| First Author | Huntington ND | Year | 2006 |
| Journal | Nat Immunol | Volume | 7 |
| Issue | 2 | Pages | 190-8 |
| PubMed ID | 16378097 | Mgi Jnum | J:112560 |
| Mgi Id | MGI:3662781 | Doi | 10.1038/ni1292 |
| Citation | Huntington ND, et al. (2006) CD45 links the B cell receptor with cell survival and is required for the persistence of germinal centers. Nat Immunol 7(2):190-8 |
| abstractText | To segregate the many contributions that B cell receptor (BCR)-mediated signals make to immune responses, we have analyzed here B cells deficient in the 'pan-leukocyte' marker CD45. BCR ligation of Cd45-/- B cells failed to activate phosphatidylinositol-3-OH kinase, NF-kappaB, Erk1 or Erk2 kinases or to upregulate cell survival proteins and instead induced apoptosis. Immunization of Cd45-/- B cell chimeras induced germinal centers and antigen-specific immunoglobulin G1 antibody-forming cells early, but both cellular compartments decreased by day 14. Proliferation of Cd45-/- B cells induced by CD40 ligand in vitro was impaired as a result of abrogation by BCR ligation of the upregulation of prosurvival proteins. In contrast, enforced expression of the antiapoptotic factor Bcl-xL prevented the collapse of Cd45-/- B cell germinal centers. These results show mechanistic differences in B cell survival during germinal center initiation and propagation; CD40 signaling is sufficient for the former, whereas the latter requires signaling from the BCR. |
