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Updated: Oct 9, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020
Role of TGF-beta in immune-evasion of cancer
C Beck1, H Schreiber, D Rowley
1Immunology Division, Department of Pathology, University of Chicago, Chicago, Illinois 60637, USA. c.beck@med2.uni-kiel.de
Abstract:
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-beta) in this context. TGF-beta 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-beta (IgG-TGF-beta), secreted by activated B cells, and a cell of myeloid origin. This mononuclear "Veto" cell presumably binds IgG-TGF-beta through Fc-receptors and activates latent TGF-beta. 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-beta are discussed.
Insights
Transforming growth factor beta (TGF-beta), bound by immunoglobulin G (IgG-TGF-beta) and secreted by B cells, may suppress anti-tumor immunity. This mechanism, mediated by myeloid cells, offers targets for enhancing cancer immunity.
Area of Science:
- Immunology
- Cancer Biology
- Molecular Biology
Background:
- Tumor-immunology faces challenges with malignant tumor growth despite immune recognition.
- Transforming growth factor beta (TGF-beta) is a cytokine with diverse roles, including immunoregulation.
- Cytolytic T cells (CTL) are crucial for immune elimination of cancers.
Purpose of the Study:
- To review the potential role of TGF-beta in tumor immune evasion.
- To propose a novel mechanism of CTL suppression mediated by immunoglobulin-bound TGF-beta (IgG-TGF-beta).
Main Methods:
- Review of existing literature on TGF-beta and tumor immunology.
- Proposal of a hypothetical mechanism involving IgG-TGF-beta and myeloid "Veto" cells.
- Analysis of supporting evidence from B cell-deficient mouse models.
Main Results:
- TGF-beta is implicated in immune regulation and potentially tumor immune evasion.
- A mechanism is proposed where IgG-TGF-beta, secreted by B cells and myeloid cells, suppresses CTL responses.
- B cell activity appears to influence tumor rejection, as suggested by studies in deficient mice.
Conclusions:
- IgG-TGF-beta secreted by B cells and myeloid cells may be a key factor in tumor immune evasion by suppressing CTLs.
- Interfering with the IgG-TGF-beta network presents a potential strategy for enhancing anti-cancer immunity.
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