoral Immunity by Complement

2012

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Summary The complement system of innate immunity plays an important role in regulating humoral immunity in large part through the complement receptor CR2 which forms a co-receptor on B cells during antigen-induced activation and retains antigens on follicular dendritic cells, which are critical for maintenance of germinal centers. Recent studies, identify a third important pathway in which naïve B cells pick-up complement C3-coated immune complexes within the lymphatics via CR2 and deliver them to follicular dendritic cells in the B cell compartment. These findings, combined with the recent report on the co-crystal structure of CR2 and its ligand C3d, present additional opportunities for dissecting a possible role for this pathway in regulating autoimmune responses.

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Section: Complement Receptor Cr2 In Humoral Immunitymentioning

confidence: 99%

Regulation of Humoral Immunity by Complement

2012

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“…However, neither approach seems to be promising for producing vaccines. The first approach is limited by the significant costs of first producing the monoclonal antibody and then coupling it to the antigen, while the second approach is handicapped by the genetic instability of tandem C3d genes (2).…”

mentioning

confidence: 99%

The Oligomerization Domain of C4-Binding Protein (C4bp) Acts as an Adjuvant, and the Fusion Protein Comprised of the 19-Kilodalton Merozoite Surface Protein 1 Fused with the Murine C4bp Domain Protects Mice against Malaria

Ogun¹,

et al. 2008

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Highly purified protein antigens are usually poor immunogens; in practice, adjuvants are needed to obtain satisfactory immune responses. Plasmodium yoelii 19-kDa merozoite surface protein 1 (MSP1 19 ) is a weak antigen, but mice vaccinated with this antigen in strong adjuvants can survive an otherwise lethal parasite challenge. Fusion proteins comprising this antigen fused to the oligomerization domain of the murine complement inhibitor C4-binding protein (C4bp) and a series of homologues have been produced. These C4bp domains acted as adjuvants for the fused antigen; the MSP1 19 -murine C4bp fusion protein induced protective immunity in BALB/c mice. Because this fusion protein also induced antibodies against circulating murine C4bp, distantly related C4bp oligomerization domains fused to the same antigen were tested. These homologous domains did not induce antibodies against murine C4bp and, surprisingly, induced higher antibody titers against the antigen than the murine C4bp domain induced. These results demonstrate a new adjuvantlike effect of C4bp oligomerization domains.

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“…A number of experiments have shown that binding of the C3 fragment C3dg to an antigen acts as a strong adjuvant to promote both humoral and cell-meditated immune responses. The magnitude of this adjuvant effect is similar to that of Freund's adjuvant, and C3 fragments have been put forward as potential components of vaccines (33,34). It is therefore reasonable to expect that complement activation and C3dg binding will trigger an immune response that can lead to an adaptive immune response against a graft.…”

Section: Discussionmentioning

confidence: 91%