When a micro-organism penetrates the body, defensive mechanisms of the non-specific innate immune system come into play, such as soluble chemical factors (bactericidal lysozyme, acute phase proteins, interferons), extracellular killing (NK cells, eosinophils), and phagocytosis (macrophages, polymorphonuclear neutrophils). This innate immune system is supported by the specific acquired immune system which comprises of B- and Tlymphocytes. These lymphocytes are educated to distinguish between self (host) and non-self (foreign) molecules by means of specific receptors on their cell surface and are further endowed with specific memory. B lymphocytes, called so because they differentiate in the bone marrow, participate in the immune response by producing antibodies that fix to antigen by their specific recognition site. These antibodies can mediate different functions, including opsonization, complement activation, antibody-dependent cell mediated cytolysis and neutrophil, basophil, or eosinophil activation. T cells, designated thus because they differentiate in the thymus, control the activation of cells of the innate and acquired immune system by producing lymphokines and playa role in killing aberrant cells such as virally infected cells and some tumour cells. Although we generally benefit from the actions of the immune system, there is an other side of the coin. When a diseased organ is replaced by a healthy transplant of another individual (not being the recipients identical twin-brother or sister), the cells of this transplant are regarded as non-self by the immune system of the recipient. As a result, the recipient's immune system will bring all its power into play to get rid of this "intruder". To prevent allograft rejection, the immunity of the transplant recipient is reduced with immunosuppressive drugs which must be taken throughout the patient's life.

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Erasmus University Rotterdam
hdl.handle.net/1765/17138
Erasmus MC: University Medical Center Rotterdam

van Emmerik, N. (1998, June 24). The involvement of donor specific CTL in cardiac transplant rejection: relevance of avidity. Retrieved from http://hdl.handle.net/1765/17138