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Homograft Rejection by Neonatally Thymectomized Germ-free Mice¹

Lobund Laboratory, Department of Microbiology, University of Notre Dame, Notre Dame, Indiana

A response to tissue transplantation was elicited in germ-free neonatally thymectomized CFW and C3H mice by challenge with homotransplantations of methylcholanthrene-induced tumor cells and neoplastic lymph node cells. Germ-free thymectomized mice of both CFW and C3H strains accepted all isologous transplants and rejected all homologous transplants with only 1 exception. When these thymectomized mice were irradiated, their immune response seemed to be effectively depressed and homologous transplants made 3 days after irradiation were accepted by both strains. In CFW thymectomized and irradiated mice the tumor enlarged and eventually killed the mouse, but in C3H thymectomized and irradiated mice the tumor did not enlarge, but persisted until 6 weeks, when the experiment was terminated and the animals were sacrificed and autopsied. However, when transplantation of C3H tumors to CFW mice was delayed until 2 months after irradiation to permit recovery of immunologically active tissues, most of the tumors were rejected after a brief period of acceptance.

Results of transplantation of neoplastic lymph node cells from C3H mice infected with leukemia were comparable to those from the tumor transplants. Both germ-free and germ-free thymectomized CFW mice were able to reject homologous lymph node cells from C3H mice; all but 1 of the C3H control mice developed leukemia.

Neonatal thymectomy alone does not deprive CFW and C3H mice of the ability to reject tumor homotransplants, nor does exposure to 300 R of X-radiation abolish this response in these thymectomized mice. The assault by microorganisms on the conventional mouse at a time when it has been deprived of most of its lymphoid tissue appears to overtax its immunologic defense and to induce a debilitated state in which it cannot successfully respond to a homotransplant.

¹ This work was supported by funds from the Office of Naval Research, NOnr-1623 [15]. P. M. Bealmear was supported by NIH Fellowship 1-Fl-GM-23, 250-01.

Received 5/27/66. Accepted 9/23/66.