AN important characteristic of the immune system is the ability to discriminate between antigens expressed on normal tissues within the individual and the many foreign antigens expressed on normal tissues of other species (xenoantigens) and even on normal tissues of members of the same species (alloantigens). Thus, although the immune system readily destroys inoculated xenogeneic and allogeneic tissue, autoimmune damage to normal, autologous tissue is rare. The rejection of inoculated foreign tissue is thought to reflect an immune surveillance mechanism by which an individual could detect and eliminate his own aberrant cells expressing abnormal surface antigens1. This mechanism may be important in restricting the development of many nascent tumours1–3. Little is known, however, concerning either the mechanism by which the immune system destroys nascent tumours or the mechanism preventing the immune system from inflicting autoimmune disease. The finding of near normal tumour incidence in congenitally athymic (nude) mice has suggested that immune surveillance may not involve the activity of thymus-dependent immunity but rather be a function of humoral immunity4. In this respect it is interesting that sera of both normal and nude mice contain antibodies reactive with a wide variety of tumour cells5,6. There is no evidence, however, that these antibodies function in the destruction of nascent tumours or that they are necessarily directed against tumour specific rather than normal tissue associated antigens. It has been demonstrated that naturally occurring antibodies (NOA) reactive with the neural tumour cell line NB1 can be specifically absorbed by syngeneic normal brain tissue6. We demonstrate further the autoantibody nature of certain NOA by documenting the occurrence in normal mouse sera of IgM antibodies reactive with autologous thymus cells.
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About this article
Springer Seminars in Immunopathology (2005)
Clinical Rheumatology (1986)