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Claude Wildmann

Researcher at Ludwig Institute for Cancer Research

Publications -  14
Citations -  1400

Claude Wildmann is an academic researcher from Ludwig Institute for Cancer Research. The author has contributed to research in topics: Antigen & CTL*. The author has an hindex of 9, co-authored 14 publications receiving 1311 citations.

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Bage - a New Gene Encoding An Antigen Recognized On Human Melanomas By Cytolytic T-lymphocytes

TL;DR: The identification of a new gene that codes for a putative protein of 43 aa and seems to belong to a family of several genes, which may prove useful for cancer immunotherapy.
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Autologous cytolytic T lymphocytes recognize a MAGE-1 nonapeptide on melanomas expressing HLA-Cw*1601

TL;DR: The identification of a gene, named MAGE‐1, which codes for antigen MZ2‐E which is presented by HLA‐A1 is reported and the range of tumor patients who could be eligible for immunization against MAGE antigens is extended.
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Structure of the gene of tum- transplantation antigen P198: a point mutation generates a new antigenic peptide.

TL;DR: It is concluded that tum- mutation P198 generates a new epitope recognized by syngeneic T cells that is able to compete for binding to major histocompatibility complex molecule Kd.
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A tyrosinase nonapeptide presented by HLA-B44 is recognized on a human melanoma by autologous cytolytic T lymphocytes

TL;DR: The human tyrosinase gene has been reported previously to code for two distinct antigens recognized on HLA‐A2 melanoma cells by autologous cytolytic T lymphocytes by stimulating lymphocytes of melanoma patient MZ2 with a subclone of the tumor cell line of this patient, and a CTL clone was obtained which recognized tumor cells expressing tyrosInase and HLA•B*4402.
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Galectin-3 captures interferon-gamma in the tumor matrix reducing chemokine gradient production and T-cell tumor infiltration

TL;DR: It is shown that galectin-3 secreted by tumours binds both glycosylated IFNγ and glycoproteins of the tumour extracellular matrix, thus avoiding IFNνγ diffusion and the formation of anIFNγ-induced chemokine gradient required for T cell infiltration.