| First Author | de Vinuesa CG | Year | 2000 |
| Journal | J Exp Med | Volume | 191 |
| Issue | 3 | Pages | 485-94 |
| PubMed ID | 10662794 | Mgi Jnum | J:60255 |
| Mgi Id | MGI:1353096 | Doi | 10.1084/jem.191.3.485 |
| Citation | de Vinuesa CG, et al. (2000) Germinal centers without T cells. J Exp Med 191(3):485-94 |
| abstractText | Germinal centers are critical for affinity maturation of antibody (Ab) responses. This process allows the production of high-efficiency neutralizing Ab that protects against virus infection and bacterial exotoxins. In germinal centers, responding B cells selectively mutate the genes that encode their receptors for antigen. This process can change Ab affinity and specificity. The mutated cells that produce high-affinity Ab are selected to become Ab-forming or memory B cells, whereas cells that have lost affinity or acquired autoreactivity are eliminated. Normally, T cells are critical for germinal center formation and subsequent B cell selection. Both processes involve engagement of CD40 on B cells by T cells. This report describes how high-affinity B cells can be induced to form large germinal centers in response to (4-hydroxy-3-nitrophenyl) acetyl (NP)-Ficoll in the absence of T cells or signaling through CD40 or CD28. This requires extensive cross-linking of the B cell receptors, and a frequency of antigen-specific B cells of at least 1 in 1,000. These germinal centers abort dramatically at the time when mutated high-affinity B cells are normally selected by T cells. Thus, there is a fail-safe mechanism against autoreactivity, even in the event of thymus-independent germinal center formation. |
