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Screening Bioactive Nanoparticles in Phagocytic Immune Cells for Inhibitors of Toll-like Receptor Signaling
Published on: July 26, 2017
Toll like receptors and pancreatic diseases: From a pathogenetic mechanism to a therapeutic target
Matteo Santoni1, Kalliopi Andrikou1, Valeria Sotte1
1Clinica di Oncologia Medica, AOU "Ospedali Riuniti", Università Politecnica delle Marche, via Conca 71, 60126 Ancona, Italy.
Abstract:
Toll-like receptors (TLRs) mediate interactions between environmental stimuli and innate immunity. TLRs play a major role in the development of numerous pancreatic diseases, making these molecules attractive as potential therapeutic targets. TLR2, TLR7 and TLR9 are involved in the initiation of type 1 diabetes mellitus (T1DM), whereas TLR2 and TLR4 play a major role in the onset of type 2 diabetes mellitus (T2DM). Furthermore, TLRs cause derangements in several tumor suppressor proteins (such as p16, p21, p27, p53 and pRb), induce STAT3 activation and promote epithelial-mesenchymal transition as well as oncogene-induced senescence. In this review we will focus on the contribution of TLRs in pancreatic disease including cancer and we describe recent progress in TLR-modulation for the treatment of these patients.
Insights
Toll-like receptors (TLRs) are key in pancreatic diseases like diabetes and cancer. Modulating TLRs offers promising therapeutic strategies for these conditions.
Area of Science:
- Immunology
- Endocrinology
- Oncology
Background:
- Toll-like receptors (TLRs) link environmental factors to innate immunity.
- TLRs are implicated in the pathogenesis of various pancreatic diseases, including diabetes and cancer.
- Specific TLRs (TLR2, TLR7, TLR9, TLR4) are associated with type 1 and type 2 diabetes mellitus.
Purpose of the Study:
- To review the role of TLRs in pancreatic diseases, encompassing diabetes and cancer.
- To highlight the impact of TLRs on tumor suppressor proteins and cellular processes relevant to cancer.
- To discuss recent advancements in TLR-targeting therapies for pancreatic conditions.
Main Methods:
- Literature review focusing on the involvement of TLRs in pancreatic diseases.
- Analysis of TLRs' contribution to diabetes mellitus (T1DM and T2DM) pathogenesis.
- Examination of TLR-induced molecular changes, including tumor suppressor protein derangements and epithelial-mesenchymal transition.
Main Results:
- TLRs are critical in initiating both type 1 and type 2 diabetes mellitus.
- TLRs disrupt tumor suppressor proteins (p16, p21, p27, p53, pRb) and activate STAT3.
- TLRs promote epithelial-mesenchymal transition and oncogene-induced senescence, contributing to pancreatic cancer development.
Conclusions:
- TLRs play a significant role in the development and progression of pancreatic diseases, including cancer.
- Targeting TLRs presents a viable therapeutic avenue for managing pancreatic diseases.
- Further research into TLR modulation holds promise for improved patient outcomes in pancreatic cancer and diabetes.
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