Morphostasis (tissue homeostasis) is a complex process consisting of three circumstances: (1) tissue renewal from stem cells, (2) preservation of tissue cells in a proper differentiated state and (3) maintenance of tissue quantity. This can be executed by a tissue control system (TCS) consisting of vascular pericytes, immune system-related components--monocyte-derived cells (MDC), T cells and immunoglobulins and autonomic innervation. Morphostasis is established epigenetically, during the critical developmental period corresponding to the morphogenetic immune adaptation. Subsequently, the tissues are maintained in a state of differentiation reached during the adaptation by a 'stop effect' of MDC influencing markers of differentiating tissue cells and presenting self-antigens to T cells. Retardation or acceleration of certain tissue differentiation during adaptation results in its persistent functional immaturity or premature ageing. The tissues being absent during adaptation, like ovarian corpus luteum, are handled as a 'graft.' Morphostasis is altered with age advancement, because of the degenerative changes of the immune system. That is why the ageing of individuals and increased incidence of neoplasia and degenerative diseases occur. Hybridization of tumour stem cells with normal tissue cells causes an augmentation of neoplasia by host pericytes and MDC stimulating a 'regeneration' of depleted functional cells. Degenerative diseases are associated with apoptosis. If we are able to change morphostasis in particular tissue, we may disrupt apoptotic process of the cell. An ability to manage the 'stop effect' of MDC may provide treatment for early post-natal tissue disorders, improve regenerative medicine and delay physical, mental and hormonal ageing.
© 2011 The Author. Scandinavian Journal of Immunology © 2011 Blackwell Publishing Ltd.