title: Interleukin-13 stimulation of the mediastinal B-cell lymphoma cell line Karpas-1106P induces a phenotype resembling the Hodgkin lymphoma cell line L1236.
abstract: OBJECTIVE
  Primary mediastinal B-cell lymphoma (PMBCL) and Hodgkin lymphoma (HL) share many biological and clinical characteristics supporting a common pathogenetic pathway. Interleukin (IL)-13 has an important pathophysiological role in HL. In this study, we asked the question of whether IL-13 is a major contributor to the observed difference in features of inflammation between HL and PMBCL.
  
  
  METHODS
  Expression of IL-13 and IL-4 receptors was studied by flow cytometry, expression of a functional cysteinyl leukotriene receptor type 1 (CysLT1R) was investigated by calcium flux measurement, expression and activity of 15-lipoxygenase type 1 (15-LO-1) was determined by Western blot and reversed-phase high-performance liquid chromatography, respectively, and cytokines were quantified by Bioplex detection.
  
  
  RESULTS
  Stimulation of the PMBCL cell line Karpas-1106P with IL-13 or IL-4 induced a proinflammatory phenotype similar to that of the HL cell line L1236. Upon interleukin stimulation of the PMBCL cell line, the cellular size increased and cells became multinucleated. Cells also expressed CysLT1R and 15-LO-1, and produced the proinflammatory eoxins. The IL-13 or IL-4 treated PMBCL cell line and the HL cell line secreted a similar set of cytokines such as IL-6, tumor necrosis factor-alpha, interferon-inducible protein-10, interferon-gamma, and RANTES.
  
  
  CONCLUSIONS
  IL-13 or IL-4 stimulation of the PMBCL cell line Karpas-1106P induced an inflammatory phenotype that resembles that of the HL cell line. Our results suggest that the autocrine release of IL-13 in HL is one critical factor that can at least partly explain the difference in phenotype between these two lymphoma entities.
authors.affiliation: Department of Medicine, Karolinska Institutet and Karolinska University Hospital, Solna, Sweden. erik.andersson@orexo.com
authors.forename: Erik
authors.initials: E
authors.lastname: Andersson
authors.forename: Frida
authors.initials: F
authors.lastname: Schain
authors.forename: Jan
authors.initials: J
authors.lastname: Sjöberg
authors.forename: Magnus
authors.initials: M
authors.lastname: Björkholm
authors.forename: Hans-Erik
authors.initials: HE
authors.lastname: Claesson
mesh_terms: D001093:Arachidonate 15-Lipoxygenase / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D045744:Cell Line, Tumor; D002467:Cell Nucleus / Q000648:ultrastructure; D048429:Cell Size; D016207:Cytokines / Q000378:metabolism; D006689:Hodgkin Disease / Q000473:pathology* / Q000503:physiopathology*; D006801:Humans; D007249:Inflammation / Q000473:pathology; D018793:Interleukin-13 / Q000494:pharmacology*; D015847:Interleukin-4 / Q000494:pharmacology; D015289:Leukotrienes / Q000096:biosynthesis; D016393:Lymphoma, B-Cell / Q000473:pathology* / Q000503:physiopathology* / Q000648:ultrastructure; D010641:Phenotype; D018077:Receptors, Leukotriene / Q000502:physiology
chemical_list: D016207:Cytokines; D018793:Interleukin-13; D015289:Leukotrienes; D018077:Receptors, Leukotriene; D015847:Interleukin-4; D001093:Arachidonate 15-Lipoxygenase; C083169:leukotriene D4 receptor; D002118:Calcium