Perspectives for immunotherapy in endocrine cancer

  1. D Führer1,2
  1. 1Department of Endocrinology and Metabolism, University Hospital Essen, University of Duisburg-Essen, Essen, Germany
  2. 2Endocrine Tumour Center at West German Cancer Center (WTZ), Essen, Germany
  3. 3Department of Dermatology, Venereology and Allergology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany
  4. 4German Cancer Consortium (DKTK), Heidelberg, Germany
  1. Correspondence should be addressed to D Führer; Email: Dagmar.fuehrer{at}uk-essen.de
  1. Figure 1

    Scheme of tumor microenvironment containing tumor cells, tumor vessels, pericyte support fibroblast and cells of innate and adaptive immune system. HIF-1α, hypoxia-inducible factors; TAMs, tumor-associated macrophages; TGF-β, transforming growth factor-β.

  2. Figure 2

    T-cell activation in a lymph node after antigen presentation by APC via TCR/MHCII complex and co-stimulatory signal B7. Right: CTLA-4 binding to B7 together with TCR complex results in T-cell inactivation. Left: Anti-CTLA-4 antibodies block the interaction of CTLA-4 and B7 and thereby confer T-cell activation. MHC, major histocompatibility complex; TCR, T-cell receptor.

  3. Figure 3

    Interaction of T cells with tumor cells within the tumor microenvironment. Right: Tumor cells expressing PD-L1/2 are able to inactivate T cells via PD-1 pathway. Left: Tumor cells lose this ability when PD-1 and/or PD-L1/2 are blocked by antibodies and an appropriate T-cell response occurs resulting in killing of tumor cells. MHC, major histocompatibility complex; TCR, T-cell receptor.

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