PATHOLOGY OF THE IMMUNE RESPONSE 



many strains of haemolytic streptococci and R pneumo- 

 cocci. Neither of these tests is generally regarded as being 

 more than indicative of the presence of abnormal adven- 

 titiously reactive globulin in the serum. The Cavelti's (1945) 

 finding that tissue extracts from relevant tissues treated with 

 streptococci reacted specifically has not been confirmed. 

 There is, however, a considerable number of individually 

 not very impressive experiments which suggest that the co- 

 existence of streptococcal or staphylococcal infection or of 

 products from these organisms confers 'antigenicity' on 

 otherwise non-antigenic body components. 



The problem of the aetiology and pathogenesis of the 

 collagen diseases is far from solved. In all probability the 

 causation is multiple and genetic, infective, immuno- 

 logical and 'stress' components may all play a part. Here 

 we are concerned only to suggest that the clonal selection 

 approach may have something to offer for the understanding 

 of the immunological aspects of these diseases. 



In view of the importance that has been ascribed to the 

 lymphoid cells in immune processes, the primary approach 

 will be to seek an explanation for the infiltration of lympho- 

 cytes and plasma cells in the tissues involved in the process. 

 These cells are associated with areas of connective tissue that 

 have undergone fibrinoid degeneration. Largely on the basis 

 of Rich and Gregory's (1943 a, b; 1944) experiments, in 

 which rabbits received large doses of soluble foreign proteins 

 intravenously, such a histological picture is widely held to be 

 an index of the occurrence of antigen-antibody reaction in 

 the tissues. Even in the case of rheumatic fever or acute 

 nephritis, where there is clear association with streptococcal 

 infection, there is no real evidence that streptococcal antigens 

 are located in the target organs. If there is an immune reac- 

 tion concerned, it is directed against tissue components. 



As in the case of the haemolytic anaemias, the most 

 promising approach is on the assumption of a dysfunction of 

 some of the cells producing antibody globulin. Again some- 



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