The first part of the reversal immune surveillance hypothesis (RISH. I) describes the conceptual framework of the immune system as a homoeostatic mechanism for the control of cell differentiation and replication. The thymic dependent lymphocytes (T-cells) are considered to be tissue specific and identify aberrations in the cell surface pattern (antigens), that represent that particular cell type. The T-cells may then recruit antibody forming B-lymphocytes (B-cells) to produce antibodies (humoral response) to the cell surface antigens in order to return the cell surface pattern to its correct state. The antigens may also be removed from the cell surface as immune complexes by the complement system, which under normal conditions does not cause cell lysis. The cellular arm of the immune system, that of killer cells or activated macrophages are considered to be primarily involved with tissue remodelling. Whether or not the humoral or cellular arm of the immune system is activated depends upon the antigens displayed by the stimulating cell. The proposed system, which is self monitoring, is considered to have ovolved from the invertebrates through to the vertebrates to become more complex in the mammals. Therefore the immune system is considered to be based on the identification of self and self-foreignness, rather than on foreignness per se. In RISH. II the original concept of RISH. I has been refined and discussed in more detail. The necessity for lymphocyte motility, in order to inspect cells in their care, and the effect of antigen stimulation on this motility is considered in terms of tissue specific T-cells. Although lymphocyte motility does not depend upon major histocompatability antigens (MHCA), these antigens do appear to be involved in tissue specific cell surface patterns. It is possible that the MHCA evolved among single cellular organisms, as a clone or species identification system and with the evolution of multicellular organisms, these antigens become partly incorporated into tissue specific cell surface patterns. Such a situation may explain the presence of a common T-cell antigen which may enable T-cells to identify and monitor each other. In addition thymic dependent lymphocytes may undergo maturation in the thymus to become cell surface pattern restricted, which may involve some MHCA. The tissue specific T-cell is considered to function both as a helper and suppressor cell in the humoral response by increasing or down regulating its receptors for IgM and IgG respectively. The regulation of the immunoglobulin receptors on the T-cell being determined by the amount of antibody synthesised by the B-cell, which may regulate its own antibody synthesis by a similar immunoglobulin receptor mechanism. Depending on the antigen eliciting the immune response, the tissue specific T-cell may also function as a killer cell (tissue remodelling) using a mechanism of immunoglobulin receptor regulation for IgM and IgG. If “free” antigen or immune complexes are available the macrophages may enter the system described and act as an amplification step. Both the humoral and cellular response can be intergrated by the macrophage and thus both types of responses may occur at similar times. The regulation of the proposed system is considered to operated on a feedback network, whereby the first set of responding cells is inhibited by a second set in an exponential fashion. Based on the above system antibody synthesis would follow a pulsatile pattern. In addition such antibodies may be involved in regulating enzyme activities and the transcription of DNA in modulating cell surface patterns. Based on RISH the immunology of pregnancy, embryogenesis, ageing, autoimmunity and cancer are discussed.