FAS IS HIGHLY EXPRESSED IN THE GERMINAL CENTER BUT IS NOT REQUIRED FOR REGULATION OF THE B-CELL RESPONSE TO ANTIGEN
- Author(s)
- Smith, KGC; Nossal, GJV; Tarlinton, DM;
- Details
- Publication Year 1995-12-05,Volume 92,Issue #25,Page 11628-11632
- Journal Title
- PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Publication Type
- Journal Article
- Abstract
- In establishing the memory B-cell population and maintaining self-tolerance during an immune response, apoptosis mediates the removal of early, low-affinity antibody-forming cells, unselected germinal center (GC) cells, and, potentially, self-reactive B cells, To address the role of the apoptosis-signaling cell surface molecule FAS in the B-cell response to antigen, we have examined the T-cell-dependent B cell response to the carrier-conjugated hapten (4-hydroxy-3-nitrophenyl)acetyl (NP) in lpr mice in which the fas gene is mutated. High levels of FAS were expressed on normal GC B cells but the absence of FAS did not perturb the progressive decline in numbers of either GC B cells or extrafollicular antibody-forming cells, Furthermore, the rate of formation and eventual size of the NP-specific memory B-cell population in lpr mice were normal, The accumulation of cells with affinity-enhancing mutations and the appearance of high-affinity anti-NP IgG1 antibody in the serum were also normal in lpr mice, Thus, although high levels of FAS are expressed on GC B cells, FAS is not required for GC selection or for regulation of the major antigen-specific B-cell compartments. The results suggest that the size and composition of B-cell compartments in the humoral immune response are regulated by mechanisms that do not require FAS.
- Publisher
- NATL ACAD SCIENCES
- Keywords
- MOLECULAR CHARACTERIZATION; SOMATIC HYPERMUTATION; TRANSGENIC MICE; MEMORY; SINGLE; BCL-2; LYMPHOPROLIFERATION; MATURATION; APOPTOSIS; AFFINITY
- Publisher's Version
- https://doi.org/10.1073/pnas.92.25.11628
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- Refer to copyright notice on published article.
Creation Date: 1995-12-05 12:00:00