AIM: To investigate the capability of retinal pigment epithelium (RPE) cells to phagocytose T lymphocytes and to further analyse the immunobiological consequences of this phagocytosis. METHODS: Human RPE cells pretreated or not by cytochalasin, a phagocytosis inhibitor, were co-cultured with T lymphocytes for different time points. Phagocytosis was investigated by optic microscopy, electron microscopy, and flow cytometry. T cell proliferation was measured by (3)H thymidine incorporation. RPE interleukin 1beta mRNA expression was quantified by real time PCR. RESULTS: RPE cells phagocytose apoptotic and non-apoptotic T lymphocytes, in a time dependent manner. This is an active process mediated through actin polymerisation, blocked by cytochalasin E treatment. Inhibition of RPE cell phagocytosis capabilities within RPE-T cell co-cultures led to an increase of lectin induced T cell proliferation and an upregulation of interleukin 1beta mRNA expression in RPE cells. CONCLUSIONS: It is postulated that T lymphocyte phagocytosis by RPE cells might, by decreasing the total number of T lymphocytes, removing apoptotic lymphocytes, and downregulating the expression of IL-1beta, participate in vivo in the induction and maintenance of the immune privilege of the eye, preventing the development of intraocular inflammation.
AIM: To investigate the capability of retinal pigment epithelium (RPE) cells to phagocytose T lymphocytes and to further analyse the immunobiological consequences of this phagocytosis. METHODS:Human RPE cells pretreated or not by cytochalasin, a phagocytosis inhibitor, were co-cultured with T lymphocytes for different time points. Phagocytosis was investigated by optic microscopy, electron microscopy, and flow cytometry. T cell proliferation was measured by (3)H thymidine incorporation. RPE interleukin 1beta mRNA expression was quantified by real time PCR. RESULTS: RPE cells phagocytose apoptotic and non-apoptotic T lymphocytes, in a time dependent manner. This is an active process mediated through actin polymerisation, blocked by cytochalasin E treatment. Inhibition of RPE cell phagocytosis capabilities within RPE-T cell co-cultures led to an increase of lectin induced T cell proliferation and an upregulation of interleukin 1beta mRNA expression in RPE cells. CONCLUSIONS: It is postulated that T lymphocyte phagocytosis by RPE cells might, by decreasing the total number of T lymphocytes, removing apoptotic lymphocytes, and downregulating the expression of IL-1beta, participate in vivo in the induction and maintenance of the immune privilege of the eye, preventing the development of intraocular inflammation.
Authors: L Farrokh-Siar; K A Rezai; E M Palmer; S C Patel; J T Ernest; G A van Seventer Journal: Invest Ophthalmol Vis Sci Date: 2000-11 Impact factor: 4.799
Authors: F Willermain; L Caspers-Velu; N Baudson; C Dubois; M Hamdane; F Willems; T Velu; C Bruyns Journal: Invest Ophthalmol Vis Sci Date: 2000-10 Impact factor: 4.799
Authors: Kevin P Kennelly; Toby M Holmes; Deborah M Wallace; Cliona O'Farrelly; David J Keegan Journal: Cell Transplant Date: 2017-01-20 Impact factor: 4.064