Expression of mouse CD43 in the B cell lineage of transgenic mice causes impaired immune responses to T‐independent antigens

摘要

AbstractCD43 (leukosialin), a sialylated glycoprotein expressed on the surface of most hematopoietic cells, has been implicated in cell adhesion and signaling. However, its precise physiological function remains unclear. We used mouse CD43 (mCD43)‐immunoglobulin enhancer‐transgenic (TG) mice to study the role of mCD43in vivo.Previous work revealed that mCD43 expression on mature B cells in these mice resulted in immunodeficiency to T‐dependent (TD) antigens (Ag), possibly by impairing B‐T cell interactions. In the present study we have immunized the TG mice with the T‐independent (TI) Ag fluorescein‐(Fl) lipopolysaccharide (LPS) (TI type 1 Ag) and Fl‐Ficoll (TI type 2 Ag). Surprisingly, the mCD43‐Ig enhancer expressing mice were impaired in their ability to mount humoral responses to both Fl‐LPS and Fl‐Ficoll, and had decreased numbers of cells responding to Agin vivo.Flow cytometric analysis was performed on peritoneal B‐1 cells, a population which often plays a major role in humoral responses to TI Ag such as bacterial Ag. This analysis revealed similar B220, IgM and CD5 expression patterns for the TG and nontransgenic (NTG) B‐1 cells. In addition, purified peritoneal B‐1 cells from TG and NTG mice were able to respond to LPS. Stimulation of splenic B cellsin vitrowith Fl‐LPS and Fl‐Ficoll revealed that, in contrast to NTG B cell responses, TG B cell responses could not be enhanced by co‐culture with T cells. However, soluble T cell factor enhancement of the TG B cell responses was normal. These data suggest that the mCD43 expression on B cells may inhibit cell interactions that are important for enhanced TI Ag responses. The anti‐adhesive forces of mucins in general may thus be critical in regulating