This suggests that MSC may represent a novel therapeutic target either independently or by inhibiting the effects of MSC on cadherin expression in breast cancer cells. To this aim, Th17 cells appear at sites of inflammation with rapid kinetics and possibly bridge the gap between innate and adaptive immunity by attracting other Th cells to the inflammatory site. Various recent studies have emerged suggesting that Th17 cells are essential in autoimmune diseases. First, mice deficient for the Th1 effector cytokine IFNc develop enhanced experimental autoimmune encephalomyelitis, and the absence of IL-23, results in a lack of Th17 cells and protection from EAE and collagen-induced arthritis. Second, IL-17 has been found to be increased in patients with rheumatoid arthritis, multiple sclerosis, inflammatory bowel disease, psoriasis and seronegative spondylarthritides. The populations considered in this paper have first evolved with different error rates for a number of generations, large enough to reach mutation-selection equilibrium. Their degree of adaptation at equilibrium decreases with the BIBW2992 EGFR/HER2 inhibitor mutation rate. However, when confronted with a new selective pressure, these populations can experience adaptive advantages if they vary their mutation rate. This means that the optimal mutation rate for an adapting population can be quite different from the optimal mutation rate under conditions that remain constant for a long time. In particular, for populations optimized at low mutation rates an increase of this parameter may be favourable, while for populations replicating under high mutation rates a decrease would be advantageous. These results can be partially explained as a consequence of the different dynamics of the adaptive process at different mutation rates, and by the influence of the composition of the population in its subsequent ability to adapt to new selective pressures. Adaptation is a complex phenomenon in which, in addition to the diversity generated de novo, the nature and distribution of existing mutants plays an important role. In our simulations, populations able to attain a high degree of adaptation to a new selective pressure in a short time were those previously optimized at moderate to high values of m1. After changing the target structure, populations optimized at high mutation rates give rise to highly diverse, non-adapted populations, which contain in their mutant distributions molecules closer to S2 at g=0 than populations optimized at lower error rates. These populations respond better when the mutation rate is decreased, thus enhancing the presence of structures close to S2. On the other hand, populations optimized at m1 =0.002 benefit from an increase in the mutation rate to rapidly adapt to the new target structure. At g=0, these populations display lower diversity, and the molecules closest to S2 have typical distances larger than those in populations optimized at high error rates.