Abstract
Basic features of the symmetrical network theory are reviewed briefly. Postulated differences in network connectivity between helper and suppressor cells are then related to the properties of the cell surface antigens they each express. A resolution of the I-J paradox is suggested in the context of the symmetrical network theory. A “centre pole” model for I-J is described, in which I-J is antianti-self. The theory includes the experimentally testable hypothesis that the difference in I-J between the two key strains B10.A(3R) and B10.A(5R) is not genetic, but rather reflects differences between self-stabilizing sets of T cell idiotypes, that are transmitted from generation to generation via a maternal influence on developing T cell repertoires.
Ziegler and Stites (1986) have published an autoimmunity theory of acquired immunodeficiency syndrome (AIDS). The I-J centre pole model leads to a network theory of AIDS, that is similar to the Ziegler-Stites theory, but a little more complete. It is suggested that the disease involves anti-anti-self and anti-anti-anti-self immune responses, resulting in a fundamental destabilization of the network. The theory provides several new experimentally testable predictions, including ideas on how to prevent the disease.
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Hoffmann, G.W. (1988). On I-J, a Network Centre Pole and AIDS. In: Sercarz, E.E., Celada, F., Mitchison, N.A., Tada, T. (eds) The Semiotics of Cellular Communication in the Immune System. NATO ASI Series, vol 23. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-73145-7_24
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DOI: https://doi.org/10.1007/978-3-642-73145-7_24
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