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Gewählte Publikation:

BECKER, JC; BRABLETZ, T; CZERNY, C; TERMEER, C; BROCKER, EB.
TUMOR ESCAPE MECHANISMS FROM IMMUNOSURVEILLANCE - INDUCTION OF UNRESPONSIVENESS IN A SPECIFIC MHC-RESTRICTED CD4+ HUMAN T-CELL CLONE BY THE AUTOLOGOUS MHC CLASS-II+ MELANOMA
INT IMMUNOL. 1993; 5(12): 1501-1508. Doi: 10.1093/intimm/5.12.1501 [OPEN ACCESS]
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Führende Autor*innen der Med Uni Graz

Becker Jürgen Christian

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Abstract:

The co-existence of tumor specific immunity with a progressing tumor is observed in a variety of experimental systems and remains one of the major paradoxes of tumor immunology. We now report that a human melanoma cell line (SMC) expressing MHC class II was able to induce clonal anergy in a specific, MHC-restricted CD4+ T cell clone (STC3). Clonal anergy is a mechanism of T lymphocyte tolerance induced by antigen receptor stimulation in the absence of co-stimulation. We observed that a CD4+ T cell clone and an autologous melanoma cell line form conjugates with each other that leads to an increase of [Ca++]i in the T cell clone; however, this interaction failed to induce IL-2 production or proliferation of the T cell clone. Furthermore, this interaction rendered this T cell clone unresponsive to subsequent stimulation. All these effects were MHC class II restricted. Therefore, the human melanoma cell line SMC was capable of delivering antigen-specific signals to the T cell clone, but did not deliver the co-stimulatory signals, e.g. a B7/CD28 interaction, necessary for full T cell activation. Transfection of the melanoma cells with an expression vector containing a B7 cDNA that resulted in subsequent expression of B7 on its cell surface rendered it into a fully competent antigen presenting cell, which is able to induce a nuclear factor binding to the IL-2 promoter in the specific T cell clone resulting in enhanced IL-2 transcription, synthesis, and T cell proliferation. These findings suggest that manipulation of co-stimulation may offer new strategies for future tumor immunotherapy.

Find related publications in this database (Keywords)

CD4+

IMMUNOSURVEILLANCE

MHC

TUMOR

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