Paul-Bunnell antigen in murine T cell differentiation: abnormal expression in MRL/Mp-lpr/lpr mice.

Expression of Paul-Bunnell (P-B) antigen was studied on lymphoid cells of normal mice, autoimmune MRL/Mp-lpr/lpr (lpr), and congenic MRL/Mp-+/+(+/+) mice. Evidence was presented that the P-B antigen is a differentiation-associated antigen of murine T cells: Cells with high P-B pattern and density on normal T cells increased as their differentiation proceeded in the peripheral lymphoid tissues. In thymus, P-B antigen was predominantly expressed on hydrocortisone resistant and PNA nonagglutinable cells. The degree of P-B expression on T cells of peripheral lymphoid tissues correlated well with that of Lyt-1 and Lyt-2 antigens (r greater than 0.7). Similar studies on lymphocytes obtained from lpr and +/+ mice at different ages revealed that P-B antigen on the peripheral T cells of lpr mice began to decrease at 6 to 8 wk of age and that the majority of the cells became low P-B cells by 10 wk, accompanied by decrease in expression of Lyt-1 antigen. In contrast, its expression on lpr thymocytes did not differ from that of +/+ or normal mice. The lymph node cell population of lpr mice at the height of the lymphadenopathy was composed of 80% of low P-B and dull Lyt-1 cells and less than 15% of "normal" P-B and Lyt-1 positive cells. These results indicate distorted differentiation of the lpr peripheral lymphocytes that are responsible for the massive lymphadenopathy and the morbid processes.