IL-3 gene expression within tumors leads to host-cell infiltration, particu
larly by macrophages, slower tumor growth, and enhanced immunogenicity, Sur
prisingly, tumor-associated macrophages (TAMs) from within FSAN-JmIL3 tumor
s had decreased expression of TNF-alpha and iNOS. On short-term culture, TA
Ms from FSAN-JmIL3 tumors regained their capacity to produce TNF-alpha and
NO, indicating that they were primed in vivo, In vitro experiments were una
ble to demonstrate differences between FSAN-JmIL3 and FSAN tumor cells in t
heir ability to stimulate TNF-alpha production by TAMs. In the absence of e
vidence that TAM activation was responsible for the slower growth of FSAN-J
mIL3 turners, the response of tumor cells to these effector molecules was s
tudied. TNF-alpha and NO were cytotoxic for FSAN-JmIL3 cells but growth sti
mulatory for FSAN, These tumor-related phenotypic changes may contribute as
much if not more than functional changes in host infiltrating cells to the
slower growth of FSAN-JmIL3 tumors in vivo.