American journal of ophthalmology · 2003
The T-lymphocyte chemoattractant Mig is highly expressed in vernal keratoconjunctivitis.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Abu El-Asrar Ahmed M, Struyf Sofie, Al-Kharashi Soliman A, Missotten Luc, Van Damme Jo, Geboes Karel
Аннотация
PURPOSE: To examine the expression of the three interferon-gamma-inducible CXCR3-binding chemokines, CXCL10/IP-10 (interferon-gamma-inducible protein of 10 KDa), CXCL9/Mig (monokine induced by interferon-gamma), and CXCL11/I-TAC (interferon-inducible T-cell alpha chemoattractant) in the conjunctiva of patients with vernal keratoconjunctivitis (VKC). These chemokines exhibit potent T-lymphocyte chemoattractant activity.
DESIGN: Immunohistochemical study.
METHODS: Conjunctival biopsy specimens from 16 patients with active VKC and nine control subjects were studied by immunohistochemical techniques using monoclonal antibodies directed against IP-10, Mig, and I-TAC. The phenotype of inflammatory cells expressing chemokines was examined by double immunohistochemistry.
RESULTS: In the normal conjunctiva, very weak Mig immunoreactivity was observed on basal epithelial cells and on vascular endothelial cells in the upper substantia propria. There was no immunoreactivity for the other chemokines. In all VKC specimens, strong immunoreactivity for Mig was expressed by epithelial cells, vascular endothelial cells, and inflammatory mononuclear cells. Inflammatory mononuclear cells expressing IP-10 and I-TAC were noted in 10 and nine specimens, respectively. The numbers of Mig(+) inflammatory cells were significantly higher than the numbers of IP-10(+) and I-TAC(+) inflammatory cells (P <.001). Inflammatory cells expressing Mig were CD4(+) T-helper/inducer cells (71.6 +/- 3.2%), CD8(+) T-cytotoxic/suppressor cells (19.5 +/- 1.5%), and CD68(+) monocytes/macrophages (5.3 +/- 5%). All inflammatory cells expressing IP-10 and I-TAC were CD68(+) monocytes/macrophages.
CONCLUSIONS: The CXC chemokine Mig is selectively and highly expressed in VKC suggesting a pathogenic role of the chemokine receptor CXCR3 and the ligand Mig in the recruitment of activated T lymphocytes.
DESIGN: Immunohistochemical study.
METHODS: Conjunctival biopsy specimens from 16 patients with active VKC and nine control subjects were studied by immunohistochemical techniques using monoclonal antibodies directed against IP-10, Mig, and I-TAC. The phenotype of inflammatory cells expressing chemokines was examined by double immunohistochemistry.
RESULTS: In the normal conjunctiva, very weak Mig immunoreactivity was observed on basal epithelial cells and on vascular endothelial cells in the upper substantia propria. There was no immunoreactivity for the other chemokines. In all VKC specimens, strong immunoreactivity for Mig was expressed by epithelial cells, vascular endothelial cells, and inflammatory mononuclear cells. Inflammatory mononuclear cells expressing IP-10 and I-TAC were noted in 10 and nine specimens, respectively. The numbers of Mig(+) inflammatory cells were significantly higher than the numbers of IP-10(+) and I-TAC(+) inflammatory cells (P <.001). Inflammatory cells expressing Mig were CD4(+) T-helper/inducer cells (71.6 +/- 3.2%), CD8(+) T-cytotoxic/suppressor cells (19.5 +/- 1.5%), and CD68(+) monocytes/macrophages (5.3 +/- 5%). All inflammatory cells expressing IP-10 and I-TAC were CD68(+) monocytes/macrophages.
CONCLUSIONS: The CXC chemokine Mig is selectively and highly expressed in VKC suggesting a pathogenic role of the chemokine receptor CXCR3 and the ligand Mig in the recruitment of activated T lymphocytes.
Предметные рубрики MeSH
AdolescentAdultAntigens, CDAntigens, Differentiation, MyelomonocyticBiopsyCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesChemokine CXCL10Chemokine CXCL11Chemokine CXCL9Chemokines, CXCChildConjunctivaConjunctivitis, AllergicEndothelium, VascularEpithelial CellsFemaleHumansImmunoenzyme TechniquesImmunophenotypingIntercellular Signaling Peptides and ProteinsInterferon-gammaMacrophagesMaleMonocytesCD68 Molecule