Interleukin 5 Regulation of Peritoneal B-Cell Proliferation and Antibody Secretion

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Abstract
The influence of recombinant interleukin 5 (rIL-5) on murine peritoneal B-cell proliferation and antibody secretion was examined. Larger, low buoyant density peritoneal B cells proliferated better with rIL-5 than the smaller resting B cells. This was also true for splenic B cells; however, comparison of the respective populations showed the large peritoneal B-cell responses to be superior. Limiting dilution analyses showed that from 25% to about 40% of large peritoneal B cells proliferated in response to rIL-5 when lipopolysaccharide (LPS) was present. No detectable difference in the fraction of proliferating splenic B cells was seen in the presence of rIL-5. These results are consistent with expression of IL-5 receptors on about 70% of low-density peritoneal B cells as determined by fluorescent staining with anti-IL-5 receptor monoclonal antibody (MoAb). IL-5 also enhanced spontaneous and mitogen-driven IgM secretion by both peritoneal and splenic B lymphocytes; the increases exhibited by peritoneal B cells, however, were at least twice those exhibited by splenic B cells. Spontaneous and mitogen-driven secretion of auto-antibodies to bromelain-treated mouse erythrocytes (BrMRBC) by peritoneal B cells were also increased by this interleukin. Furthermore, rIL-5 enhanced peritoneal B-cell plaque-forming cell (PFC) responses to TNP-LPS but not TNP-Ficoll. Both an anti-IL-5R MoAb and an anti-IL-5 MoAb blocked the rIL-5-induced enhancement of proliferation and auto-antibody PFC responses. Hence, IL-5 appears to be important for the regulation of proliferation and antibody secretion by many murine peritoneal B cells.