It is proposed that immunosuppression may be the end result of a multitude of events all leading to microangiopathic changes in the bone marrow. The mechanisms by which medullary microangiopathy leads to immunoparalysis are not understood but it is reasonable to assume that local ischemia may interfere with angiogenic production of immunocytes. Secondly, it is recognized that immunohomeostasis is dependent on a large complexity of commonly evolved systems including the clotting, inflammatory, fibrinolytic, complemental and immune processes at play with endotoxin, insoluble surfaces, metabolic analogues and immunogenic glycoprotein elements offered by exogenous biopathogens and/or somatic mutants. Finally, it appears that neurochemical mediation and hypothalamic nuclei may have a direct influence on those coevolved systems and determine the ultimate direction and kinetics of their reactions.
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