Key points are not available for this paper at this time.
One of the major obstacles in tumor-immunology is the outgrowth of malignant tumors despite their immunogenicity and recognition by the immune-system. Multiple mechanisms for this phenomenon have been proposed. We review the possible involvement of transforming growth factor beta (TGF-β) in this context. TGF-β is a cytokine with pleiotropic functions, involved in multiple physiologic processes including immunoregulation. Immune elimination of most cancers ultimately depends on cytolytic T cells (CTL). We propose a mechanism of specific suppression of cytolytic T cell (CTL)-responses mediated through immunoglobulin-bound TGF-β (IgG-TGF-β), secreted by activated B cells, and a cell of myeloid origin. This mononuclear “Veto” cell presumably binds IgG-TGF-β through Fc-receptors and activates latent TGF-β. The suggestion that B cell responses can inhibit tumor rejection is supported by observations in B cell–deficient mice. Ways for enhancing effective cancer immunity by interfering with the network of interactions involving IgG-TGF-β are discussed. Microsc. Res. Tech. 52:387–395, 2001. © 2001 Wiley-Liss, Inc.
Beck et al. (Mon,) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: