This returns us to our original question, namely, the relationship between what is to be eliminated and what is to be induced. Neither the pathogen alone (pathogenicity, danger) nor the host alone (localization, context, tuning) could be the source of signalling information
to determine class. The pathogen is recognized by paratopes that are informationless with respect to effector class. The normal tissue is protected by tolerance and, therefore, has no need to signal class discrimination. selleckchem Further, there could be no selection pressure for host self-components to signal optimization of their own destruction, and the same could be said for pathogens. Only the pathogen–host interaction, which has an appropriate traumatic consequence for the host tissue, can initiate a meaningful signal. Given three effector ecosystems to which the M-ecosystem can differentiate, a minimum of three
trauma signals need be postulated. What elements of the M-ecosystem read them? After passing through Module 2, the activated T/B cells of the M-ecosystem enter Module 3. The eTh0 delivering Signal 2 is required to activate the iT/B-cell preparatory to their differentiation into the various effector classes. Given this, the host-Eliminon trauma signal can be envisaged to be read either: 1 directly by the iT or iB cell undergoing activation, or There are all manners of variation Dynein that can be envisaged for these pathways but, for our purpose, consideration of the three extremes is sufficiently check details illustrative. To determine whether the pathway is direct
or indirect will require that the tissue-pathogen trauma signals be identified (see discussion of Hypothesis VII in ref. ). Here, let us focus on the difficult question of the relationship between the postulated trauma signals and the effector ecosystem which is induced. In the end, these signals must originate from the Eliminon–tissue interaction. The innate system that recognizes directly a portion of the pathogenic universe can contribute to effector class determination, but it is predictably limited. One reasonable postulate to explore would be that there is a family of differentiation signals originating from the Eliminon–tissue interaction that is read by the initial state iTh to become one or another member of the eTh-family that regulates which defensive effector ecosystem will be optimal. As the pathogenic universe is large compared to the number of effector ecosystems, the immune system must have a way to group Eliminons. This grouping must be based on germline-selected recognition of the signals from traumatized tissues (referred to as the ‘Trauma Model’)[6, 8].