Abstract：
:Toll-like receptor (TLR) agonists are considered adjuvants in clinical trials of cancer immunotherapy. Here, we investigated the modulation of gammadelta T cell-mediated tumor cell lysis by TLR ligands. gammadelta T-cell cytotoxicity and granzyme A/B production were enhanced after pretreatment of tumor cells with TLR3 [poly(I:C)] or TLR7 ligand (imiquimod). We examined TLR3- and TLR7-expressing pancreatic adenocarcinomas, squamous cell carcinomas of head and neck and lung carcinomas. Poly(I:C) treatment of pancreatic adenocarcinomas followed by coculture with gammadelta T cells resulted in an upregulation of CD54 on the tumor cells. The interaction of CD54 and the corresponding ligand CD11a/CD18 expressed on gammadelta T cells is responsible for triggering effector function in gammadelta T cells. Moreover, treatment with imiquimod downregulated MHC class I molecules on tumor cells possibly resulting in a reduced binding affinity for inhibitory receptor NKG2A expressed on gammadelta T cells. These results indicate that TLR3 or TLR7 ligand stimulation of tumor cells enhances the cytotoxic activity of expanded gammadelta T cells of cancer patients in vitro.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Shojaei H,Oberg HH,Juricke M,Marischen L,Kunz M,Mundhenke C,Gieseler F,Kabelitz D,Wesch Ddoi
10.1158/0008-5472.CAN-09-1602subject
Has Abstractpub_date
2009-11-15 00:00:00pages
8710-7issue
22eissn
0008-5472issn
1538-7445pii
0008-5472.CAN-09-1602journal_volume
69pub_type
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