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Original Article |
Duke University Medical Center, Jones Bldg., Rm. 316, Box 3010, Research Dr., Durham, NC 27710.919-684-8982919-613-7821
mchey002{at}duke.edu
The mechanisms that regulate B cell memory and the rapid recall response to antigen remain poorly defined. This study focuses on the rapid expression of B cell memory upon antigen recall in vivo, and the replenishment of quiescent B cell memory that follows. Based on expression of CD138 and B220, we reveal a unique and major subtype of antigen-specific memory B cells (B220–CD138–) that are distinct from antibody-secreting B cells (B220+/–CD138+) and B220+CD138– memory B cells. These nonsecreting somatically mutated B220– memory responders rapidly dominate the splenic response and comprise >95% of antigen-specific memory B cells that migrate to the bone marrow. By day 42 after recall, the predominant quiescent memory B cell population in the spleen (75–85%) and the bone marrow (>95%) expresses the B220– phenotype. Upon adoptive transfer, B220– memory B cells proliferate to a lesser degree but produce greater amounts of antibody than their B220+ counterparts. The pattern of cellular differentiation after transfer indicates that B220– memory B cells act as stable self-replenishing intermediates that arise from B220+ memory B cells and produce antibody-secreting cells on rechallenge with antigen. Cell surface phenotype and Ig isotype expression divide the B220– compartment into two main subsets with distinct patterns of integrin and coreceptor expression. Thus, we identify new cellular components of B cell memory and propose a model for long-term protective immunity that is regulated by a complex balance of committed memory B cells with subspecialized immune function.
Key Words: antigen-specific immunity • immunological memory • B lymphocyte memory • B lymphocyte subset • mice
© 2000 The Rockefeller University Press
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