Impaired antibody responses but normal proliferation of specific CD4 + T cells in mice lacking complement receptors 1 and 2

Abstract

Severely impaired Ab responses are seen in animals lacking C (complement) factors C2, C3 or C4 as well as CR1-2 (C receptors 1 and 2). The molecular mechanism behind this phenomenon is not understood. One possibility is that C-containing immune complexes are endocytosed via CR2 on B cells and presented to specific CD4+ T cells, which would then proliferate and provide efficient help to specific B cells. In vitro, B cells can endocytose immune complexes via CR1-2 and present the Ag to T cells. Whether absence of this Ag presenting function in Cr2--- mice (mice lacking CR1-2) explains their low Ab response is unclear. To address this question, Cr2--- and wild type mice were transferred with OVA-specific T cells, obtained from the DO11.10 strain which has a transgenic TCR recognizing an OVA peptide. The animals were subsequently immunized with sheep red blood cells (SRBC) conjugated to OVA. Interestingly, proliferation of the OVA-specific T cells was normal in Cr2--- mice, although their Ab response to both SRBC and OVA was severely impaired. These observations suggest that the impaired Ab response in Cr2--- mice cannot be explained by a lack of appropriate induction of T cell help. © 2009 Blackwell Publishing Ltd.