Mechanism of T-cell Specific Immunosuppression Induced by Prodigiosin

  • Kim, Hwan-Mook (Korea Research Institute of Bioacience and Biotechnology (KRIBB)) ;
  • Park, Se-Hyung (Korea Research Institute of Bioacience and Biotechnology (KRIBB)) ;
  • Jeon, Young-Jin (Korea Research Institute of Bioacience and Biotechnology (KRIBB)) ;
  • Lee, Sang-Han (Korea Research Institute of Bioacience and Biotechnology (KRIBB)) ;
  • Kim, Hyung-Chin (Korea Research Institute of Bioacience and Biotechnology (KRIBB)) ;
  • Yang, Kyu-Hwan (Department of Biological Sciences, KAIST) ;
  • Han, Sang-Bae (Department of Biological Sciences, KAIST)
  • Published : 2001.07.01

Abstract

In a series of our screening for immunomodulating substances, we isolated prodigiosin from the culture broth qf Serratia marcescens B-1231. This compound inhibited the T cell-mediated immune responses such as concanavalin A-induced proliferation, mixed lymphocyte response, local graft versus host reaction and T-dependent antibody response at nontoxic concentrations. However. prodigiosin did not effect B cell-mediated immune functions such as lipopolysaccharide-induced proliferation and -activated polyclonal antibody production at the same concentrations. Prodigiosin did not cause death in vitro to lymphocytes at effective concentrations (<100 nM) and also did not show toxicity in vivo to lymphoid organs at effective dos-ages (10 and 30 mg/kg). The pharmacological potencies were comparable to the activities of well-known T-cell specific immunosuppressants such as cyclosporin A. In our continuing study, mechanism of action of PDG is investigated with respect to the effect of PDG on IL-2/IL-2R pathway and transcription factor.

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