A role for microchimerism in obesity and evolution?

Cells exchanged between individuals, such as those passing the placenta from the mother to the child and vice versa, may survive in the fetal or maternal circulation and tissues for decades and result in microchimerism. Microchimeric cells may play a role in tissue repair, but they have also been implicated as inducers of chronic inflammation, leading to autoimmunity or even cancer. Here we propose that microchimerism may play a more fundamental role in health and evolution by setting a limit to genomic variability within populations. This means that microchimerism allows immune recognition of genomic differences between donor and host which may, depending on the level of variability, cause chronic inflammation. Since chronic inflammation has been experimentally linked to metabolic syndrome, we propose that genomic variability could affect the individual's weight. Thus, metabolic syndrome, which is a growing health problem, may not only result from our lifestyle, but in part be caused by global migration and the increasingly diverse origin of the present human population. Moreover, since in nature weight gain is associated with an increased risk of predation, we discuss the possibility that immunological incompatibility normally promotes the continuous development of new species.