PARTICIPATION OF NK1.1(-CELLS IN THE REJECTION OF LPR ALPHA-BETA-T CELLS WHEN BONE-MARROW CELLS OF LPR MICE ARE TRANSPLANTED INTO B6 MICE()T)

When C57BL/6 (B6) mice were irradiated (9 Gy) and received bone marrow (BM) cells of B6-lpr/lpr mouse origin (i.e., lpr-->B6), all mice died within 6 days. In the irradiated B6 mice, radioresistant CD3(-) IL-2R beta NK cells and IL-2R beta(+) CD3(int) cells (i.e., CD3(int) cells of extrathymic origin) remained, especially in the liver, There were t wo subsets, NK1.1(+) and NK1.1(-), among the IL-2R beta(+) CD3(int) ce lls. However, the NK1.1(+) subset (i.e. NK1.1(+) T cells) was much mor e radioresistant, and the majority of CD3(int) cells belonged to this subset in irradiated mice. The expansion of lymphocytes from injected BM cells did not occur in the irradiated B6 mice. However, such expans ion did take place in irradiated B6-lpr/lpr mice injected with both BM cells of B6-lpr/lpr and B6 origin. As a result, the mice subjected to BM cells survived. Irradiated B6 mice were treated in vivo with anti- NK1.1 mAb or anti-asialoGM(1) antibody to eliminate NK cells alone or both NK cells and NK1.1(+) T cells. When irradiated B6 mice were pretr eated with anti-NK1.1 mAb, the mice could survive. These results sugge st that intact NK1.1(+) T cells of extrathymic origin may recognize ab normal BM cells with the lpr gene and inhibit the expansion of lymphoc ytes, including abnormal double-negative CD4(-) 8(-) cells, in B6-lpr/ lpr mice. To inhibit the expansion of lymphocytes, mechanisms other th an Fas ligand/Fas molecules on extrathymic T cells may be responsible.