Now we are in a position to consider the elements that should be factored into a model of the regulation of class. 1  There are effective

and ineffective classes in ridding a given Eliminon. The ineffective classes can either block the functioning of the effective classes and/or be a serious source of immunopathology. Therefore, a choice must be made between them [8]. The adaptive immune response cannot be lit up like a Christmas tree. The question how many categories of response and how many incompatible classes there FDA-approved Drug Library solubility dmso are needs analysis. Associative recognition of antigen is obligatory if coherence and independence are to be respected. As cited earlier, two solutions as to mechanism have been proposed, either the unique STAT inhibitor usage of the B cell as an APC for the activation of T-helpers [35] or presentation of the antigen-derived peptides by an APC in a signalling patch [6, 8]. This should be an active area of investigation as a solution to the mechanism of T-T interactions in ARA (or its functional equivalent) on an APC is central. 4  The induction of a given class of regulatory eTh requires (i) processing and presentation of the Eliminon by the APC and

(ii) an interaction in ARA of iTh-APC-eTh (delivery of Signal 2) in the presence of a class-determining trauma signal referred to as Signal 3. Given these considerations, what questions should we ask that must be answered by

any model? Any paratope that binds multiple NS epitopes has an increased probability of seeing in the host’s antigenic load two Eliminons that require different effector classes to rid them. Polyspecificity tends to blur the ability of the system to maintain coherence and independence of responsiveness. The acceptable limits on the degree of polyspecificity need a detailed analysis by modelling. This is a to-be-resolved problem that is cited here simply for completeness. This question was introduced earlier but because it is the single most important issue to settle Teicoplanin before constructing a model that we return to it. The adaptive system sees pathogens and their products to which the innate system is blind. Further, the adaptive system sees everything that the innate system sees. Therefore, it appeared reasonable that a somatically generated random repertoire would be coupled to the appropriate effector using a somatic learning process. Such a process could only be based on a biological assay of the effectiveness with which the Eliminon is ridded. This led to a very seductive theory that was termed the Adapton Model [6, 45]. The theory failed, interestingly enough, not because of any definitive experimental test, but because it could not be reduced to a testable mechanism.