Purpose. To investigate the density, distribution, and morphology of macrophages (bone marrow-derived microglia) and major histocompatibility complex (MHC) class II-positive cells in the retina of Lewis rats and the dynamics of these cells after systemic lipopolysaccharide (LPS) injection. Methods. Immunohistochemistry was carried out using monoclonal antibodies specific to monocytes and macrophages (ED1, ED2) and MHC class II-positive cells (OX-6) on whole-mounts of the retina obtained from Lewis rats before and at different time points after footpad injection of 200 g of LPS. Results. The inner layers of the normal retina contained a network of macrophages, whereby ED1 and ED2 staining revealed similar results. Macrophages were either dendritiform or pleiomorphic in morphology, with the former predominant. The density of positive cells was higher at the peripheral part and the periequatorial part (271

Purpose: Recent studies have shown that experimental uveitis can be induced by the appropriate administration of various retinal antigens. Little is known about the in-situ interactions between immune cells in the retina as a prerequisite for understanding the mechanisms involving the presentation of antigens by local antigen-presenting cells (APC) to invading T cells. The study described here was therefore designed to investigate the presence of immunocompetent cells with a focus on the characterization of retinal APCs. Materials and methods: Retinal whole mounts, cytospins, and ocular sections were prepared from eyebank eyes obtained within 24 hours postmortem. Immunohistochemistry (single staining and double staining) was performed on the retinal wholemounts, cytospins, and the ocular sections using monoclonal antibodies specific for HLA-DR (MHC class II), CD45 (leukocytes), CD68 (macrophages), CD2z (B cells), CD3 (T cells), and CDLa (dendritic cells). Results: CD68 positive macrophages were observed in one layer of the retina, whereas HLA-DR~ and CD45+ cells were seen in two distinct planes: one mainly at the level of the inner nuclear layer to outer plexiform layer (deep layer) and the other mainly at the nerve fiber and ganglion cell layer (shallow layer). There was a significant difference between the different parts of the retina with regard to the density of these cells. Cell density decreased when going from the peripheral to the posterior areas of the retina. The positive cells in the deep layer were frequently associated with blood vessels, whereas the cells in the shallow layer were distributed evenly throughout the retina. Most positive cells displayed a dendritiform appearance, whereas few cells showed a pleiomorphic morphology. Very few CDIa-positive cells were noted in the retina. Neither T cells (CD3) nor B cells (CD22) could be detected in the normal human retina. Double staining showed that the majority (83.7%) of the CD45~ cell population Was I-ILA-DR-positive, whereas approximately half (56.8%) the CD68~Cell population was HLA-DR-positive. Conclusions: This study shows that the human retina contains a number of different microglia populations, some of which express HLA-DR and could thus be involved in antigen presentation. Marked differences in cell density can be observed within the retina, with the most abundant presence seen in the peripheral retina. The normal retina contains few professional antigen-presenting cells (CDI+).

Retinal microglia originate flom hemopoietic cells and invade the retina from the retinal margin and the optic disc, most likely via the blood vessels of the ciliary body and iris, and the retinal vasculature. respectively. The microglial precursors that appear in the retina 34-325oJerent microglia popula.prior to vascularization arc major histocompatibilily complex (MHC) class 1-and II-positive and express the CD45 marker, but lack specific macrophage markers. They differentiate into ramified parenchymal microglia in the adult retina. A second category of microglial precursors, which do express specific macrophage markers, migrate into the retina along with vascular precursors. They appear around blood vessels in the adult retina and are similar to macrophages or cells of the mononuclear phagocyte series (MPS). Microglia are distributed in the outer plexiform laver (OPL), outer nuclear laver (ONL), inner plexiform layer (IPL), ganglion cell layer (GCL), and nerve fiber laver (NFL) of the primate retina. The pattern of microglial distribution in the avascular retina of the quail indicates that blood vessels are not responsible for the final location of microglia in the retina. In the human retina, microglia express MHC class l, MHC class II, CD45. CD68, and $22 markers. In the rat and mouse retina. OX41, OX42, OX3, OX6. OX18, ED1, Mac-l, F4/80, 5D4 anti-keralan sulfate, and lectins are used to recognize microglia. Microglial cells play an important role in host defense against invading microorganisms, immunoregulation, and tissue repair. During neurodegeneration, activated microglial cells participate in the phagocytosis ol debris and facilitate regenerative processes. In autoimnmne disease, microglia have dual functions: initialing uveoretinitis, but also limifing subsequent inflame marion. Retinal microglia may he associated wiih vitreoretinopathy, diabetic retinopathy, glaucoma, and age-related macular degeneration. The goal of this article was to review the present knowledge about retinal microglia and the function of retinal microglia in pathological conditions.

Aim: To investigate T-bet mRNA and protein expression on peripheral blood monanuclear cells (PBMC) in patients with Behcet's disease with active uveitis. Methods: Blood samples were taken from 24 patients with Behcet's disease who had active uveitis and 16 healthy individuals. PBMC were subjected to analysis of T-bet mRNA nd protein expression using semiquatitative reverse tran scriptase-polymerase chain reaction (RT-PCR) and western blot, respectively. The products from PCR were sequenced. In order to determine the influence of activation on T-bet expression, the phytohaemagglutinin (PHA) stimulated PBMC from each sample were also evaluated for expression of T-bet mRNA and protein. Results: A significantly increased T-bet mRNA accumulation was detected in the samples from patients with active Behcet's disease compared with that in controls. A 62 kDa band was detectable in patients with active Behcet's disease, but not in controls. No difference was found between patients with Behcet's disease who had active uveitis and normal controls concerning the expression of either T-bet mRNA or its protein after stimulation with PHA for 72 hours. Conclusion: Behcet's disease is associated with an upregulation of T-bet expression, which supports a role for the Thl subset of T cells in the pathogenesis of this disease.