| First Author | Jacobson AC | Year | 2008 |
| Journal | J Immunol | Volume | 180 |
| Issue | 7 | Pages | 5057-66 |
| PubMed ID | 18354231 | Mgi Jnum | J:133369 |
| Mgi Id | MGI:3778338 | Doi | 10.4049/jimmunol.180.7.5057 |
| Citation | Jacobson AC, et al. (2008) Complement receptors 1 and 2 influence the immune environment in a B cell receptor-independent manner. J Immunol 180(7):5057-66 |
| abstractText | The CD21/35 proteins are complement receptors implicated in controlling and interpreting activation states of the innate and acquired immune responses. One defect of CD21/35(-/-) animals is depressed production of Ag-specific IgG3 which we show is evident in vivo but not in vitro. Gene expression profiles obtained from naive wild-type and CD21/35(-/-) splenocytes demonstrated enhanced expression of inflammatory mediators from CD11b(+) splenocytes in the CD21/35(-/-) animals. Splenocyte populations between wild-type and CD21/35(-/-) mice were similar except for a moderate increase in GR1(low)CD31(+) immature myeloid cells. Furthermore, depletion of neutrophils and other GR1-expressing cells alleviates elevated inflammatory gene expression in the CD21/35(-/-) spleen. Complement activation also plays a key role in the differential gene expression observed in the CD21/35-deficient mouse as depletion of C3 or inhibition of C3a receptor signaling within the animal returned inflammatory gene expression within the spleen to wild-type levels. Finally, C3 depletion before immunization allowed for the enhanced production of Ag-specific IgG3 production in the CD21/35(-/-) mouse compared with mock-depleted animals. These data suggest that the overall environment of the CD21/35(-/-) spleen is quite different from that of the wild-type animal perhaps due to altered complement convertase activity. This difference may be responsible for a number of the phenotypes ascribed to the deficiency of CD21/35 proteins on B cells and follicular dendritic cells. |
