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  • 1
    Electronic Resource
    Electronic Resource
    Heat shock protein expression in oral lichen planus (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of oral pathology & medicine 24 (1995), S. 0 
    Details
    ISSN: 1600-0714
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: To assess the potential role of heat shock protein (HSP) in the pathogenesis of oral lichen planus (OLP), sections of OLP, normal oral mucosa, non-specific oral ulceration (NSOU) and dysplastic OLP were assessed for HSP expression using avidin-biotin complex immunohistochemistry with an anti-HSP 70 polyclonal antibody. There were statistically significant differences in both the vertical and horizontal staining distribution when other groups were compared with the OLP group (p〈0.01). Using microdensitometry, the mean staining intensity in OLP, dysplastic OLP and NSOU was elevated in comparison with normal oral mucosa (p〈0.001). In a standard tritiated thymidine uptake assay, lymphocytes extracted from nine OLP lesions demonstrated significant proliferation when stimulated with purified protein derivative (PPD), of which HSP is a major constituent, with stimulation indices ranging from 2 to 132. These results are consistent with the hypothesis that, in OLP patients, diverse exogenous agenst may cause upregulated expression of HSP by oral mucosal keratinocytes. A reaction of cytotoxic T lymphocytes to these activated keratinocytes may then result in the tissue destruction which is characteristic of OLP lesions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-0714.1995.tb01121.x
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  • 2
    Electronic Resource
    Electronic Resource
    Mast cell/T cell interactions in oral lichen planus (2002)
    Oxford, UK : Blackwell Science, Ltd
    Journal of oral pathology & medicine 31 (2002), S. 0 
    Details
    ISSN: 1600-0714
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Lichen planus is a disorder characterized by lesions of the skin and oral mucous membranes. Although many patients have involvement of both skin and oral mucosa at some stage during the progress of the disease, a larger group has oral involvement alone. It has been reported that oral lichen planus (OLP) affects one to two percent of the general population and has the potential for malignant transformation in some cases (1, 2). Like many chronic inflammatory skin diseases, it often persists for many years. Numerous disorders may be associated with OLP such as graft-vs.-host disease and Hepatitis C virus infection (3), however, it is unclear how such diverse influences elicit the disease and indeed whether they are identical to idiopathic OLP.Available evidence supports the view that OLP is a cell-mediated immunological response to an induced antigenic change in the mucosa (4–6). Studies of the immunopathogenesis of OLP aim to provide specific novel treatments as well as contributing to our understanding of other cell-mediated inflammatory diseases. In this paper, the interactions between mast cells and T cells are explored from the standpoint of immune regulation. From these data, a unifying hypothesis for the immunopathogenesis of OLP is then developed and presented.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1600-0714.2002.310401.x
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  • 3
    Electronic Resource
    Electronic Resource
    Clonal expansion of lymphocytes from oral lichen planus lesions (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of oral pathology & medicine 22 (1993), S. 0 
    Details
    ISSN: 1600-0714
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Lymphocytes were extracted from 11 biopsy specimens of oral lichen planus (OLP) by collagenase digestion, and cell lines were expanded with repetitive cycles of stimulation (with phytohaemagglutinin) and rest in media supplemented with interleukin 2. Four OLP lines contained a majority of CD3 + CD4 −CD8 + cells, in six lines the CD4:CD8 ratio was between I and 2, and in one line the CD4:CD8 ratio was 5:1. Limiting dilution of nine lines at 0.3 and 1.0 cells/well resulted in viable wells (putative clones) with plating efficiencies ranging from 0.0 to 18.1 percent and 0.0 to 22.2 percent respectively. The majority of clones were CD3 + CD4–CD8 +αβ+γδ-, although three clones were CD3 + CD4 + CD8 - αβ+γδ - and one clone was CD3 + CD4 - CDS - and expressed the γδ T cell receptor. T cell clones derived from lymphocytes extracted from OLP lesions may be generated and maintained in culture providing opportunity for their further phenotypic and functional characterisation. This strategy may facilitate the identification of a putative oral lichen planus-specific antigen and indicate the frequency of lichen planus-specific T cells within lesions of OLP.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-0714.1993.tb01043.x
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  • 4
    Electronic Resource
    Electronic Resource
    Phenotypic and functional analysis of peripheral blood lymphocytes in oral lichen planus (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of oral pathology & medicine 21 (1992), S. 0 
    Details
    ISSN: 1600-0714
