Keratinocyte-lymphocyte interaction in cutaneous T-cell lymphoma - Modulation of keratinocyte antigen My7 by a soluble factor produced by T lymphocytes

被引:7
作者
Celerier, P [1 ]
Bureau, B [1 ]
Litoux, P [1 ]
Dreno, B [1 ]
机构
[1] HOP HOTEL DIEU,DEPT IMMUNODERMATOL,NANTES,FRANCE
关键词
D O I
10.1001/archderm.133.7.837
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
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). Design: In vitro study with reconstituted skin model. Setting: Department of Dermatology of Universitary Hospital, Nantes, France. Patients: Lymphocytes extracted from 11 skin samples with lesions of epidermotropic CTCL (mycosis fungoides, stages Ila 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 re constituted skin. Intervention: None. Main Outcome Measures: 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.
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页码:837 / 840
页数:4
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