PURPOSE: The aim of this study was to survey the histopathological and immunohistochemical features of rejected human corneal allografts. METHODS: Following graft failure in each case due to rejection, paraffin-embedded specimens of 17 corneal transplants which had been replaced were examined by light microscopy and immunohistochemistry. Specimens were either first (n = 9), second (n = 4) or third (n = 4) grafts and were removed at varying intervals from 4 weeks following documented rejection. RESULTS: Those grafts which were removed earliest following onset of rejection had the most intense graft inflammatory infiltrates. Immunohistochemical staining showed a high proportion of graft stroma-infiltrating cells expressing leucocyte common antigen, and many of these cells also bore T cell or macrophage markers. Leucocyte-keratocyte apposition and regional loss of keratocytes were observed in all rejection specimens, but not in non-rejected control grafts. In situ end-labelling of DNA double-strand breaks and morphological features identified keratocyte apoptosis in 5 of 12 specimens examined for this phenomenon. Corneal endothelial cells were absent in 7 specimens and present in reduced numbers in the remaining 10 specimens. CONCLUSIONS: Endothelial cell monolayer attenuation and keratocyte loss are consistent findings in grafts removed subsequent to clinically observed endothelial rejection. Death of donor corneal cells is mediated, at least in part, by apoptosis. The stromal inflammatory infiltrate consists mainly of T lymphocytes and macrophages, which may be responsible for induction of keratocyte apoptosis.
PURPOSE: The aim of this study was to survey the histopathological and immunohistochemical features of rejected human corneal allografts. METHODS: Following graft failure in each case due to rejection, paraffin-embedded specimens of 17 corneal transplants which had been replaced were examined by light microscopy and immunohistochemistry. Specimens were either first (n = 9), second (n = 4) or third (n = 4) grafts and were removed at varying intervals from 4 weeks following documented rejection. RESULTS: Those grafts which were removed earliest following onset of rejection had the most intense graft inflammatory infiltrates. Immunohistochemical staining showed a high proportion of graft stroma-infiltrating cells expressing leucocyte common antigen, and many of these cells also bore T cell or macrophage markers. Leucocyte-keratocyte apposition and regional loss of keratocytes were observed in all rejection specimens, but not in non-rejected control grafts. In situ end-labelling of DNA double-strand breaks and morphological features identified keratocyte apoptosis in 5 of 12 specimens examined for this phenomenon. Corneal endothelial cells were absent in 7 specimens and present in reduced numbers in the remaining 10 specimens. CONCLUSIONS: Endothelial cell monolayer attenuation and keratocyte loss are consistent findings in grafts removed subsequent to clinically observed endothelial rejection. Death of donor corneal cells is mediated, at least in part, by apoptosis. The stromal inflammatory infiltrate consists mainly of T lymphocytes and macrophages, which may be responsible for induction of keratocyte apoptosis.
Authors: Hidetaka Hara; Naoko Koike; Cassandra Long; Jordan Piluek; Danny S Roh; Nirmala SundarRaj; James L Funderburgh; Yoshiaki Mizuguchi; Kumiko Isse; Carol J Phelps; Suyapa F Ball; David L Ayares; David K C Cooper Journal: Invest Ophthalmol Vis Sci Date: 2011-07-15 Impact factor: 4.799
Authors: Tanja P A M Slegers; Gerard van der Veen; L Joep A Hermans; Lidy Broersma; Nico van Rooijen; Hendrika J Völker-Dieben; Gabriel van Rij; Ruth van der Gaag Journal: Graefes Arch Clin Exp Ophthalmol Date: 2003-04-16 Impact factor: 3.117
Authors: T Hudde; R M Comer; M T Kinsella; L Buttery; P J Luthert; J M Polak; A J T George; D F P Larkin Journal: Br J Ophthalmol Date: 2002-09 Impact factor: 4.638