Objective. In order to shed light on the role of splenic B1 cells in disease pathogenesis in lupus-prone mice, this study was undertaken to determine how efficiently these cells can serve as antigen-presenting cells (APC) and to ascertain which murine lupus susceptibility loci dictate the expansion of these cells. Methods. Spleens and peritoneal cavities (PerC) of NZM2410 lupus-prone mice, as well as of control B6 and New Zealand white mice, were examined for the prevalence, surface phenotype, and possible anatomic location of B1 cells. The antigen-presenting ability of fluorescence-sorted splenic B1a cells was assessed. Levels of B1 cells were examined in B6 mice congenic for 4 different lupus susceptibility intervals. Results. NZM2410 lupus mice showed an expansion of splenic and PerC B1a cells at all ages. These cells expressed high levels of B71, B72, CD24, lymphocyte function-associated antigen 1, and intercellular adhesion molecule 1, and had the functional capability to serve as APC. Among the lupus susceptibility intervals studied, Sle2, but not Sle1, Sle3, or the H2 locus, affected the expansion of B1 cells. Conclusion. These findings raise the possibility that the genetically determined expansion of splenic B1a cells in lupus-prone mice might contribute to disease pathogenesis by augmenting the presentation of autoantigens to pathogenic T cells.
|Original language||English (US)|
|Number of pages||11|
|Journal||Arthritis and rheumatism|
|State||Published - Sep 1 1998|
ASJC Scopus subject areas
- Immunology and Allergy
- Pharmacology (medical)