Structure of Lymphocytic Scries of Cells in Relation to Disease 271 



of the blast and as its extensive cytoplasm retracts freeing the cell and 

 increasing its basophilia but depressing the cytoplasmic-nuclear ratio. In 

 the study of hematopoiesis in the bone marrow after the fetal period and in 

 the study of peripheral blood cells, such an oversight is understandable 

 because nonleukemic, heterologous blood formation from reticulum cell 

 through hematopoietic RI-. cell to the myeloid elements requires an almost 

 cataclysmic stimulus (e.g., atomic radiation, 36 untreated subacute bacterial 



Fig. 19-8. Hematopoietic reticulum cell (top center) from a lymph 

 node imprint in infectious mononucleosis. This reticulum cell is well 

 on its way to blood cell formation. Leishman stain, (x 1100) 



endocarditis 111 ) for its demonstration in those locations. In contrast is the 

 ease with which heterologous lymphocyte formation can be followed in 

 lymph nodes responding to even moderate antigenic stimuli or to stimuli 

 responsible for lymphocyte formation. Imprints of any node reacting to 

 such stimuli, and the majority of otherwise "normal" nodes are so reacting, 

 will yield for study examples of all stages in the transformation of inactive 

 reticulum cells first to hematopoietic reticulum cells and only then to lym- 

 phoblasts. 



In the transformation of the inactive or undifferentiated reticulum cell 

 (Fig. 19-1) to the cell capable of forming blood cells, the first change is the 

 enlargement of the nucleus and an accentuation of the chromatin pieces 

 forming the irregular network or stippled pattern with its now larger but 

 still irregularly outlined, colorless parachromatin interstices (Fig. 19-7). The 

 cyptoplasm then retracts and becomes increasingly basophilic (Fig. 19-8); 



