THE PROBABLE MECHANISM OF THE REACTION 109 



amount of antiferment present in the exudate which, of course, 

 inhibits digestion. If now the antiferment is lowered, either because 

 of the change in the reaction or because it is saturated by protease 

 mobilized from some other organ, while at the same time protease 

 and ereptase are liberated locally, the patient will be detoxicated 

 promptly as digestion changes from a state of inhibition to one of 

 acceleration. In this case the liberation of the true protease would 

 be associated with detoxication. 



Let us assume on the other hand that we are dealing with a 

 quiescent tubercle, one that is sufficiently protected by a connective 

 tissue encapsulation to prevent the absorption of toxic material from 

 the focus that has been walled off. If for any reason the identical 

 serum reaction or local reaction that has been hypothecated above 

 should occur in such a patient quite the opposite clinical effect would 

 ensue. The liberation of protease would, along with the reduction 

 of the antiferment (protective) titer, promptly begin to digest away 

 the connective tissue of the capsule and allow some of the toxic 

 material from the focus and the native proteins of the focus as well, 

 to escape into the general circulation with a resulting intoxication of 

 the patient and activation of the focus. Fluctuation of the protease 

 titer can therefore be assumed to influence pathological processes in 

 a fundamental way and at times with diametrically opposite clinical 

 results. But this fluctuation of the protease is under the control 

 to a certain extent of the antiferment or inhibitory substance, which 

 thereby becomes an integral part of the balance which we have 

 under consideration. Here we leave the enzymes and have to deal 

 very probably with lipoid substances. The antiferment is not an 

 antibody in the immunological sense, although it was early so con- 

 sidered; it consists of the highly dispersed unsaturated lipoids of 

 the serum and of the lymph and the tissues.* Its titer varies there- 

 fore with at least three conditions: (1) the amount of the lipoids 

 present, (2) the dispersion of the lipoids, (3) and the chemical struc- 

 ture, that is, the degree of unsaturation. All these conditions are 

 subject to considerable variation and any of them may cause a 

 change in the titer. 



Thus changing of the dispersion by acidifying, by salting and 

 by heating to a sufficient degree inactivate the antiferment, physical 

 adsorption by certain chemically inert adsorbing surfaces such as 

 fuller's earth, barium sulphate, agar, etc., lowers the titer; solution 

 of the lipoids by chloroform, ether, acteone, and certain of the alco- 

 hols removes the antiferment from the serum. The soaps of the 

 unsaturated fatty acids are perhaps the most comparable substances 

 which are available and with them one can simulate many of the 



* The evidence concerning the nature of the antiferment is conflicting. Bach 

 and Teal were not able to coafirm the results of Jobling and Petersen. The 

 papers of Tachigara, Fujimoto, etc., should be consulted. 



