title: Interleukin-2 stimulation activates mesothelial cellular functioning against autologous tumor cells.
abstract: BACKGROUND
  The present study was designed to determine the different effects of cytokines or antibodies (IL-2, IL-4, IL-7, IL-10, IL-12, alphaCD3) in stimulating the cellular functions of mesothelial cells isolated from malignant pleural effusion.
  
  
  METHODS
  Mesothelial cells were isolated from 27 patients with malignant pleural effusion. The cultured cellular interferon-gamma (IFNgamma) and IL-10 production, proliferative response, and cytolytic activity against autologous tumors and K-562 cells were measured.
  
  
  RESULTS
  Stimulation with IL-2 alone significantly increased the mesothelial cells' proliferative response (p < 0.001) and cytolytic activity against autologous tumors (p = 0.025). The further addition of other cytokines did not increase these functions. The IFNgamma/IL-10 ratio data showed that the T-helper (Th) pathway was shifted from the Th-2 pathway to the Th-1 pathway (increase of IFNgamma/IL-10 ratio) when mesothelial cells were stimulated with IL-2. Further stimulation with IL-2 plus IL-12 or alphaCD3 shifted the Th pathway further in the Th-1 direction, but without statistical significance.
  
  
  CONCLUSIONS
  The mesothelial cell proliferative response is enhanced with IL-2 stimulation alone. The T-helper pathway is also shifted from the Th-2 to the Th-1 response (increase of IFNgamma/IL-10 ratio) after IL-2 stimulation of mesothelial cells. Mesothelial cells had cytolytic activity against tumor cells, and this activity could be augmented by IL-2 stimulation.
authors.affiliation: Chest Department, Taipei Veterans General Hospital and National Yang-Ming University School of Medicine, Taipei, Taiwan, ROC. ymchen@vghtpe.gov.tw
authors.forename: Yuh-Min
authors.initials: YM
authors.lastname: Chen
authors.forename: Yi-Lin
authors.initials: YL
authors.lastname: Hsieh
authors.forename: Chun-Ming
authors.initials: CM
authors.lastname: Tsai
authors.forename: Reury-Perng
authors.initials: RP
authors.lastname: Perng
mesh_terms: D000911:Antibodies, Monoclonal / Q000494:pharmacology; D017252:CD3 Complex / Q000276:immunology; D003602:Cytotoxicity, Immunologic / Q000187:drug effects; D004797:Enzyme-Linked Immunosorbent Assay; D004847:Epithelial Cells / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D006801:Humans; D007371:Interferon-gamma / Q000032:analysis; D016753:Interleukin-10 / Q000032:analysis / Q000276:immunology / Q000494:pharmacology; D018664:Interleukin-12 / Q000276:immunology / Q000494:pharmacology; D007376:Interleukin-2 / Q000276:immunology / Q000494:pharmacology*; D015847:Interleukin-4 / Q000276:immunology / Q000494:pharmacology; D015851:Interleukin-7 / Q000276:immunology / Q000494:pharmacology; D016066:Pleural Effusion, Malignant / Q000503:physiopathology; D015398:Signal Transduction / Q000187:drug effects; D018417:Th1 Cells / Q000187:drug effects / Q000378:metabolism; D018418:Th2 Cells / Q000187:drug effects / Q000378:metabolism; D014407:Tumor Cells, Cultured
chemical_list: D000911:Antibodies, Monoclonal; D017252:CD3 Complex; D007376:Interleukin-2; D015851:Interleukin-7; D016753:Interleukin-10; D018664:Interleukin-12; D015847:Interleukin-4; D007371:Interferon-gamma