* Department of Atomic Science, Tsing Hua University, Hsinchu 30013, Taiwan;
Department of Radiation Oncology, Chang Gung Memorial Hospital, Tao-Yuan 30033, Taiwan; and
Roy E. Coats Laboratories, Department of Radiation Oncology, University of California, Los Angeles, California
Correspondence: Chi-Shiun Chiang, Ph.D., Department of Atomic Science, Tsing Hua University, 101 Sec. 2, Kuang-Fu Road, Hsinchu 30013, Taiwan. E-mail: cschiang{at}mx.nthu.edu.tw
IL-3 gene expression within tumors leads to host-cell infiltration,
particularly by macrophages, slower tumor growth, and enhanced
immunogenicity. Surprisingly, tumor-associated macrophages (TAMs) from
within FSAN-JmIL3 tumors had decreased expression of TNF-
and iNOS.
On short-term culture, TAMs from FSAN-JmIL3 tumors regained their
capacity to produce TNF- and NO, indicating that they were primed
in vivo. In vitro experiments were unable to
demonstrate differences between FSAN-JmIL3 and FSAN tumor cells in
their ability to stimulate TNF- production by TAMs. In the absence
of evidence that TAM activation was responsible for the slower growth
of FSAN-JmIL3 tumors, the response of tumor cells to these effector
molecules was studied. TNF- and NO were cytotoxic for FSAN-JmIL3
cells but growth stimulatory 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.
Key Words: cytokine • TNF • NO • iNOS • immunotherapy
