摘要：

Summary. There is, to date, no firm experimental proof of a direct or indirect causal relationship between the presence of the type 'C' virus particles and any of the aberrations shown by the NZB mice. There are, nevertheless, considerable precedents for assuming that the virus may be responsible for the malignant proliferation of the reticulum cells, notably its ultrastructural similarity to other murine leukaemia viruses known to cause lymphocytic, erythroid, or myeloid leukaemia. There murine leukaemia viruses have certain important characteristics which must affect their biological activities. There is also little doubt that viruses can modify both the target cells and the immunological apparatus of their hosts and so could, theoretically, precipitate autoimmune reactions. They can cause proliferation of erythroblasts, or of im-munocytes such as lymphocytes, and the transmissible agent of Aleutian mink disease undoubtedly evokes plasmacytosis and an increase in serum immunoglobulin. Viruses can provoke the formation of new antigens on cell surfaces, or leave their antigenic footprints within cell nuclei, or elicit the production of specific circulating antibody. Some murine leukaemia viruses can deprees the classical antibody response to exogenous antigenic stimulation, and some are present in prenatal life and possibly induce a state of tolerance. As far as the: NZB mice are concerned, the experimental evidence available points to the following conclusions. The autoantibody is predominantly IgG and can sensitize normal mouse erythrocytes. Florid positive antiglobulin reactions occur in germ-free NZB mice shielded from external viral or bacterial antigens [8] so that the precipitating stimulus is, presumably endogenous. Positive Coombs reactions develop, and can indeed be accelerated, in NZB mice depleted of lymphocytes by neonatal thymectomy [6] indicating that the immune response is humoral rather than cell mediated. Splenic germinal centres are numerous and active and the plasma cell population is often increased in intact or thymectomized conventional, as well as in germ-free NZB mice [5, 6, 8]. High serum levels of IgM are characteristic of conventional intact NZB mice and are not affected by thymectomy or isolation in a germ-free environment [6, 81. Type 'C' virus particles are ubiquitous in NZB mice of all ages, including embryos, and can bud from the surface of plasma cells, lymphoid cells, erythroblasts and reticulum cells in most organs of the body. Thus, the argument as to whether the basic flaw responsible for the autoimmune reactions unique to this strain is an abnormality of the target erythrocytes or of the antibody-producing cells remains unresolved.

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