Human natural killer‐like activity against mouse spleen cells

Academic Article


  • Unstimulated human peripheral lymphocytes were cytotoxic for normal mouse spleen cells and suppressed the in vitro antibody plaque‐forming cell (PFC) response of these cells to sheep red blood cells and dinitrophenylated Ficoll. The cells in the lymphocyte population that were responsible for the immunosuppression had properties of natural killer (NK) or NK‐like cells in that they were: (a) non‐E‐rosetting, (b) nonadherent, (c) unaffected by treatment with anti‐human immunoglobulin plus complement, (d) cytotoxic against an established human NK target, K562 leukemic cells, and (e) partially inactivated by mitomycin C. Addition of the human NK‐like cells to mouse spleen cell cultures at the time of antigen addition and at an effector cell to target cell ratio as low as 0.67:1 resulted in 85 to 96% suppression of the PFC response. Addition of NK‐like cells to cultures 18 h before harvesting in 5‐day cultures required higher concentrations and ratios (2.7 : 1) of effector to target cells to significantly suppress the PFC response. The data suggest that human NK‐like activity in suppression of the mouse PFC response is due to killing of the targets. The mouse spleen cell PFC system represents a potential model for assessment of human NK activity that is quite dramatic in its effect and can be used in addition to the well known 51Cr‐release assay. Also, since the mouse spleen cell is a normal cell, it provides a model in the PFC system for studying the mechanism of NK regulation of normal cellular function. An additional finding of this study was the observation that E‐rosetting T cells significanty enhanced the mouse PFC response. Thus, human peripheral lymphocytes contain discrete cellular populations that either enhance or suppress the mouse PFC response. Copyright © 1982 WILEY‐VCH Verlag GmbH & Co. KGaA
  • Published In

    Digital Object Identifier (doi)

    Author List

  • Yamamoto JK; Edwin Blalock J; Johnson HM
  • Start Page

  • 222
  • End Page

  • 227
  • Volume

  • 12
  • Issue

  • 3