| First Author | Heiser RA | Year | 2011 |
| Journal | J Immunol | Volume | 187 |
| Issue | 1 | Pages | 212-21 |
| PubMed ID | 21622866 | Mgi Jnum | J:175935 |
| Mgi Id | MGI:5287948 | Doi | 10.4049/jimmunol.1002328 |
| Citation | Heiser RA, et al. (2011) Aborted germinal center reactions and B cell memory by follicular T cells specific for a B cell receptor V region peptide. J Immunol 187(1):212-21 |
| abstractText | A fundamental problem in immunoregulation is how CD4(+) T cells react to immunogenic peptides derived from the V region of the BCR that are created by somatic mechanisms, presented in MHC II, and amplified to abundance by B cell clonal expansion during immunity. BCR neo Ags open a potentially dangerous avenue of T cell help in violation of the principle of linked Ag recognition. To analyze this issue, we developed a murine adoptive transfer model using paired donor B cells and CD4 T cells specific for a BCR-derived peptide. BCR peptide-specific T cells aborted ongoing germinal center reactions and impeded the secondary immune response. Instead, they induced the B cells to differentiate into short-lived extrafollicular plasmablasts that secreted modest quantities of Ig. These results uncover an immunoregulatory process that restricts the memory pathway to B cells that communicate with CD4 T cells via exogenous foreign Ag. |
