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. 1997 Aug;81(8):677–682. doi: 10.1136/bjo.81.8.677

Tenascin-C expression in normal, inflamed, and scarred human corneas

H Maseruka 1, R Bonshek 1, A Tullo 1
PMCID: PMC1722281  PMID: 9349157

Abstract

AIMS/BACKGROUND—In adult tissues the expression of tenascin-cytotactin (TN-C), an extracellular matrix glycoprotein, is limited to tumours and regions of continuous renewal. It is also transiently expressed in cutaneous and corneal wound healing. There are limited data regarding its expression in inflammation and scarring of the adult human cornea. In this study, TN-C expression patterns in normal, inflamed, and scarred human corneas have been examined.
METHODS—Penetrating keratoplasty specimens were selected from cases of herpes simplex keratitis, herpes zoster ophthalmicus, rheumatoid arthritis ulceration, bacterial keratitis, rosacea keratitis, interstitial keratitis, and previous surgery so as to encompass varying degrees of active and chronic inflammation and scarring. TN-C in these and in normal corneas was immunodetected using TN2, a monoclonal antibody to human TN-C.
RESULTS—There was no TN2 immunopositivity in normal corneas except at the corneoscleral interface. In pathological corneas, TN2 immunopositivity was localised in and around regions of active inflammation, fibrosis, and neovascularisation. TN2 positivity was less in acute inflammation than in active chronic inflammation. Mature, avascular scar tissue and epithelial downgrowth were TN2 negative.
CONCLUSION—These results indicate that in the adult human cornea, TN-C expression is induced in regions of inflammation, fibrosis, and neovascularisation, but that expression is absent in mature, avascular scar tissue. This suggests a role for this glycoprotein in inflammation, healing, and extracellular matrix reorganisation of the cornea.



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Figure 1  .

Figure 1  

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Normal cornea and corneoscleral interface. There is TN2 immunopositivity of the sclera (small arrows) including the scleral spur (large arrow). Corneal tissue is TN2 immunonegative (× 18).

Figure 2  .

Figure 2  

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Bacterial keratitis, with ulcer and stromal abscess. Strong TN2 immunopositivity in and around the edges of the acutely inflamed tissue. The ulcer, epithelium, and stroma immediately adjacent are negative. There is also subepithelial TN2 immunopositivity in an area of epithelial lifting from oedematous stroma (small arrows) (× 38).

Figure 3  .

Figure 3  

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Bacterial keratitis, higher magnification. Occasional TN2 positive keratocytes are seen in the acutely inflamed area. However, the strongest TN2 immunoreaction is in the posterior stroma where there is a chronic inflammatory cell infiltrate, rather than in the acutely inflamed tissue of mid stroma. The chronic inflammatory cells are negative, but the stromal tissue is positive. Note that Descemet's membrane is negative, but there is a band of TN2 immunopositivity at the interface between posterior stroma and Descemet's membrane (arrowheads). Endothelium has been lost from this cornea (× 185).

Figure 4  .

Figure 4  

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Herpes simplex keratitis cornea. There is stromal TN2 immunopositivity associated with chronic inflammation in the posterior stroma. Inflammatory cells are negative. Note that, as in Figure 3, there is also focal positivity at the interface between posterior stroma and Descement's membrane (arrowheads). Endothelium is intact (× 370).

Figure 5  .

Figure 5  

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Rheumatoid perforation with an area of epithelium bridging a stromal defect. There is diffuse, extracellular, stromal TN2 immunopositivity around the defect. The small amount of subepithelial tissue remaining beneath the undermined epithelium is also strongly positive (small arrows). Iris pigment (IP) is present as discrete deposits in the posterior stroma below and adjacent to the perforation. Very few inflammatory cells are present (× 38).

Figure 6  .

Figure 6  

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Previous surgery. There is patchy chronic inflammation and vascularisation. TN2 immunopositivity is present in the stroma where there is an aggregate of chronic inflammatory cells. Here, occasional lymphocytes have cytoplasmic membrane staining. Elsewhere, there is cytoplasmic labelling of some vascular endothelial cells. There is also granular cytoplasmic staining of epithelial cells overlying this area (× 450, oil immersion).

Figure 7  .

Figure 7  

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Healed 2 year old surgical incision. There is minimal fibroblastic reaction and no vascularisation or inflammation. TN2 immunoreaction is negative in the mature scar tissue (arrows). There is faint granular TN2 immunopositivity in the epithelium above the scar (× 450, oil immersion).

Figure 8  .

Figure 8  

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Epithelial downgrowth that fills a previous relaxing incision. TN2 immunoreaction is negative in both stroma and epithelium (× 180, differential interference contrast (DIC)).

Selected References

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