Immunity to carcinogen-induced transplantable fibrosarcomas in B2/B2 chickens. IV. Effect of whole-body gamma radiation on localization and growth of intravenously injected tumor cells.
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Biomedical subjects
Publications and source records attributed to M A Palladino.
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Delayed hypersensitivity (DH) reaction to human Ig, corynebacterium parvum or allogeneic cells at the site of tumor cell injection, suppressed the fibrosarcoma (SCFS) growth in chickens. Spleen cells of SC chickens sensitized to human Ig or C. parvum suppressed SCFS growth when adoptively transferred with tumor cells, but only when the sensitizing antigen was present locally. This suppression did not occur in irradiated recipients, SCFS I cells injected into wattles of chickens immune to the tumor, provoked a local DH reaction. Spleen cells from donors sensitized to SCFS I adoptively transferred immunity to both SCFS I and SCFS II when cells of the two tumors were mixed together before injection, but not when SCFS II cells were injected alone. Tumor-specific and nontumor-specific DH may be essential for local suppression of fibrosarcoma growth in chickens.
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Presensitization of BX donors with B cells appears obligatory in order for their T cells to acquire suppressor capacity against the adoptive humoral antibody response of bursa cells to B. abortus. Although anti-Ig + C treatment of bursa cells removes their capacity to "immunize" BX chickens for suppressor activity, BX chickens cannot be sensitized for this effect by the injection of chicken IgM + IgG. Both embryonic and allogeneic bursa cells can "immunize" the T cells of BX chickens. The observation that spleen cells from BX chickens can cause absence of plasma cells and germinal centers in the spleen and mucosal lining of cecal tonsils of histocompatible recipients within 1-2 weeks after transfer suggests that the suppressor cells mediate their effect by acting directly on B cells at one or more stages during their development.
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Transplantable fibrosarcomas were developed in two B-locus-defined chicken strains from primary tumors induced by im injection of 2 mg 7,12-dimethylbenz[a]anthracene in 0.1 ml dimethyl sulfoxide into 1- to 2-week-old chicks. Viruses were not important factors in transmission of these tumors as evidenced by 1) transplantability only within the chicken strain of origin, 2) lack of evidence for a filterable agent, 3) maintenance of donor karyotypic characteristics upon transplantation, 4) lack of DNA polymerase and avian leukosis virus group-specific protein production in vitro. Bursectomized inbred SC chickens had a higher incidence of tumor induction than did normals of the same strain. Although the exact interpretation of this finding posed some problems, as discussed, an important function of enhancing antibody in tumor growth appeared excluded.
Transfer of lymphoid cells from agammaglobulinemic donor chickens into 3- to 4-week-old irradiated recipients that had been surgically bursectomized at 2 to 3 weeks of age significantly depressed the ability of the antibody-forming apparatus to recover from irradiation. Antibody production to Brucella abortus and sheep erythrocytes remained much below control levels in BX donor-cell recipients of both chicken strains studied (SC and FP). Progressive loss of serum IgM and IgG was observed primarily in the FP strain resulting in complete agammaglobulinemia within 4 to 6 weeks after transfer of BX donor spleen cells. Serial transfer of this phenomenon was demonstrated in the SC strain.