Molecular Cloning of Rat NK Target Structure -The Possibility of CD44 Involvement in NK Cell-Mediated Lysis

J-STAGE
  • Kanki Kazushige
    Department of Pathology, Sapporo Medical University School of Medicine
  • Torigoe Toshihiko
    Department of Pathology, Sapporo Medical University School of Medicine
  • Hirai Itaru
    Department of Pathology, Sapporo Medical University School of Medicine
  • Sahara Hiroeki
    Department of Pathology, Sapporo Medical University School of Medicine
  • Kamiguchi Kenjiro
    Department of Pathology, Sapporo Medical University School of Medicine
  • Tamura Yasuaki
    Department of Pathology, Sapporo Medical University School of Medicine
  • Yagihashi Atsuhito
    Department of Laboratory Diagnosis, Sapporo Medical University School of Medicine
  • Sato Noriyuki
    Department of Pathology, Sapporo Medical University School of Medicine

抄録

The nature of target molecules of natural killer (NK) cell-mediated lysis remains to be elucidated. As we previously reported, mAb 109 recognizes one of the tumor-associated antigens, designated as 109 antigen (Ag), expressed on the cell surface of rat fibrosarcomas W31 and W14, which are transformants of WFB (rat fetal fibroblast cell line) with H-ras oncogene. 109Ag was thought to be a target structure of NK cells since mAb 109 inhibited NK cell-mediated lysis against W31 and W14. Here, we demonstrate by molecular cloning that 109Ag is identical to rat CD44. Immunoprecipitation and immunoblotting studies also showed that mAb 109 and anti-rat CD44 mAb OX-50 recognize the same protein of W31 cell lysates with an 86kDa molecular size. CD44 was suggested to be a target structure of NK cell-mediated lysis; however, rat CD44 cDNA transfection alone into CD44 null cell lines did not result in up-regulation of target cell susceptibility to NK cell-mediated lysis. Our results therefore indicated that CD44 may play a crucial role as one of the target structures in our rat fibrosarcoma system though the cell surface expression of CD44 alone does not affect NK susceptibility of the target cells.

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