title: Keratinocyte-lymphocyte interaction in cutaneous T-cell lymphoma. Modulation of keratinocyte antigen My7 by a soluble factor produced by T lymphocytes.
abstract: OBJECTIVE
  To test the hypothesis that the modulation of My7 antigen in the basal keratinocytes is directly related to the effect of dermal lymphocyte infiltrate of epidermotropic cutaneous T-cell lymphoma (CTCL).
  
  
  METHODS
  In vitro study with reconstituted skin model.
  
  
  METHODS
  Department of Dermatology of University Hospital, Nantes, France.
  
  
  METHODS
  Lymphocytes extracted from 11 skin samples with lesions of epidermotropic CTCL (mycosis fungoides, stages IIa to IV) and 6 skin samples with lesions of atopic dermatitis (control population) together with the supernatants of these infiltrating lymphocytes were incubated with normal reconstituted skin samples either alone or in the presence of interferon alfa-2a (10(2) IU/ mL). Moreover, normal peripheral blood mononuclear cells of 7 patients and 4 controls were incubated with reconstituted skin.
  
  
  METHODS
  None
  
  
  METHODS
  None.
  
  
  RESULTS
  Ten of 11 samples of lymphocytes extracted from CTCL and 7 of 11 of their supernatants inhibited partially or completely My7 expression by basal cells. NO inhibition was noted for lymphocytes extracted from inflammatory skin or their supernatants. Addition of interferon alfa-2a in a culture medium of extracted lymphocytes or their supernatants blocked inhibition of My7 expression by keratinocytes in 8 of 10 reconstituted skin samples. No abrogation of My7 expression was noted with peripheral mononuclear cells.
  
  
  CONCLUSIONS
  Our in vitro study demonstrated a direct and specific interaction between the tumor infiltrate of CTCL and keratinocytes. Moreover, this interaction appeared to be closely associated with a soluble factor produced by the tumor T-cell infiltrate and was at least partially blocked by interferon alfa-2a.
authors.affiliation: Department of Immuno-Dermatology, Hotel Dieu, Nantes, France.
authors.forename: P
authors.initials: P
authors.lastname: Célérier
authors.forename: B
authors.initials: B
authors.lastname: Bureau
authors.forename: P
authors.initials: P
authors.lastname: Litoux
authors.forename: B
authors.initials: B
authors.lastname: Dréno
mesh_terms: D000911:Antibodies, Monoclonal; D018826:CD13 Antigens / Q000037:antagonists & inhibitors / Q000235:genetics*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000473:pathology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology / Q000473:pathology; D002450:Cell Communication / Q000276:immunology; D003876:Dermatitis, Atopic / Q000276:immunology / Q000473:pathology; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000276:immunology / Q000494:pharmacology; D015603:Keratinocytes / Q000276:immunology / Q000473:pathology*; D007963:Leukocytes, Mononuclear / Q000166:cytology / Q000276:immunology; D016246:Lymphocytes, Tumor-Infiltrating / Q000276:immunology / Q000473:pathology*; D009182:Mycosis Fungoides / Q000276:immunology / Q000473:pathology*; D010641:Phenotype; D011994:Recombinant Proteins; D012867:Skin / Q000473:pathology; D012878:Skin Neoplasms / Q000276:immunology / Q000473:pathology*; D013491:Suppressor Factors, Immunologic / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology / Q000473:pathology*; D014407:Tumor Cells, Cultured
chemical_list: D000911:Antibodies, Monoclonal; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D011994:Recombinant Proteins; D013491:Suppressor Factors, Immunologic; D018826:CD13 Antigens