The Journal of Experimental Medicine
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Published 5 May 2003. doi:10.1084/jem.20022232
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© Rockefeller University Press, 0022-1007/2003/5/1183 $5.00
The Journal of Experimental Medicine, Volume 197, Number 9, 1183-1190

A Role for Complement in Feedback Enhancement of Antibody Responses by IgG3

Teresita Díaz de Ståhl1, Jörgen Dahlström1, Michael C. Carroll2 and Birgitta Heyman1

1 Department of Genetics and Pathology, Rudbeck Laboratory, Uppsala University, SE-751 85 Uppsala, Sweden
2 Center for Blood Research, Harvard Medical School, Boston, MA 02115

Address correspondence to Birgitta Heyman, Department of Genetics and Pathology, Rudbeck Laboratory, Uppsala University, SE-751 85 Uppsala, Sweden. Phone: 46-18-6113868; Fax: 46-18-55-89-31; E-mail: Birgitta.Heyman{at}genpat.uu.se

IgG1, IgG2a, and IgG2b, passively administered with soluble Ags, enhance specific Ab responses. The effect of IgG3 in this type of feedback regulation has not been studied previously. We immunized mice with trinitrophenyl (TNP)-coupled carrier proteins (bovine serum albumin [BSA] or ovalbumin [OVA]) alone or complexed to monoclonal TNP-specific IgG3. The carrier-specific Ab responses were enhanced by several hundred-fold by IgG3. Enhancement was significantly impaired in mice depleted of complement factor C3 and in mice lacking complement receptors 1 and 2 (Cr2-/-). In contrast, mice lacking the common Fc-receptor gamma chain (FcR{gamma}-/-), resulting in reduced expression of Fc{gamma}RI and lack of Fc{gamma}RIII, and mice lacking Fc{gamma}RIIB (Fc{gamma}RIIB-/-), responded equally well to immunization with IgG3-complexed Ag as wild-type controls. These findings demonstrate that IgG3 can induce feedback enhancement and that IgG3, in analogy with IgM, uses the complement system for this function.

Key Words: rodents • Fc receptors • cellular activation • transgenic/knockout


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