ACCUMULATION OF SPLENIC B1A CELLS WITH POTENT ANTIGEN-PRESENTING CAPABILITY IN NZM2410 LUPUS-PRONE MICE

Objective. In order to shed light on the role of splenic B1 cells in d isease pathogenesis in lupus-prone mice, this study was undertaken to determine how efficiently these cells can serve as antigen-presenting cells (LPC) and to ascertain which murine lupus susceptibility loci di ctate the expansion of these cells. Methods. Spleens and peritoneal ca vities (PerC) of NZM2410 lupus-prone mice, as well as of control B6 an d New Zealand white mice, were examined for the prevalence, surface ph enotype, and possible anatomic location of B1 cells. The antigen-prese nting ability of fluorescence-sorted splenic B1a cells was assessed. L evels of B1 cells were examined in B6 mice congenic for 4 different lu pus susceptibility intervals. Results. NZM2410 lupus mice showed an ex pansion of splenic and PerC B1a cells at all ages. These cells express ed high levels of B71, B72, CD24, lymphocyte function-associated antig en 1, and intercellular adhesion molecule 1, and had the functional ca pability to serve as APC, Among the lupus susceptibility intervals stu died, Sle2, but not Sle1, Sle3, or the H2 locus, affected the expansio n of B1 cells. Conclusion. These findings raise the possibility that t he genetically determined expansion of splenic B1a cells in lupus-pron e mice might contribute to disease pathogenesis by augmenting the pres entation of autoantigens to pathogenic T cells.