Structure of Lymphocytic Series of Cells in Relation to Disease 283 



that they serve to recapitulate current concepts of heterologous and homol- 

 ogous lymphocyte formation (Table 19-1). Sabin" ,L> presented evidence for the 

 participation of the reticulum cell in antibody formation. Just a little earlier 

 Kolouch 34 ' 35 associated heterologous plasmacytopoiesis from the reticulum 

 cell with antibody formation responding to repeated antigenic stimuli. 

 Fasraeus, 22 Coons 8 and Enrich 19 further established the close association of 

 homologous plasmacytopoiesis with antibody production, usually after re- 

 peated antigenic stimulation. Dougherty, White, and their associates, 1 '' '■"' 

 the Harrises,- 1 "- -'••• 4T and Wesslen 01 have demonstrated homologous lym- 

 phocytopoiesis and the lymphocyte as a cellular source of antibodies usually 



Table 19-3. Antibody Formation 



reticulum cell (Sabin) macrophage (Roberts, Dixon) 



(Kolouch) 



LYMPHOBLAST 



\ 



PROLYMPHOCYTE 



LYMPHOCYTE 



(Harrises, Dougherty, 

 White, Rebuck, Wesslen) 



* PLASMABLAST 



\ 



PROPLASMACYTE 



(Roberts, Dixon) \f 



-►plasma cell (Fagraeus, Coons, 

 Ehrich) 



(Campbell, Good) 



MACROPHAGE 



in response to a single antigenic stimulus. Roberts, Dixon, and Weigie 51 have 

 shown further that transferred lymphocytes are capable of antibody forma- 

 tion but transform into plasma cells in the process. Finally, Campbell and 

 Good"' and Roberts and his associates"' 1 have similarly demonstrated the 

 transformation of sessile macrophages (histiocytes) into plasma cells con- 

 current with their production of antibodies. Had this information been 

 available to earlier workers, it would have been apparent that multiple 

 myeloma is but a malignant caricature of heterologous plasmacytopoiesis 

 in which the reticulum cell forms malignant reticular plasmablasts and 

 proplasmacytes diagnostic of this condition (Fig. 1!)-17). Inherent abnormali- 

 ties of gloubulin formation are thus warranted. Similarly, in our experi- 

 ence Waldenstrom's syndrome complicating lymphocytic malignancies of the 

 mature lymphocytic cell type is explained by retention on the part of the 

 leukemic or malignant adult lymphocyte of its propensity for plasma cell 

 formation (Fig. 19-18), resulting in excess globulin formation even though 

 in such cases the globulin formed is a giant polymer. 



