期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 191, 期 3, 页码 485-493出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.191.3.485
关键词
quasimonoclonal mice; (4-hydroxy-3-nitrophenyl) acetyl-Ficoll; germinal centers; CD40 ligation; thymus independent
资金
- NIAID NIH HHS [R01AI41570, R01 AI041570] Funding Source: Medline
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.
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