PATHOLOGY OF THE IMMUNE RESPONSE 



giant cells in measles. This suggests that in addition to the 

 protection which is known to be mediated by circulating 

 antibody, immunity is also associated with cellular changes 

 which are sufficient to prevent multiplication in lymphoid 

 tissue. The possibility that these viruses of long incubation 

 period actually spend the period of incubation in potentially 

 antibody-producing cells, may provide a fertile working 

 hypothesis for the interpretation of what is, despite Fenner's 

 work on ectromelia, still one of the major unsolved problems 

 of pathology. It would be of special interest to know the 

 response of a child with agammaglobulinaemia to a virus of 

 the yellow fever or mosquito-borne encephalitis type in 

 which viraemia occurs early and in which current teaching 

 ascribes immunity wholly to serological factors. 



(ii) On the interpretation of haemolytic disease presented 

 earlier, we must consider that in Rohn's case the same basic 

 change in one or more mesenchymal clones has occurred. 

 The occurrence of excessive erythrophagocytosis might have 

 several interpretations not mutually exclusive, {a) Abnormal 

 'stickiness' of lymphocytes in the spleen for erythrocytes 

 might hold undue numbers to the walls of the sinusoids, and 

 phagocytosis by macrophage cells would be expected to 

 follow, {b) Contact of red cell determinant with specifically 

 modified lymphocyte might detach cytoplasmic fragments 

 which would sensitize the erythrocyte for phagocytosis. 

 {c) Macrophages might develop from modified clones and 

 show specific phagocytic activity for the red cells. This third 

 alternative is a little out of line with our general conceptions 

 and could only be considered if the other two were 

 inadmissible. 



(iii) In more than one place in our discussion of the 

 pathology of the immune response, we have spoken of the 

 necessity for some homeostatic mechanism to eliminate or 

 temper the effect of the inevitable occasional mutation to 

 a 'forbidden' pattern. It may be that the frequency with 

 which young persons with agammaglobulinaemia develop 



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