CD18/CD54(+CD102), CD2/CD58 pathway-independent killing of lymphokine-activated killer (LAK) cells against glioblastoma cell lines T98G and U373MG

For natural killer cell-mediated cytolysis (NK-lysis) and lymphokine-activa ted killer cell-mediated cytolysis (LAK-lysis), the co-stimulatory signals of CD18/CD54(+CD102) and CD2/CD58 pathways are essential. However, in this report, we describe a LAK-lysis that does not depend upon these two pathway s. The killed cells were glioblastoma cell lines T98G and U373MG. The LAK c ells were induced from peripheral blood lymphocytes in the presence of inte rleukin-2. 1) The T98G and U373MG did not express CD54 or CD102, but expres sed CD58. 2) However, when they were pretreated with an anti-CD58 (TS2/9), the LAK-lysis was not blocked. 3) The LAK-lysis was markedly inhibited by p retreating with Concanamycin A and slightly inhibited by treating with anti tumor necrosis factor-related apoptosis-inducing ligand (anti-TRAIL) antibo dy. 4) Nineteen percent of the LAK cells adhered to the T98G. The adhered L AK cells killed it. But nonadherent LAK cells could not kill the T98G or U3 73MG but killed lymphoblastoma cell lines Raji and NALM-6. These findings s uggested that this type of the LAK-lysis might not depend upon the CD18/CD5 4(+CD102) pathway or CD2/CD58 pathway. The effector cells that killed the T 98G and U373MG might not always be the same as the effector cells that kill ed the other cell lines. The LAK cells contain several subsets, and one of the subsets might kill these two target cell lines.