Many chronic bacterial diseases, including tuberculosis and leprosy are characterized by bacterium with extremely slow growth rates. At the same time, it has been suggested that the ability of these microorganisms to survive for long periods Indaconitine within the host may be due, in part, to the SB225002 induction of peripheral tolerance as a result of a lacking ��signal�� required for T cell activation. We show that this as yet uncharacterized ��signal�� is growth of the pathogen itself, and that slow growing pathogens may be particularly effective at inducing chronic infection because, among other immune evasion tactics that they employ, they can actively ��trick�� the GDP mechanism. As an example, we consider leprosy. To emulate the 2 day doubling period of the leprosy bacterium relative to the more typical 100 minute doubling period of faster growing bacteria, we ran a simulation of the GDP system assuming a pathogen with a replication rate that is 29 times slower than the replication rate used to generate Figure 2 a). In Figure 5 we show that this extremely slow growing infection can, indeed, induce peripheral tolerance, minimizing T cell activation and potentially allowing the pathogen to invade the host against relatively little resistance. Just as the immune system occasionally fails to mount an adequate attack against a pathogen invader, it can also mistakenly trigger a vigorous immune response against a relatively harmless environmental antigen. When this happens, the stage is set for an allergic reaction, either immediately or, more commonly, upon a second encounter with that same stimulus. This type of immune system failure can also be explained in the context of GDP activation. As an example, in Figure 6 we repeat the GDP simulation for sudden injection of a non-replicating antigen. This time, however, we assume that the rate of diffusion of the antigen into and through the blood stream is slightly slower, and also that the foreign material has a slightly lower natural decay rate. In contrast to the earlier simulation, which suggested the development of peripheral tolerance towards the injection, the simulation in Figure 6 implies the onset of an immune response.