Recognition of heterogeneous lymphokine-activated killer (LAK) receptors on Kaposi's sarcoma cells, endothelial cells, and monocytes/macrophages: Evidence of distinct LAK-cell antigen on Kaposi's sarcoma cells?Potential for use of LAK cells for immunotherapy

Abstract

The purpose of this study was to determine the potential use of lymphokine-activated killer (LAK) cells against Kaposi's sarcoma (KS) cells. We used chromium release cold-target inhibition assay for understanding the expression of heterogeneous LAK-cell antigens (Ags) on KS cells, endothelial cells (ECs), and monocytes/macrophages (M phi) which could allow for the utilization of LAK-cell immunotherapy in KS without side effects. Our data show that (i) all three cell types express the CD18 Ag of LFA-1 or Leu-CAM, (ii) rare KS cells from eyes cannot cold target-inhibit ECs, (iii) KS cells express a distinct LAK-cell Ag, which we have called LAK-KS Ag, and (iv) LAK-KS Ag allows for cold-target inhibition between different KS cells. The identification of LAK-KS Ag and a monoclonal antibody capable of inhibiting lysis of ECs and M phi without obstructing LAK-KS Ag would be important.

Primary Research: Short Communication: Evidence Supporting Rare AIDS-Kaposi's Sarcoma Metastasis In Keeping With Their Vascular Endothelial Evolution

“…Our results herein showed that although RH1-38 did not inhibit killing of AIDS-KS21 cells, it concomitantly inhibited rupture of AIDS-KS10 cells, vascular ECs and MΦ (Table 1). Combining this finding with our previous data, where AIDS-KS21 cells failed to cold-target inhibit lysis of vascular ECs, as otherwise demonstrated by AIDS-KS10 cells [10], summarize that AIDS-KS21 cells bore either diminished or negative CD54 Ag composition. Published papers to date have reported CD54 Ags on several other AIDS-KS cell lines unaffected following multiple passages in vitro [14], and that no significant immunophenotyping differences exist between AIDS-KS3, -KS6 and -KS8 cells at comparable stages [15].…”

“…In our earlier paper, we specified that AIDS-KS21 cells originated from an eye lesion, whereas, AIDS-KS10, -KS8 and -KS3 cells were cutaneous, visceral and pleural fluid isolates, respectively [10]. Juxtaposed was put the observation that the differences in reactions of AIDS-KS21 cells may be related to location, however, a plausible explanation could not be proposed [10].…”

“…In addition, the Ag mediated interactions of LAK effectors also target and cause cytotoxicity to vascular ECs and monocytes/macrophages (MΦ) [8,9]. It was therefore proposed that the presence of heterogeneous LAK-cell Ags on vascular ECs, MΦ and tumor cells would make it possible to obviate of the complicating injury to ECs and MΦ in LAK-cell immunotherapy via the application of monoclonal antibodies (mAbs) to selectively inhibit EC and MΦ damage [10]. …”

“…Pursuant to this approach, we incorporated the cold-target inhibition technique [11] in chromium release assays to detect possible heterogeneity of LAK-cell Ags on AIDS-KSCs, vascular ECs and MΦ[10]. Data accumulated then showed that unlike cutaneous AIDS-KS10 cells, AIDS-KS21 cells collected from ocular lesions did not cold-target inhibit EC lysis [10].…”

“…Data accumulated then showed that unlike cutaneous AIDS-KS10 cells, AIDS-KS21 cells collected from ocular lesions did not cold-target inhibit EC lysis [10]. This suggested differences in LAK-cell Ags of AIDS-KS21 cells versus AIDS-KS10 cells and ECs, specifically, pointing to intercellular adhesion molecule-1 (ICAM-1) or CD54 Ags as studies have repeatedly elucidated ICAM-1 on targets binding to lymphocyte function associated antigen-1 (LFA-1) on LAK effectors in LAK-cell attacks [12].…”