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Complex Immune Evasion Strategies in Classical Hodgkin Lymphoma.
Wein, Frederik; Weniger, Marc A; Höing, Benedikt; Arnolds, Judith; Hüttmann, Andreas; Hansmann, Martin-Leo; Hartmann, Sylvia; Küppers, Ralf.
Afiliación
  • Wein F; Institute of Cell Biology (Cancer Research), Medical Faculty, University of Duisburg-Essen, Essen, Germany.
  • Weniger MA; Institute of Cell Biology (Cancer Research), Medical Faculty, University of Duisburg-Essen, Essen, Germany.
  • Höing B; Department of Otorhinolaryngology, University Hospital Essen, Essen, Germany.
  • Arnolds J; Department of Otorhinolaryngology, University Hospital Essen, Essen, Germany.
  • Hüttmann A; Department of Hematology, University Hospital Essen, Essen, Germany.
  • Hansmann ML; Dr. Senckenberg Institute of Pathology, Goethe-University of Frankfurt/Main, Medical School, Frankfurt/Main, Germany.
  • Hartmann S; Dr. Senckenberg Institute of Pathology, Goethe-University of Frankfurt/Main, Medical School, Frankfurt/Main, Germany.
  • Küppers R; Institute of Cell Biology (Cancer Research), Medical Faculty, University of Duisburg-Essen, Essen, Germany. ralf.kueppers@uk-essen.de.
Cancer Immunol Res ; 5(12): 1122-1132, 2017 12.
Article en En | MEDLINE | ID: mdl-29070649
The cellular microenvironment in classical Hodgkin lymphoma (cHL) is dominated by a mixed infiltrate of inflammatory cells with typically only about 1% Hodgkin and Reed/Sternberg (HRS) tumor cells. T cells are usually the largest population of cells in the cHL microenvironment, encompassing T helper (Th) cells, regulatory T cells (Tregs), and cytotoxic T cells. Th cells and Tregs presumably provide essential survival signals for HRS cells. Tregs are also involved in rescuing HRS cells from antitumor immune responses. An understanding of the immune evasion strategies of HRS cells is not only relevant for a characterization of the pathophysiology of cHL but is also clinically relevant, given the current treatment approaches targeting checkpoint inhibitors. Here, we characterized the cHL-specific CD4+ T-cell infiltrate regarding its role in immune evasion. Global gene expression analysis of CD4+ Th cells and Tregs isolated from cHL lymph nodes and reactive tonsils revealed that Treg signatures were enriched in CD4+ Th cells of cHL. Hence, HRS cells may induce Treg differentiation in Th cells, a conclusion supported by in vitro studies with Th cells and cHL cell lines. We also found evidence for immune-suppressive purinergic signaling and a role of the inhibitory receptor-ligand pairs B- and T-cell lymphocyte attenuator-herpesvirus entry mediator and CD200R-CD200 in promoting immune evasion. Taken together, this study highlights the relevance of Treg induction and reveals new immune checkpoint-driven immune evasion strategies in cHL. Cancer Immunol Res; 5(12); 1122-32. ©2017 AACR.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Enfermedad de Hodgkin / Evasión Inmune Límite: Humans Idioma: En Revista: Cancer Immunol Res Año: 2017 Tipo del documento: Article País de afiliación: Alemania Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Enfermedad de Hodgkin / Evasión Inmune Límite: Humans Idioma: En Revista: Cancer Immunol Res Año: 2017 Tipo del documento: Article País de afiliación: Alemania Pais de publicación: Estados Unidos