AUTOCYTOTOXINS' 537 



tained, it is hardly conceivable that specific somatogenic cytotoxins 

 can be produced. 



Autocytotoxins. While these toxins possess some theoretic interest, 

 they are of very rare occurrence in experimental work. Certainly cells 

 of the kidney, liver, and other organs are constantly dying and being 

 replaced by new cells; the receptors of these cells are thereby set free, 

 and are capable of forming a union with the receptors of other cells, and 

 the possibility for the formation of autocytotoxins is established. Ac- 

 cording to Ehrlich, however, the side-arms anchoring the receptors of 

 the dead cells are sessile in nature, and are unlikely to cause overproduc- 

 tion, as in the case of antibodies for bacterial substances or for the cells 

 of other species. On the other hand, a simultaneous production of 

 antiautotoxins that counteract the autotoxins and preserve a delicate 

 physiologic equilibrium may occur, the whole subject being, however, 

 still in the experimental stage. 



Of most interest in this connection are the theoretic autonephrotoxins. 

 These may be produced when part of a kidney becomes disorganized 

 in the living body, as by means of a toxin. Theoretic autotoxins may 

 then be produced, which, acting upon other kidney cells, institute a 

 vicious cycle. Acting upon these assumptions, Ascoli and Figari 1 and 

 Lindeman 2 have proposed a new theory as to the pathogenesis of certain 

 of the nephritides. These observers would account for the cardiac 

 hypertrophy of nephritis by attributing it to the action of the nephro- 

 toxic serum in causing contraction of the peripheral vessels, with con- 

 sequent increase of blood-pressure; the nephritic nervous symptoms, 

 they believe, are due to the fact that the serum contains a neurotoxic 

 constituent. 



Lindeman has produced a toxic nephritis in dogs by giving them 

 injections of potassium bichromate, and found that the serum, although 

 free from the chromate, was toxic to other dogs, a finding he believed 

 due to the presence of antonephrotoxins produced in the first dog as a 

 result of the destruction of kidney cells. According to this view, the 

 original toxic cause of a degenerative nephritis would be less responsible 

 for the continuance of the process than would the formation of an 

 autonephrotoxin. While these conclusions are somewhat far-reaching, 

 they serve to indicate that the same processes operative in bacterial 

 infection and immunity may have an important relation to other patho- 

 logic conditions. 



1 Berl. klin. Wochenschr., 1902, xxxix, 634. 



2 Ann. de 1'Inst. Pasteur, 1900, xiv, 49. 



