Abstract
Abstract New Zealand black mice (NZB)2 develop disease spontaneously which is similar in many ways to human systemic lupus erythematosis (SLE) and is characterized by autoantibodies, nephritis, (1, 2) and perivascular cellular infiltration. These mice have also shown a decreased capacity with ageing to reject tumors induced by Moloney sarcoma virus (3). Cantor and co-workers (4) have demonstrated that the capacity of spleen cells from NZB mice to mount a graft-vs-host reaction also decreases with age. Both of these observations indicate reduced efficacy of the thymus-dependent immune system or thymus-dependent lymphocytes (T cells), but do not show whether programmed T cells are responsible for some of the cellular autoimmunity in this disease. We have investigated the ability of spleen cells from diseased NZB mice to elicit a cytotoxic effect against fetal target cells, in vitro, by a modified form of the colony inhibition, or lymphocyte cytotoxicity system (5, 6).
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