Theory of Mechanical Immunology

Numerous autoimmune illnesses are not only caused by defects of the immune system but may also be caused by defects in anatomical barriers. Morphologically, most of these barriers consist of basal membranes combined with epithelial cells or, more precisely, their cell membranes. In many organs, these barriers are associated with specialized, phagocytizing cells (e.g. histiocytes, macrophages, microglial cells A and B cells in joints). A collapse of these anatomical barriers caused either by mechanical effects (invasion by micro-organisms) or destructive tumor growth, leads to contact between macrophages and the CD4 lymphocytes, with protein structures of the cell interior. In principle, many intracellular structures should be able to function, on this basis, as potential antigens via MHC II. Contact between intracellular structures and the immune system first leads to a restricted local immune reaction and then to local autoantibody production. In order that a systemic immune reaction can take place, the contact between macrophages, CD4 cells and intracellular structures must occur over a long period and with high intensity. As a desirable, remote target, new clinical therapeutic strategies can be developed from this theory, for example, for patients with cell damage. Examples of such illnesses are, amongst others, cardiac infarcts and strokes as well as accident traumas. An immunosuppressive therapy should reduce the immune reply in all the patients mentioned and thus reduce the volume of the cell damage, giving the patient an advantage.