Inflammation identity crisis: pathogenic nature of platelet-derived transforming growth factor β in chronic inflammatory conditions
- 1Department of Immunology and Microbiology, University of Rochester School of Medicine and Dentistry
- 2Department of Neurology, University of Rochester School of Medicine and Dentistry
- 3Department of Neuroscience, University of Rochester School of Medicine and Dentistry
Abstract
Chronic inflammatory conditions are associated with sustained platelet activation and subsequent release of platelet-derived immunomodulatory factors. Among these, platelets are the largest circulating reservoir of transforming growth factor β (TGFβ), and as such can be implicated in all physiological processes where TGFβ plays a crucial role. TGFβ is associated with immune regulation via dampening of Th ₁ responses, amplification of regulatory T lymphocyte polarization, and reduced inflammation, which can be beneficial in mitigating autoimmune diseases. However, in the case of solid tumors or persistent viral infections, this function can result in aberrant immune suppression and increased disease severity and pathology. TGFβ is also implicated in tissue remodeling and wound healing, however, in conditions associated with chronic platelet activation, such as diabetes, hypertension, and HIV infection, increased levels of platelet-derived TGFβ can exacerbate fibrosis, resulting in tissue and organ damage. Thus, whether TGFβ plays a pathogenic or pro-homeostatic role is dependent on the disease context. In order to harness the therapeutic potential of platelet-derived TGFβ, it is crucial to first understand how its mechanism of action varies across physiologic and pathologic conditions. In this review, we aim to emphasize the highly pleiotropic nature of TGFβ, highlight what is currently known about platelet-derived TGFβ across disease states, and to reinforce the importance of considering platelet-derived mediators as regulators of immunity and tissue responses, especially in the presence of chronic inflammation.
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BibTeX
@article{sutton2026inflammation,
title = {{Inflammation identity crisis: pathogenic nature of platelet-derived transforming growth factor β in chronic inflammatory conditions}},
author = {Karli R. Sutton and Rachel C. Eisenhart and Meera V. Singh},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1938898},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1938898/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Inflammation identity crisis: pathogenic nature of platelet-derived transforming growth factor β in chronic inflammatory conditions
AU - Karli R. Sutton
AU - Rachel C. Eisenhart
AU - Meera V. Singh
PY - 2026
DA - 2026/10/05
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1938898
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1938898/full
AB - Chronic inflammatory conditions are associated with sustained platelet activation and subsequent release of platelet-derived immunomodulatory factors. Among these, platelets are the largest circulating reservoir of transforming growth factor β (TGFβ), and as such can be implicated in all physiological processes where TGFβ plays a crucial role. TGFβ is associated with immune regulation via dampening of Th ₁ responses, amplification of regulatory T lymphocyte polarization, and reduced inflammation, which can be beneficial in mitigating autoimmune diseases. However, in the case of solid tumors or persistent viral infections, this function can result in aberrant immune suppression and increased disease severity and pathology. TGFβ is also implicated in tissue remodeling and wound healing, however, in conditions associated with chronic platelet activation, such as diabetes, hypertension, and HIV infection, increased levels of platelet-derived TGFβ can exacerbate fibrosis, resulting in tissue and organ damage. Thus, whether TGFβ plays a pathogenic or pro-homeostatic role is dependent on the disease context. In order to harness the therapeutic potential of platelet-derived TGFβ, it is crucial to first understand how its mechanism of action varies across physiologic and pathologic conditions. In this review, we aim to emphasize the highly pleiotropic nature of TGFβ, highlight what is currently known about platelet-derived TGFβ across disease states, and to reinforce the importance of considering platelet-derived mediators as regulators of immunity and tissue responses, especially in the presence of chronic inflammation.
SN - 1664-3224
ER -