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Mechanisms mediating the effects of IL‐3 gene expression on tumor growth
Author(s) -
Wu YuanZhau,
Hong JiHong,
Huang HsinHong,
Dougherty Graeme J.,
McBride William H.,
Chiang ChiShiun
Publication year - 2000
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.68.6.890
Subject(s) - biology , effector , tumor necrosis factor alpha , in vivo , cytotoxic t cell , immunogenicity , cancer research , gene expression , infiltration (hvac) , in vitro , phenotype , microbiology and biotechnology , immune system , immunology , gene , genetics , physics , thermodynamics
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‐α and iNOS. On short‐term culture, TAMs from FSAN‐JmIL3 tumors regained their capacity to produce TNF‐α 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‐α 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‐α 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 .