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Integrated Department of Immunology, National Jewish Medical and Research Center and University of Colorado School of Medicine, Denver, CO 80206
Normal animals contain an autoreactive B lymphocyte subset, the B-1
subset, which is controlled by undefined mechanisms to prevent
autoimmunity. Using a VH11V
9 Ig transgenic
mouse, with a specificity prototypic of the subset, we have explored
conditions responsible for the previously reported Ag
hyporesponsiveness of these cells. We report that peritoneal
VH11V9 B cells exhibit typical B-1 behavior
with high basal intracellular free Ca2+ and negligible
receptor-mediated calcium mobilization. However, splenic B cells from
this mouse, while phenotypically similar to their peritoneal
counterparts, including expression of CD5, mount robust B-2-like
responses to Ag as measured by calcium influx and altered tyrosine
phosphorylation responses. When these splenic cells are adoptively
transferred to the peritoneal cavity and encounter their cognate
self-Ag, they acquire a B-1 signaling phenotype. The ensuing
hyporesponsiveness is characterized by increases in both basal
intracellular calcium and resting tyrosyl phosphorylation levels and is
highlighted by a marked abrogation of B cell receptor-mediated calcium
mobilization. Thus, we show that self-Ag recognition in specific
microenvironments such as the peritoneum, and we would propose other
privileged sites, confers a unique form of anergy on activated B cells.
This may explain how autoreactive B-1 cells can exist while
autoimmunity is avoided.
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