230 J. R. BATCHELOR AND M. S. SILVERMAN 



Should the principle be upheld that excess circulating humoral 

 antibody tends to suppress the induction and activity of cells in a 

 state of delayed hypersensitivity, it may be of value in the treat- 

 ment of some autoimmune diseases. Some authors believe that 

 the action of hypersensitive lymphoid cells plays a major role in 

 the tissue destruction. If high titres of humoral antibody are not 

 toxic per se, the suppression of the sensitized cells may be accom- 

 plished by this means. 



Suttittiary 



The intraperitoneal growth of the C3H ascites sarcoma, BP 8, 

 in non-immune recipients is inhibited by mixing the tumour 

 inoculum vs^ith lymphoid cells derived from isogenic mice 

 previously sensitized against BP 8. Interference by host strain 

 anti-BP 8 isoantibody v^ith the protective effect of immune cells 

 has been demonstrated. Passive immunization of BALB/c and 

 BALB/c X C57BL hosts injected v^ith BP 8 did not inhibit the 

 development of a host cellular reaction; but despite the presence 

 of host reactive cells, graft rejection was not completed. It is 

 concluded that such cells function less effectively in an environ- 

 ment of humoral antibody excess. 



Enhancing activity has been transferred by pooled immune 

 spleen and lymph node cells to C3H cJ hosts. Splenectomy has 

 been found to increase the resistance of C3H (Js to an A-strain 

 mammary tumour, and BALB/c hosts to BP 8. 



The implications of these fmdings are discussed in relation to 

 immunological enhancement, and delayed hypersensitivity 

 reactions. 



Acknowledgements 



The authors are deeply indebted to the late Dr. P. A. Gorer F.R.S., on whose 

 ideas they have freely drawn. Thanks are due to Miss A. Carsons and Miss 

 B. Hand for technical assistance and to the Medical Illustrations Department for 

 help with Table I. 



