Physiological Role of the Immune Reaction
DOI:
https://doi.org/10.5644/Radovi.175Abstract
There are experimental data which suggest that the immune reaction should have a physiological role, the usual immune response being only an expression of the same phenomenon resulting upon the inoculation of unfamiliar antigenic molecules.
Besides experimental data the attention should be paid to the well-known “instructive” and “selective” theories of the immunological reaction. If »instruction« of immunologically competent cells would play a predominant role in the immunological response, then the cells should be omnipotent. This would imply in responsible cells occurring either change or depression of pacific gene(s) upon inoculation of an unfamiliar antigen. Whatsoever the mechanisms of changes in stimulated cells are, the ability of cells to accept all kinds of antigens could be explained by assuming the existence of a great many of different antigen receptors being scattered over the cell membrane.
This way of thinking conduces to the study of receptors for proteins (also protein hormones) on the surface of cell membrane. Differentiated cells have specific receptors on the surface of their cell membranes, and there is no reason to call in question this quality in immunologically competent cells. These postulates are in the ground of the Burnet’s clonal selection theory. Receptors as well as antigens are expressions of the gene’s activity in cells. Thereafter it appears conceivable that the cells displaying the same function and producing the same product possess common antigens even if they originate from different species (organ-specific antigens). Despite the existence of organ-specific antigens the autoagressive diseases are however infrequent. This phenomenon of autoagressive diseases belongs to the problem of “self-not self-recognition”, or even “self-tolerance”. It seems that the tolerance of allogeneic or xenogeneic antigens in chimeric organisms as well as of tumour antigens in tumorous organisms belongs to the same phenomenon.
There appears to be nothing for it, but to assume that organisms cover antigenic sites of “own” cells with complementary proteins (immunoglobulins, protein-hormones or other proteins). Consequently, the same should occur in chimeric animals and in tumour bearing organisms. By covering the antigenic sites of “own”, foreign or tumour cells they become inaccessible to the destructive action of cellular immunity. However, these protein coats could act as integral part of cell membranes thus enabling the cells to function and to survive.
Some data speak strongly in favour of the described hypothesis. Anaphylactic reaction is known to be mainly due to the reaction of immunoglobulins adsorbed on the surface of cell membranes of” shock-organ(s)”.
Tanned and trypsinized erythrocytes are suitable for adsorption of proteins. Erythrocytes and polymorphonuclear leukocytes can be washed from coating immunoglobulins thus undergoing the loss of their function as well as the ability to survive.
It appears interesting to note that Wistar rats displaying a high incidence of experimental allergic encephalomyelitis have in serum a low titter of complement fixating antibrain antibodies. Lewis rats show an opposite picture.
Enhancement of tumour growth with complementary immunoglobulins speaks strongly in favour of the theory of the protective activity of proteins coating the specific antigenic sites of cell membranes.
It has been tried to produce de-enhancement by anti-serum antibodies and cathepsins acting mostly specifically upon gamma, (and beta) globulins. Indeed, rats inoculated with Yoshida ascites sarcoma cells survived longer if injected intravenously with rabbit antiserum against rat serum or cathepsins from leukocytes of swine blood.
Regarding to cellular immunity the best way to learn its physiological role seems to be by understanding the phenomenon lying in the ground of the hypothesis of allogeneic inhibition. This mechanism would be responsible for the elimination of all newformed cells or antigen(s) which were not suitable to be protected by coating proteins.
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