Cell-mediated and neural control of morphostasis

Abstract

Morphostasis refers to the maintenance of the differentiated state of tissues in an adult individual and it represents a basal event of homeostasis and the organism's existence. Most of the cells in the body are arrested in their differentiation at a certain point related to their optimal function. Evidence is rapidly accumulating on the general role of immunoglobulin-gene superfamily (IGSF) domains in the non-immune control of behavior of cells in various tissues. A novel ‘tissue control system’ (TCS) has been suggested, supporting the differentiation of tissue cells in an adult organism and functioning via the IGSF domains and cell-mediated control of morphostasis. We assume here that the morphostasis is established epigenitically during the early adaptive period. With its termination, coinciding with the attainment of an organism's immunocompetence, the combination of cell surface markers of the most mature cells in tissues are encoded in the TCS as the stop-signal (SS). This stage of tissue differentiation is maintained during further life: upon recognition of SS the committed TCS element does not stimulate further differentiation of the cell, i.e. it exhibits a stop-effect (SE). Each tissue-specific cell line has only one or no SE established depending on its presence or absence during development, respectively. The only way to escape an established SE and continue in differentiation is to change at least a portion of the SS. Hormones might act here directly, by conformation of their cell surface receptors recognized as a portion of SS, or indirectly, by influencing proteosynthesis of cell surface markers. A genetic disposition to certain disease can be viewed as a genetic alteration of an appropriate timing of a certain tissue development during the early adaptive period. Additionally, late adaptive periods may occur during further life under circumstances that alter the integrity of TCS. This can be beneficial for appropriate adaptation to the environment, but an altered adaptation to certain tissue may be the source of tissue dysfunction and serious diseases. The TCS is suggested to be supervised by the autonomic nervous system maintaining the proportionality of all tissues. Age-related regressive changes in the CNS are expected to also be responsible for regressive changes in TCS function with subsequent decline of TCS-dependent function of certain tissues. The later the tissue differentiates in ontegeny, the earlier the TCS support of its function expires. Discovery of factors determining and ensuring morphostasis may provide a basis for revolutionary changes in the clinical treatment of diseases associated with morphofunctional alteration which lead to metabolic dysfunction, autoimmunity, chronic inflammation or hyperproliferation.