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Biomedical subjects

R Stiemer

Publications and source records attributed to R Stiemer.

7 recordsLinked to original sources
PubMed2001

Immunology and growth characteristics of ocular basal cell carcinoma.

BACKGROUND: Knowledge about immunological features and growth characteristics of palpebral (ocular) basal cell carcinomas (BCCs) is limited. In particular, it is unclear whether ocular BCC represents in this regard a special BCC entity or not. METHODS: Twenty BCCs of the lid area (ocular BCCs) were investigated immunohistologically using monoclonal antibodies against CD4, CD8, CD45Ro, CD50, CD68, HECA-452, Ki67 (MIB1), and the p53 epitope. For comparison, nine BCCs excised distant from the eye (non-ocular BCCs) were evaluated. RESULTS: In BCCs the distribution of the immunocompetent cells investigated is markedly irregular. These cells are localized mainly around BCC islands. Only a few of them invade tumour cell aggregates. The CD4:CD8 ratio as detected by immunohistochemistry is >1 in 82% of ocular BCCs and in 88% of nonocular BCCs. Often there are dense infiltrations of CD68+ cells (macrophages) and HECA-452+ cells adjacent to tumour cell aggregates. The growth fraction [percentage of proliferating (Ki67+/MIB 1+) cells] varies from 0% to more than 30%. Proliferative activity is enhanced at the invasion front. Additionally, the amount of p53+ cells differs considerably among the BCCs. CONCLUSIONS: CD4+ T cells seem to be the most important cell population for BCC immunosurveillance, offering the chance for conservative interferon therapy. The role of CD68+ and HECA-452+ cells has to be further elucidated. In many tumours the large amount of proliferating cells contrasts to the usually slow growth of BCCs, indicating strong apoptotic processes. The results can be regarded only as semiquantitative. So far, ocular and nonocular BCCs exhibit no essential differences regarding immunocompetent cell infiltration and growth characteristics. According to this, palpebral BCCs are "normal" BCCs and not a special BCC variant. Therefore, results from dermatological research concerning BCC can be extended without limitations to their counterparts in the lid area.

Adult↗
PubMed2000

Identification of visual arrestin (S-antigen) in retinal pigmented epithelial cells.

PURPOSE: Inactivation of photolyzed rhodopsin requires phosphorylation of this receptor and binding of the 48 kDa regulatory protein arrestin (S-antigen). Arrestin is also to cause an autoimmune disease, uveoretinits, that resembles uveitis in humans. In this study we demonstrate the presence of visual arrestin in retinal pigment epithelial cells (RPE) in culture. METHODS: Bovine RPE were isolated. Mouse and rat monoclonal and rabbit polyclonal antibodies against visual arrestin, and a synthetic peptide "GFLGELTSSEVATEVPFRLM" (a pathogenic sequence corresponding to residues 340 to 359 of human visual arrestin), and rabbit polyclonal antibody against the specific peptide "EDPDTAKESFQ" for bovine visual arrestin were used to detect arrestin in RPE cells. Using visual arrestin specific primer, RT-PCR of RNA from RPE was performed. RESULTS: By western blots analysis a 48 kDa protein, corresponding to visual arrestin was detected with both mAb and polyclonal antibodies in extracts of RPE cells. RT-PCR analysis of RNA from RPE cells confirmed the presence of arrestin mRNA of predicted 377 bp and exhibited 100% homology with visual arrestin 48 kDa. CONCLUSION: Visual arrestin proteins present in RPE may be involved in the desensitization of G-protein-coupled receptors in RPE cells and in arrestin uveopathogenesis.

Amino Acid Sequence↗
PubMed1999

[High endothelial venules. Kinetics of the expression in IRBP-induced experimental autoimmune uveitis].

UNLABELLED: Experimental autoimmune uveitis (EAU) is a T-cell-mediated disease expressing high endothelial venules (HEVs) in the retina. HEVs could be responsible for the absorption of activated T-cells. The purpose of this study was to investigate the kinetics of HEV expression in the murine IRBP (interphotoreceptor retinoid binding protein) induced EAU. METHODS: B10. A mice were immunized subcutaneously with IRBP. The eyes were analysed on days 10, 18, 24 and 28 (n = 5 for each time point). While HEVs were identified with the mAb MECA 325, the control mAb MECA 20 stained all endothelial cells. RESULTS: HEVs were detectable in the intact retina from day 10. Presence of HEVs peaked on day 18 and decreased by day 28, when maximal inflammation and retinal destruction was detectable. CONCLUSION: HEV expression could play a central role in the onset of EAU, allowing homing and migration of inflammatory cells into the eye.

Animals↗
PubMed1999

[Experimental autoimmune uveitis. Characterization of retina infiltrating cells].

UNLABELLED: The chronic model of murine EAU induced by interphotoreceptor retinoid binding protein represents a disease similar to clinical chorioretinitis. In this study we characterized the kinetics of retina infiltrating T-cells, macrophages and expression of the adhesion molecules ICAM-1 and ICAM-2. METHODS: B10.A mice were immunized subcutaneously with IRBP, and the eyes were analyzed on days 10, 18, 24 and 28. The infiltrating cells were characterized by mAbs recognizing T-cell receptors (TCR) Vss6 and Vss8, T-cell markers, macrophages and ICAM-1 and ICAM-2. RESULTS: While CD8+ T-cells and ICAM-2 were detectable from day 10 (retina is intact) until day 28, CD4+ T-cells, macrophages and ICAM-1 appear with the onset of retinal destruction. Starting at day 10 the dominating TCR was Vss6; Vss8 was noticed from day 18 on. CONCLUSION: CD8+ T-cells infiltrating the intact retina and stimulating the expression of high endothelial venules (HEVs) could be responsible for the onset of uveitis.

Acute Disease↗
PubMed1997

[Physiological protective mechanisms of the eye].

The physiological mechanisms for the protection of the eye are only partly known. It becomes increasingly evident that the eye is supervised by and included in the immune system of the body. The physiological protection system of the eye consists of a mechanical and an immunological component. The lacrimal gland plays a key role for the immune system of the anterior segment. It is part of the MALT system, and the characterisation of the special ocular components of this system-including possible homing receptors-will give important informations. Research of the ocular immune system has disclosed various special features, like the anterior chamber associated immune deviation (ACAID). The distribution of antigen presenting cells and its localization, but also the distribution of T- and B-lymphocytes is an important factor for limiting ocular inflammation. The phenomenon of 'apoptosis' seems to have an important role in maintenance of the ACAID. The cornea is nearly free of cells, and infiltrating antigen presenting cells may prevent ACAID. Research regarding mechanisms which are used to tuned these various cells will give answers to the questions how the cornea contains its optical transparency, how corneal transplant rejection works, how the eye participates in systemic disorders and may also define the role of a possible dysfunction of antigen presenting cells of the retinal pigment epithelium in senile maculopathy.

Antigen-Presenting Cells↗