Abstract
AbstractThe symmetrical immune network theory is based on Jerne’s network hypothesis. An improved version of the theory is presented. The theory is characterized by symmetrical stimulatory, inhibitory and killing interactions between idiotypic and antiidiotypic immune system components. In this version killing is ascribed to IgM antibodies, while IgG antibodies are stimulatory. In the symmetrical immune network theory T cells make specific T cell factors, that have a single V region, and are cytophilic for non-specific accessory cells (A cells, including macrophages and monocytes) and play a role in the system switching between stable steady states. A recurring theme in the theory is the concept of co selection. Co-selection is the mutual positive selection of individual members from within two diverse populations, such that selection of members within each population is dependent on interaction with (recognition of) one or more members within the other population. Prior to exposure to an antigen, antigen-specific and antiidiotypic T cells are equally diverse. This equality is a form of symmetry. Immune responses with the production of IgG involve co selection of the antigen-specific and antiidiotypic classes with the breaking of this diversity symmetry, while induction of unresponsiveness involves co-selection without the breaking of diversity symmetry. The theory resolves the famous I-J paradox of the 1980s, based on co selection of helper T cells with some affinity for MHC class II and suppressor T cells that are anti-anti-MHC class II. The theory leads to three experimentally testable predictions concerning I-J. The theory includes a model for HIV pathogenesis, and suggests that polyclonal IgG from many donors given in immunogenic form may be an effective vaccine for protection against infection with HIV. Surprisingly, a mathematical model that simulates the autonomous dynamics of the system is the same as one that models a previously described neural network.
Highlights
The symmetrical immune network theory is based on Jerne’s network hypothesis
Many papers published in the 1970s and 1980s reported that T cells make molecules that were called specific T cell factors, and that are involved in the regulation of the production of antibodies by B cells
As discussed below, the I-J paradox can be resolved in the context of the symmetrical immune network theory, and the data demonstrating both the existence of I-J and the existence of tabs stands
Summary
The symmetrical immune network theory is based on Jerne’s network hypothesis. An improved version of the theory is presented. The theory is characterized by symmetrical stimulatory, inhibitory and killing interactions between idiotypic and antiidiotypic immune system components. In this version killing is ascribed to IgM antibodies, while IgG antibodies are stimulatory. Prior to exposure to an antigen, antigen-specific and antiidiotypic T cells are diverse This equality is a form of symmetry. Specific T cell factors play a central role in the symmetrical network theory, and for the sake of brevity I will call them tabs. As discussed below, the I-J paradox can be resolved in the context of the symmetrical immune network theory, and the data demonstrating both the existence of I-J and the existence of tabs stands The reasoning has been “There is no gene for I-J, I-J does not exist, molecules that express I-J determinants do not exist.” as discussed below, the I-J paradox can be resolved in the context of the symmetrical immune network theory, and the data demonstrating both the existence of I-J and the existence of tabs stands
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
