In vivo or in vitro treatments with anti-I-J alloantisera abolish immunity to AKR leukemia.

AUTOR(ES)

Meruelo, D

RESUMO

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.

Documentos Relacionados

• Involvement of I-J epitopes in the self- and allo-recognition sites of T cells: blocking of syngeneic and allogeneic mixed lymphocyte reaction-responder cells by monoclonal anti-I-J antibodies.
• Regulation of immune response to tumor antigen: interference with syngeneic tumor immunity by anti-IA alloantisera.
• The humoral immune response of NIH Swiss and SWR/J mice to vaccination with formalinized AKR or Gross murine leukemia virus.
• Mode of Action of Chemotherapy In Vivo on Human Acute Leukemia. I. DAUNOMYCIN
• Genetic alterations of RNA leukemia viruses associated with the development of spontaneous thymic leukemia in AKR/J mice.