Mice bearing the immunosuppressive
plasmacytoma TEPC-183 exhibit a marked splenic
hyperplasia. We have characterized these
tumor-reactive splenocytes on the basis of cell surface marker expression,
nonspecific esterase activity, and morphology. Although splenocyte numbers increased progressively throughout
tumor growth, B- and T-lymphocytes, as defined by
surface immunoglobulin and
Thy-1 antigen expression, respectively, did not increase significantly. Fourteen days after
tumor implantation, T-lymphocytes decreased from 70 million to 50 million per spleen. However, cells expressing
Mac-1 antigen or
nonspecific esterase activity increased from 10 to 65 million. This constituted a 6-fold increase in splenic macrophages. Further studies utilizing the expression of PC.2
antigen in conjunction with morphological examination indicated that metastatic TEPC-183 cells comprise approximately 5% of the
tumor-host splenocyte population 14 days after implantation. Ablation of
plasmacytoma by
cyclophosphamide inhibited the
tumor-associated splenocytosis and led to an increase in splenic T-cells (from 70 to 120 million). In addition, macrophage numbers returned to normal. This study also assessed the ability of splenocytes from animals with either actively growing
tumors or those from
cyclophosphamide-treated
tumor-bearing mice to mediate an antitumor response. Splenocytes, when assessed 1 wk following
tumor ablation by
cyclophosphamide, demonstrated antitumor activity in Winn neutralization assays. This activity was not detectable in splenocytes from animals with progressively growing
tumors. Additional studies revealed that the cell population involved in the antitumor effect was glass nonadherent,
nylon-wool nonadherent, and expressed
Thy-1 antigen. These observations were consistent with the expansion of the splenic T-lymphocyte population following
cyclophosphamide treatment. However, the immune response directed against primary TEPC-183
tumor cells was not inhibitory to metastatic
tumor cells.