In vivo or in vitro treatments with anti-I-J alloantisera abolish immunity to AKR leukemia.
This paper provides evidence for the involvement of immune mechanisms in conferring resistance to a spontaneous AKR leukemia. It is shown that genes in the B, J, or E subregions of the H-2 complex confer resistance to a spontaneously arisen, tissue culture-adapted AKR thymoma, BW5147. A direct correlation is demonstrated between survival to injected BW5147 cells and humoral responsiveness in various hybrids obtained from crosses of AKR mice and C57BL/10 or C3H/DiSn derived congeneic strains differing at H-2. Cellular immunity appears to play no role in resistance to the proliferation of tumor cells. It is further established that development of effective humoral immunity depends on B cells and Ly-1+, 2-, 3- helper T-cells bearing the I-Jk phenotype. These findings seem directly applicable to the spontaneous disease, and results of studies using transformed cells from an overtly leukemic AKR mouse parallel those obtained using BW1547 cells.
D000818:Animals; D000917:Antibody Formation; D005802:Genes, MHC Class II; D006183:H-2 Antigens / Q000235:genetics; D007518:Isoantibodies / Q000008:administration & dosage; D007942:Leukemia, Experimental / Q000276:immunology* / Q000517:prevention & control; D008211:Lymphocyte Cooperation; D008285:Major Histocompatibility Complex; D051379:Mice; D008806:Mice, Inbred AKR / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*
D006183:H-2 Antigens; D007518:Isoantibodies