March 2017
Volume 58, Issue 3
Open Access
Research Highlight  |   March 2017
Cross Talk Between TGF-β2 and TLR-4
Author Affiliations
  • Paul A. Knepper
    Department of Ophthalmology and Visual Sciences, University of Illinois Chicago, Chicago, Illinois, United States; Department of Ophthalmology, Northwestern University Medical School, Chicago, Illinois, United States; pknepper@northwestern.edu
Investigative Ophthalmology & Visual Science March 2017, Vol.58, 1824. doi:10.1167/iovs.17-21782
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      Paul A. Knepper; Cross Talk Between TGF-β2 and TLR-4. Invest. Ophthalmol. Vis. Sci. 2017;58(3):1824. doi: 10.1167/iovs.17-21782.

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      © ARVO (1962-2015); The Authors (2016-present)

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The innate immune system is the first line of defense in preventing infection and disease. The innate immune response is immediate and protects cells from both damage-associated molecular patterns (DAMPs) and exogenous pathogen-associated molecular patterns. Taylor et al.1 demonstrated the role of low-molecular-weight hyaluronic acid fragments as DAMPs that trigger cellular signaling through Toll-like receptor 4 (TLR-4) and CD44. Recently, Grybauskas et al.2 identified expression of TLR-4 in the trabecular meshwork (TM). Hernandez and colleagues3 have extended these studies to identify a cross-talk pathway between TGF-β2 and TLR-4 in response to the DAMP cellular fibronectin extra domain A, which leads to a profibrotic response in the TM. The authors demonstrate that a profibrotic TGF-β2–TLR-4 cross-talk mechanism is involved in the production and regulation of the extracellular matrix in the TM. Their data illustrate a novel pathway involved in TM fibrosis and may shed light on the etiology of glaucomatous TM damage. Since the discovery of increased stiffness in glaucomatous TM by Russell and Johnson,4 a clearer understanding of increased IOP has finally arrived. In principle, Hernandez and colleagues3 have given a working blueprint of the structural damage of the TM leading to increased IOP, as well as the potential to prevent fibrotic changes in the TM. The authors should be commended for their study and its potential impact on our understanding of the pathophysiology of the TM in primary open angle glaucoma. 
References
Taylor KR, Trowbridge JM, Rudisil JA, Termeer CC, Simon JC, Gallo RL. Hyaluronan fragments stimulate endothelial recognition of injury through TLR4. J Biol Chem. 2004; 279: 17079–17084.
Grybauskas A, Koga T, Kuprys PV, et al . ABCB1 transporter and Toll-like receptor 4 in trabecular meshwork cells. Mol Vis. 2015; 21: 201–212.
Hernandez H, Medina-Ortiz WE, Luan T, Clark AF, McDowell CM. Crosstalk between transforming growth factor beta-2 and toll-like receptor 4 in the trabecular meshwork. Invest Ophthalmol Vis Sci. 2017; 58: 1811–1823.
Russell P, Johnson M. Elastic modulus determination of normal and glaucomatous human trabecular meshwork. Invest Ophthalmol Vis Sci. 2012; 53: 117.
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