title: Analysis of leukemia inhibitory factor, type 1 and type 2 cytokine production in patients with eosinophilic fasciitis.
abstract: OBJECTIVE
  Eosinophilic fasciitis (EF) is a scleroderma-like disease of unknown etiology characterized by skin induration, elevated immune globulins, and peripheral eosinophilia. The hallmarks of the chronic cutaneous involvement in this syndrome are inflammation and fibrosis of the fascia. To determine how the inflammatory process in EF may be regulated, we investigated the spontaneous and mitogen induced [lipopolysaccharide (LPS), phytohemagglutinin (PHA) or both LPS+PHA] syntheses of interleukins (IL)-2, 5 and 10, interferon-gamma (IFN-gamma), and leukemia inhibitory factor (LIF) cytokines by peripheral blood mononuclear cells (PBMC) from 4 patients with active EF and compared them to those of 10 healthy individuals.
  
  
  METHODS
  We used a short term whole blood assay and culture supernatants were collected after 24 h to measure the IL-2 and IFN-gamma contents and after 48 h to evaluate IL-5, IL-10, and LIF. Supernatant cytokine concentrations were determined by ELISA.
  
  
  RESULTS
  All 4 patients had similar patterns of cytokine secretion. Cytokine production did not differ between patients and controls under basal conditions or when LPS was added to the cultures. In contrast, under PHA or LPS+PHA stimulation, significantly higher amounts of all 5 cytokines were detected in samples from patients compared to those from controls.
  
  
  CONCLUSIONS
  Overall, our data suggest that EF is characterized by an increased capacity of PBMC to produce IL-5 and IL-10, possibly leading to eosinophilia and immune globulin overexpression. In this context, the simultaneous elevations of type 1 cytokines (IL-2 and IFN-gamma) and LIF production by the same cells may be an attempt by the immune system to limit the exacerbation of a type 2 dominant response.
authors.affiliation: Service de Médicine Interne et Maladies Infectieuses, H pital Haut-Lévêque, Pessac, France.
authors.forename: J F
authors.initials: JF
authors.lastname: Viallard
authors.forename: J L
authors.initials: JL
authors.lastname: Taupin
authors.forename: V
authors.initials: V
authors.lastname: Ranchin
authors.forename: B
authors.initials: B
authors.lastname: Leng
authors.forename: J L
authors.initials: JL
authors.lastname: Pellegrin
authors.forename: J F
authors.initials: JF
authors.lastname: Moreau
mesh_terms: D000328:Adult; D000368:Aged; D002478:Cells, Cultured; D004802:Eosinophilia / Q000378:metabolism* / Q000473:pathology; D005208:Fasciitis / Q000378:metabolism* / Q000473:pathology; D005260:Female; D006131:Growth Inhibitors / Q000276:immunology / Q000378:metabolism*; D006801:Humans; D007371:Interferon-gamma / Q000096:biosynthesis / Q000276:immunology; D015850:Interleukin-6; D007378:Interleukins / Q000096:biosynthesis* / Q000276:immunology; D053605:Leukemia Inhibitory Factor; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D008070:Lipopolysaccharides; D008213:Lymphocyte Activation; D008222:Lymphokines / Q000276:immunology / Q000378:metabolism*; D008875:Middle Aged; D008934:Mitogens / Q000494:pharmacology; D010835:Phytohemagglutinins
chemical_list: D006131:Growth Inhibitors; D015850:Interleukin-6; D007378:Interleukins; C507837:LIF protein, human; D053605:Leukemia Inhibitory Factor; D008070:Lipopolysaccharides; D008222:Lymphokines; D008934:Mitogens; D010835:Phytohemagglutinins; D007371:Interferon-gamma