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: To assess cellular immunity in oral lichen planus (OLP), peripheral blood mononuclear cells (PBMC) were obtained from 19 OLP patients and 30 control subjects. The proportions of circulating CD45RA+ and CD29+ lymphocyte subsets were determined. The proliferative activity of PBMC to the non-specific plant mitogens phytohemagglutinin (PHA) and concanavalin A (Con A) was examined together with the spontaneous proliferative response and the response in the autologous mixed lymphocyte reaction (AMLR). In the OLP group, the proportion of CD4+CD45RA+ T lymphocytes was significantly less than control subjects and the proportion of CD4+ CD29+ T lymphocytes was increased significantly. The proliferative response to PHA was similar in OLP and controls subjects. Con A-stimulated PBMC proliferation was decreased significantly in the OLP group. Spontaneous PBMC proliferation in patients with non-reticular lesions was significantly less than control subjects. Despite a mildly depressed response in the AMLR in OLP patients, this result was not statistically significant. Results of the phenotypic analysis of peripheral blood lymphocytes indicate a decreased proportion of naive T cells and an increased proportion of primed memory T cells, although the antigen specificity of these memory cells remains to be determined. Results of the functional assays would seem to reflect this phenotypic shift, and as T cells responding to Con A stimulation and in the AMLR possess suppressor-inducer activity, these results may also suggest an association between OLP and defective innate T cell-mediated suppressor circuits.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-0714.1992.tb00972.x
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  • 5
    Electronic Resource
    Electronic Resource
    Expression of RANTES and CCR1 in oral lichen planus and association with mast cell migration (2002)
    Oxford, UK : Blackwell Science, Ltd
    Journal of oral pathology & medicine 31 (2002), S. 0 
    Details
    ISSN: 1600-0714
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background:  T lymphocytes and mast cells infiltrate the lamina propria in oral lichen planus (OLP). Chemokines and their receptors are involved in T cell and mast cell migration and accumulation during the inflammatory process.Methods:  In the present study, we investigated the role of RANTES and its receptors in OLP using immunohistochemistry, RT-PCR and an in vitro chemotaxis assay.Results:  RANTES and CCR1 were expressed on T cells and mast cells in OLP, while OLP lesional T cell supernatants stimulated CCR1 mRNA expression in a human leukemia mast cell line (HMC-1). TNF-α stimulated CCR1, CCR4 and CCR5 mRNA expression in the same cell line. OLP lesional T cell supernatants stimulated HMC-1 migration, which was partly inhibited by anti-RANTES antibody.Conclusions:  The present study shows, for the first time, the distribution of RANTES and CCR1 in OLP. It is hypothesized that RANTES and CCR1 may play important roles in mast cell trafficking and related events in OLP.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1600-0714.2002.310306.x
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  • 6
    Electronic Resource
    Electronic Resource
    Preliminary functional analysis of human epidermal T cells (2000)
    Springer
    Archives of dermatological research 292 (2000), S. 9-15 
    Details
    ISSN: 1432-069X
    Keywords: Key words Epidermal T cells ; Function ; Human
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The function of human epidermal T cells (ETC) is unknown. In the present study, dermal T cells (DTC), ETC and keratinocytes were cultured from normal human skin. DTC and ETC lines were expanded in medium containing interleukin 2. The autologous keratinocytes were transfected with a human papillomavirus 16 E6 and E7 plasmid to produce an immortal keratinocyte line “HEK001”. Lymphocyte migration and adhesion to HEK001 was assessed in calcein fluorimetric assays. ETC migrated towards HEK001 three to four times more than DTC. ETC adhered to HEK001 two to four times more than DTC. The proportion of ETC expressing the cutaneous lymphocyte-associated antigen was greater than that of DTC (26% and 1%, respectively). The keratinocyte line HEK001 expressed ICAM-1 following stimulation with TNF-α or IFN-γ and following coculture with autologous cutaneous T cells. A blocking anti-ICAM-1 antibody reduced DTC and ETC adhesion to HEK001 by 30% and 50%, respectively. Therefore, cutaneous T cells may upregulate keratinocyte ICAM-1 expression which mediates adhesion to autologous keratinocytes. These results are consistent with the hypothesis that the ETC and DTC populations are distinct. Both directed migration (epidermotropism) and selective retention may be involved in the development and maintenance of the ETC population in normal human skin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00007461
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  • 7
    Electronic Resource
    Electronic Resource
    Ameloblast apoptosis and IGF-1 receptor expression in the continuously erupting rat incisor model (1999)
    Springer
    Apoptosis 4 (1999), S. 441-447 
    Details
    ISSN: 1573-675X
    Keywords: ameloblasts ; amelogenesis ; apoptosis ; insulin-like growth factor.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Enamel-producing cells (ameloblasts) pass through several phenotypic and functional stages during enamel formation. In the transition between secretory and maturation stages, about one quarter of the ameloblasts suddenly undergo apoptosis. We have studied this phenomenon using the continuously erupting rat incisor model. A special feature of this model is that all stages of ameloblast differentiation are presented within a single longitudinal section of the developing tooth. This permits investigation of the temporal sequence of gene and growth factor receptor expression during ameloblast differentiation and apoptosis. We describe the light and electron microscopic morphology of ameloblast apoptosis and the pattern of insulin-like growth factor-1 receptor expression by ameloblasts in the continuously erupting rat incisor model. In the developing rat incisor, ameloblast apoptosis is associated with downregulated expression of the insulin-like growth factor-1 receptor. These data are consistent with the hypothesis that ameloblasts are “hard wired” for apoptosis and that insulin-like growth factor-1 receptor expression is required to block the default apoptotic pathway. Possible mechanisms of insulin-like growth factor-1 inhibition of ameloblast apoptosis are presented. The rat incisor model may be useful in studies of physiological apoptosis as it presents apoptosis in a predictable pattern in adult tissues.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1009600409421
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