[4][5] The scope of the symmetrical network theory developed by Hoffmann includes the phenomena of low dose and high dose tolerance, first reported for a single antigen by Avrion Mitchison,[6] and confirmed by Geoffrey Shellam and Sir Gustav Nossal,[7] the helper[8] and suppressor roles [9] of T cells, the role of non-specific accessory cells in immune responses,[10] and the very important phenomenon called I-J.
Jerne was awarded the Nobel Prize for Medicine or Physiology in 1984 partly for his work towards the clonal selection theory, as well as his proposal of the immune network concept.
[13][3] He developed a detailed immune network theory based on symmetrical stimulatory, inhibitory and killing interactions.
[3] Tabs are able to exert a powerful suppressive effect on the production of IgG antibodies in response to foreign substances (antigens), as was demonstrated rigorously by Takemori and Tada.
[14] Hoffmann and Gorczynski have reproduced the Takemori and Tada experiment, confirming the existence of specific T cell factors.
An immune network model for HIV pathogenesis was published in 1994 postulating that HIV-specific T cells are preferentially infected (Hoffmann, 1994, op cit.).
[22] These three quasispecies apply selective pressure on one another and co-evolve in such a way that the viral epitopes eventually come to mimick the V regions of the main population of T regulatory cells.
This results in the dysregulation of the immune system, and eventually to other further anti-self reactions, including against the T helper cell population.
Hence in this model, the onset of AIDS is primarily an auto-immune reaction triggered by the cross-reaction of anti-HIV antibodies with T regulatory cells.
Once this induced auto-immunity sets in, removing the HIV virus itself (for instance via HAART) would not be sufficient to restore proper immune function.
In fact such vaccines may do more harm in certain cases, since if the original infection comes from a source with a "mature" infection, those virions will have a high affinity for anti-HIV T helper cells (see above), and so increasing the anti-HIV population via vaccination only serves to provide the virus with more easy targets.
[24] This is a phenomenon that makes no sense in the context of clonal selection, without taking idiotypic network interactions into account.