Journal
SCANDINAVIAN JOURNAL OF IMMUNOLOGY
Volume 70, Issue 2, Pages 77-84Publisher
WILEY
DOI: 10.1111/j.1365-3083.2009.02274.x
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Funding
- Uppsala University
- Swedish Research Council
- Ellen, Walter and Lennart Hesselman's Foundation
- Hans von Kantzow's Foundation
- King Gustaf V:s 80 Years Foundation
- Ollie and Elof Ericsson's Foundation
- Agnes and Mac Rudberg's Foundation
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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.
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