Confirmation of the “protein-traffic-hypothesis” and the “protein-localization-hypothesis” using the diabetes-mellitus-type-1-knock-in and transgenic-murine-models and the trepitope sequences

Abstract

As possible mechanisms to explain the emergence of autoimmune diseases, the current author has suggested in earlier papers two new pathways: the “protein localization hypothesis” and the “protein traffic hypothesis”. The “protein localization hypothesis” states that an autoimmune disease develops if a protein accumulates in a previously unoccupied compartment, that did not previously contain that protein. Similarly, the “protein traffic hypothesis” states that a sudden error within the transport of a certain protein leads to the emergence of an autoimmune disease.The current article discusses the usefulness of the different commercially available transgenic murine models of diabetes mellitus type 1 to confirm the aforementioned hypotheses.This discussion shows that several transgenic murine models of diabetes mellitus type 1 are in-line and confirm the aforementioned hypotheses. Furthermore, these hypotheses are additionally inline with the occurrence of several newly discovered protein sequences, the so-called trepitope sequences. These sequences modulate the immune response to certain proteins. The current study analyzed to what extent the hypotheses are supported by the occurrence of these new sequences.Thereby the occurrence of the trepitope sequences provides additional evidence supporting the aforementioned hypotheses.Both the “protein localization hypothesis” and the “protein traffic hypothesis” have the potential to lead to new causal therapy concepts.The “protein localization hypothesis” and the “protein traffic hypothesis” provide conceptional explanations for the diabetes mouse models as well as for the newly discovered trepitope sequences.