caa a22 4500 469073934 CHVBK 20180323132929.0 cr unu---uuuuu 170328e19920901xx s 000 0 eng 10.1007/BF01741147 doi (NATIONALLICENCE)springer-10.1007/BF01741147 Monoclonal antibodies anti-CD3, anti-TCRαβ and anti-CD2 act synergistically with tumor cells to stimulate lymphokine-activated killer cells and tumor-infiltrating lymphocytes to secrete interferon γ [Elektronische Daten] [Anita Chong, Edgar Staren, Philip Scuderi] Summary: Peripheral blood lymphocytes cultured in interleukin-2 IL-2 acquire the ability to recognize and kill a wide range of tumor cells. Such promiscuous killer cells are termed lymphokine-activated killer (LAK) cells. We recently reported that the interaction of LAK cells with tumor cells stimulated the LAK cells to release interferon (IFN)γ. Here, we report that the release of IFNγ by LAK cells can be further enhanced by addition of the monoclonal antibodies (mAbs), anti-CD3, anti-(T cell receptor αβ) (TCRαβ) and a mitogenic combination of anti-CD2 (T112+T113). Other antibodies, including a non-mitogenic anti-CD2 mAb (Leu5b), that recognize T cell-associated antigens were not stimulatory. The same stimulatory mAbs also synergized with tumor cells to stimulate tumor-infiltrating lymphocytes (TIL) to secrete IFNγ. Additional experiments indicated that it was the T cell subset of LAK cells (LAK-T cells) that was stimulated by tumor cells and mAbs to release IFNγ. Inhibition studies with specific mAbs suggest that the stimulation of IFNγ release by LAK-T cells was dependent both on the aggregation of TCR-CD3 complexes on the LAK-T cell, and on the interaction of accessory molecules with their ligands. The accessory molecules we have identified as critical are LFA 1 and CD2/LFA-2 on LAK-T cells interacting with their respective ligands ICAM-1 and LFA3. Thus our data suggest that cytokine production in LAK-T cells can be regulated by multiple molecular interactions, involving the TCR-CD3 complex and adhesion molecules. Springer-Verlag, 1992 IFNγ nationallicence LAK nationallicence TIL nationallicence Anti-CD3 nationallicence Chong Anita Department of General Surgery, Rush-Presbyterian-St. Luke's Medical Center, 1653 W Congress Parkway, 60612, Chicago, IL, USA aut Staren Edgar Department of General Surgery, Rush-Presbyterian-St. Luke's Medical Center, 1653 W Congress Parkway, 60612, Chicago, IL, USA aut Scuderi Philip Department of Experimental Therapeutics, Miles Inc., Cutter Biologicals, 94701, Berkeley, CA, USA aut Cancer Immunology, Immunotherapy Springer-Verlag 35/5(1992-09-01), 335-341 0340-7004 35:5<335 1992 35 262 https://doi.org/10.1007/BF01741147 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF01741147 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Chong Anita Department of General Surgery, Rush-Presbyterian-St. Luke's Medical Center, 1653 W Congress Parkway, 60612, Chicago, IL, USA aut NATIONALLICENCE 700 1- Staren Edgar Department of General Surgery, Rush-Presbyterian-St. Luke's Medical Center, 1653 W Congress Parkway, 60612, Chicago, IL, USA aut NATIONALLICENCE 700 1- Scuderi Philip Department of Experimental Therapeutics, Miles Inc., Cutter Biologicals, 94701, Berkeley, CA, USA aut NATIONALLICENCE 773 0- Cancer Immunology, Immunotherapy Springer-Verlag 35/5(1992-09-01), 335-341 0340-7004 35:5<335 1992 35 262 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer