PATHOLOGY OF THE IMMUNE RESPONSE 



Mackay, 1958), which is positive in this condition, was 

 originally thought to demonstrate this. Until an organ- 

 specific antigen can be obtained, however, as it has been for 

 Hashimoto's disease, other alternatives will be more likely. 

 In sympathetic ophthalmia conditions broadly similar to 

 those of Hashimoto's disease may well be operative. 



3. Acquired haemolytic anaemias 



In the discussion of these conditions, Dacie's (1954) text-book 

 will be used as the primary source of information. He divides 

 the acquired (that is, not genetically determined) haemo- 

 lytic anaemias into primary and secondary and the antibodies 

 into warm and cold types, but stresses that detailed study 

 will show that almost every case has individual features of 

 its own. For the present purpose only conditions giving 

 a positive Coombs test will be considered as falling in the 

 auto-immune group. 



In all such disease conditions there is evidence of blood 

 destruction, anaemia, jaundice and, in acute forms, haemo- 

 globinuria, and almost always a considerable enlargement of 

 the spleen. The serum contains auto-antibodies in the sense 

 that they react with the patient's own red cells. The antibody 

 is an incomplete one which is demonstrable by the Coombs 

 test, direct or indirect, and by various technical artifices 

 such as the use of trypsin- treated cells. There is evidence that 

 the warm and cold types are physically different. Fuden- 

 berg and Kunkel (1957) have found that the cold antibodies 

 are usually associated with fast-moving gamma globulin that 

 in the ultracentrifuge shows itself to be a macroglobulin with 

 a sedimentation constant of 1 9 S. In three patients with more 

 acute haemolytic anaemia the abnormal antibody was 

 carried by globulin of the commoner molecular size with 

 a sedimentation constant of 7 S, corresponding to a molecular 

 weight of about 60,000. Human beings given foreign blood 

 by transfusion, etc., readily produce complete agglutinins, 

 so that the failure to produce them against their own cells is 



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