Lymphokine-activated Killer Activity Induced by in Vivo Interleukin 2 Therapy: Predominant Role for Lymphocytes with Increased Expression of CD2 and Leul9 Antigens but Negative Expression of CD16 Antigens

Gilda Weil-Hillman, Paul Fisch, Jeffrey A. Sosman, Jacquelyn A. Hank, Paul M. Sondel, Audrey F. Prieve

Research output: Contribution to journalArticlepeer-review

82 Scopus citations

Abstract

The phenotype and function of lymphocytes from cancer patients treated with repetitive weekly cycles of continuous i.v. infusions of recombinant interleukin 2 (IL-2) were examined. Peripheral blood lymphocytes (PBL) obtained after IL-2 therapy showed an increased percentage of cells bearing the CD16 and leul9 markers which are associated with natural killer cells. These PBL mediated significantly increased levels of IL-2-dependent lymphokine-activated killer (LAK) activity against the Daudi cell line. Depletion of CD16+ cells from PBL obtained after in vivo IL-2 caused only slight inhibition of their LAK activity or their proliferative response to IL-2 in vitro. This indicates that CD16+ cells are involved but play only a minor role in these responses. In contrast, depletion of leul9+ cells, from PBL activated in vivo with IL-2, virtually abrogated their LAK activity and their proliferative response to IL-2. Two-color flow cytometry studies showed that a Ieul9+/CD16-population was expanded by in vivo IL-2 therapy and was responsible for the majority of LAK activity by in vivo-activated PBL. Moreover, this CD16- population showed an increased density of leul9 and CD2 (E rosette receptor) antigens when compared to the resting PBL obtained prior to IL-2 treatment. These data show that the predominant population mediating in vitro LAK activity, induced by in vivo IL-2 therapy, consists of activated natural killer cells with a high density of leul9 and CD2 antigens but negative for the CD 16 antigen.

Original languageEnglish (US)
Pages (from-to)3680-3688
Number of pages9
JournalCancer Research
Volume49
Issue number13
StatePublished - Jul 1 1989

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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