Abstract：
:Tumor-associated macrophages (TAM) are a major inflammatory infiltrate in tumors and a major component of the protumor function of inflammation. TAM in established tumors generally have an M2 phenotype with defective production of interleukin-12 (IL-12) and high IL-10. Here, we report that defective responsiveness of TAM from a murine fibrosarcoma and human ovarian carcinoma to M1 activation signals was associated with a massive nuclear localization of the p50 nuclear factor-kappaB (NF-kappaB) inhibitory homodimer. p50 overexpression inhibited IL-12 expression in normal macrophages. TAM isolated from p50(-/-) mice showed normal production of M1 cytokines, associated with reduced growth of transplanted tumors. Bone marrow chimeras showed that p50 inactivation in hematopoietic cells was sufficient to result in reduced tumor growth. Thus, p50 NF-kappaB overexpression accounts for the inability of TAM to mount an effective M1 antitumor response capable of inhibiting tumor growth.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Saccani A,Schioppa T,Porta C,Biswas SK,Nebuloni M,Vago L,Bottazzi B,Colombo MP,Mantovani A,Sica Adoi
10.1158/0008-5472.CAN-06-1867subject
Has Abstractpub_date
2006-12-01 00:00:00pages
11432-40issue
23eissn
0008-5472issn
1538-7445pii
66/23/11432journal_volume
66pub_type
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