Includes nine pages of amendments. / Bibliography: leaves 140-211. / 211, [200] leaves, [12] leaves of plates : ill. (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Aims to determine the reason for the lack of ability of many myeloid leukaemic cell populations to stimulate allogeneic lymphocytes in mixed leucocyte culture (MLC), with a view to manipulating the immunogenicity of these cells for therapeutic purposes. / Thesis (Ph.D.)--University of Adelaide, Dept. of Microbiology and Immunology, 1995

Errata slip inserted at back / "August 2001." / Includes bibliographical references (leaves 254-296) / xxviii, 296, [9] leaves : charts (some col.), plates (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine, 2001

Bibliography: leaves 113-128 / xii, 128, [63] leaves, [6] leaves of plates : ill ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--University of Adelaide, Dept. of Microbiology and Immunology, 1984

Bibliography: leaves 218-251.

Bibliography: leaves 111-137.

Bibliography: leaves 129-145.

Graduation date: 2006

Prostaglandin E2 (PGE2) is an immunosuppressive factor secreted by the murine Lewis lung carcinoma (LLC). This factor can help to insure the survival of a tumor by suppressing the functions of lymphocytes and macrophages in their defense against tumors.Four weekly assays of macrophage tumoristatic activity from tumor-bearing mice were performed during the course of tumor development. Macrophages from the peritoneal cavity were cultured with LLC cells and after 48 hours the LLC growth was measured.The results of this study showed that macrophages from tumorbearing mice were suppressed in their ability to halt LLC growth in vitro. This suppression could be prevented by the use of indomethacin, a prostaglandin synthesis inhibitor. Indomethacin administration to tumor-free mice also enhanced their macrophage tumoristatic activities suggesting that the tumor was not the exclusive source of prostaglandin which suppressed anti-tumor immunity. Finally, indomethacin-fed tumor-bearing mice had smaller tumors than did mice not fed indomethacin.Ball State UniversityMuncie, IN 47306

The immune regulatory abilities of alveolar macrophages from C57B1/6 mice bearing a metastatic variant of Lewis lung carcinoma were determined. During early stages of tumor development, or before tumors metastasized to the lungs, alveolar macrophages did not affect or slightly enhanced T-lymphocyte proliferation; as tumor growth progressed, or following tumor metastasis, alveolar macrophages suppressed the T-cell response. Macrophage suppressor activity was probably not mediated by their production of PGE, since macrophages of tumor-bearing mice secreted less 2 PGE than did macrophages of normal mice. Normal alveolar 2 macrophages or macrophages preincubated in tumor cell supernatant for a short period stimulated T-cell blastogenesis and secreted PGE during in vitro culture. However, with 2 longer exposure to tumor cell supernatant, alveolar macrophages lost the capacity to augment T-cell proliferation and secreted less PGE 2.Ball State UniversityMuncie, IN 47306

published_or_final_version / Medical Sciences / Master / Master of Medical Sciences