Association of the lymphoproliferative disease inducer gene Arp with autoimmunity and resistance to tumour growth.

This report describes a biological role for the diallelic gene system, Arpa and Arpb, which codes for surface antigens on murine lymphocytes and tumour cells. Arpb is present only in a mutant strain of BALB/c which is designated BALB/c-Arpb. Normal BALB/c and all other strains of mice tested express Arpa. Cross immunizations between BALB/c and BALB/c-Arpb generated autoantibodies and autoreactive cytostatic effector cells which recognize Arp-encoded determinants on normal and tumour cells. The latter expressed quantitatively more Arp encoded products than normal cells as indicated by increased binding of autoantibodies and susceptibility to cytostasis. The anti-tumour response generated by Arp-incompatible immunizations resulted in increased resistance to challenge with syngeneic tumour cells and in some cases total suppression of tumour growth. BALB/c-Arpb mice were inherently different from BALB/c in that they generated H-2 unrestricted cytostatic effectors, produced higher levels of autoantibodies on immunization and survived longer than normal BALB/c when challenged with 10(5) Meth. A tumour cells. The role of the Arp gene in tumour immunity is discussed.