Lymphoid cell transfers between adult C57BL/6 mice differing at the LPR locus. Lack of lymphadenopathy transfer and effects on host survival.

"1 pr" is an autosomal recessive locus which determines the lymphoproliferation of an abnormal T cell subset ("T lpr" cell subset). Though a thymus is necessary for the initiation of the lymphadenopathy, adult thymectomy does not interfere with the development of disease. C57BL/6 (B6) mice (either treated with cyclophosphamide or not), lpr heterozygous at the lpr locus, or not), and nu homozygous B6 mice (either homozygous at the lpr locus, or not) are refractory to the growth and massive proliferation of grafted cells of the aberrant T lpr cell subset, which polyclonally expands in lpr homozygous B6 mice. Their lack of expansion in B6 nu, lpr mice is surprising, since such animals may develop the lymphadenopathy under certain circumstances (thymus grafting). While the injection of normal B6 lymphoid cells does not improve the health of the B6 nu, lpr mice, but may even accelerate their wasting, the injection of B6 lpr lymphoid cells into B6 nu, lpr mice causes, after a transient wasting, a remarkable prolongation of survival. B6 nu recipients of B6 lpr lymphoid cells show no sign of wasting and survive like recipients of normal B6 (B6+) cells. Thus the "lpr type" lymphoproliferative potential is neither simply carried by the T lpr subset cells themselves, nor simply determined by the lpr environment of athymic, lpr homozygous mice, and it is also not readily reconstituted by grafting T lpr cells in athymic lpr mice.