Oral lichen planus: characterization of immunocompetent cells with hybridoma antibodies

Becker, Jürgen C.; Löning, T.; Reichart, Peter A.; Hartmann, N

doi:10.1111/j.1600-0714.1983.tb00324.x

Cited by 46 publications

(33 citation statements)

References 25 publications

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“…The prominent cellular infiltrate was characterised to determine the presence of several cellular immunophenotypes. OLP showed an increase in CD4+ T cells, and CD8+ T cells in accord with several other authors (4–7, 34–37). This infiltrate was mainly represented by CD8+ suppressor‐cytotoxic cells.…”

Section: Discussionsupporting

confidence: 91%

“…This infiltrate was mainly represented by CD8+ suppressor‐cytotoxic cells. Previous studies have showed that CD8+ T cells constitute a high proportion of the cellular infiltrate in OLP (4, 6, 7, 35). However, some studies have shown a high proportion of CD4+ T cells (36, 37).…”

Section: Discussionmentioning

confidence: 99%

“…The histopathological diagnosis is based on the presence of an infiltrate of mononuclear cells in the superficial lamina propria, which disrupts the epithelium (4–7) with degeneration of basal epithelial cells and the basement membrane (8). The immunological events may begin with an external or internal antigen that alters the basal epithelial cells, rendering them susceptible to a cell‐mediated immune response involving activation of antigen‐presenting Langerhans cells, immunocompetent keratinocytes, CD4+ T‐helper–inducer cells, CD8+ T‐suppressor‐cytotoxic cells, and the production of cytokines, including chemokines (such as interleukin‐2, interferon gamma and tumour necrosis factor beta) within the epithelium and within the infiltrate by activated leucocytes (2, 4, 6, 8–14).…”

mentioning

confidence: 99%

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Oral lichen planus: immunohistology of mucosal lesions

Dorrego

Correnti

Delgado

et al. 2002

J Oral Pathology Medicine

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Oral lichen planus: immunohistology of mucosal lesions

Dorrego

Correnti

Delgado

et al. 2002

J Oral Pathology Medicine

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“…One ofthe characteristics of OLP is a bandlike subepithelial mononuclear cell infiltrate. Most of the local inflammatory cells are immunocompetent T lymphocytes, as has been demonstrated using cytoadherence (10,11), histochemistry (12,13), and, more recently, by applying T cell specific monoclonal anti- bodies (2,(14)(15)(16)(17). However, based on ultramorphology, acdvation marker expression, DNA synthesis, and secretion of lymphokines/immunoglobulin, only a small fracdon of the local T lymphocytes is blast transformed (18) although MHC class II andgen expression is common (16,18).…”

Section: Discussionmentioning

confidence: 99%

Immunoelectron microscopic study of distribution of T cell subsets in oral lichen planus

Jungell

Konttinen

Nortamo

et al. 1989

European J Oral Sciences

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– Monoclonal anti‐CD4, anti‐CD8, and anti‐GD18 antibodies were applied in avidinbiotin‐peroxidase complex staining using a pre‐embedding immunoelectron microscopy technique. Although most of the local T cells in situ were of CD4+ subtype, local CD8+ cells generally had a lower nucleus/cytoplasm ratio and contained more cell organelles than CD4+ cells. This suggests a local activation of CD8+ subpopulation, rather than activation of the numerically predominant CD4+ cells. Topographical analysis disclosed that all lymphocytes, regardless of location, were CD18+ and that most of the CD8 + cells were located subbasally and intraepithelially, whereas CD4+ cells often occurred in small clusters deeper down in the subepithelial lymphocyte‐rich band. Furthermore, CD8+ cells were often in close contact with macrophages, whereas CD4+ cells were in some instances in direct contact with plasma cells. This indicates that CD4+ cells may be involved in T cell‐dependent B cell‐mediated immunoglobulin synthesis, whereas CD8+ cytotoxic lymphocytes and tissue macrophages may be involved in the local pathogenetic process leading to basement membrane alterations.

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“…Inflammatory conditions are frequently linked to the etiology of human cancers (Templeton, 1975). Relevant to the latter is the observation that oral precancers such as leukoplakia quite often show a strong subepithelial accumulation of inflammatory cells (Becker et al, 1983). In inflammation, potent soluble mediators including the cytokines are produced, and these play a key role in initiating as well as sustaining the metabolic and immune responses (Grimble, 1992;Simpson and Hoffman-Goetz, 1993).…”

Section: Introductionmentioning

confidence: 99%

Bionutrition and Oral Cancer in Humans

Enwonwu

Meeks

1995

Critical Reviews in Oral Biology & Medicine

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Tobacco (smoking and smokeless) use and excessive consumption of alcohol are considered the main risk factors for oral cancer . Conspicuous national and international variations in oral cancer incidence and mortality rates, as well as observations in migrant populations, raise the possibility that diet and nutritional status could be an important etiologic factor in oral carcinogenesis. As shown in this report, abuse of alcohol and tobacco has serious nutritional implications for the host, and generates increased production of reactive free radicals as well as eliciting immunosuppression. Maintenance of optimal competence of the immune system is critical for cancer surveillance. Active oxygen species and other reactive free radicals mediate phenotypic and genotypic alterations that lead from mutation to neoplasia. Consequently, the most widely used chemopreventive agents against oral cancer (e.g., vitamins A, E, C, and p-carotene) are anti-oxidants/free radical scavengers. These anti-oxidants, both natural and synthetic, neutralize metabolic products (including reactive oxygen species), interfere with activation of procarcinogens, prevent binding of carcinogens to DNA, inhibit chromosome aberrations, restrain replication of the transformed cell, suppress actions of cancer promoters, and may even induce regression of precancerous oral lesions such as leukoplakia and erythroplakia. Malnutrition is characterized by marked tissue depletion of anti-oxidant nutrients, including GSH (y-glutamyl-cysteinyl-glycine), a key cellular anti-oxidant as well as a modulator of T-cell activation. GSH or its precursor cysteine inhibits activation of the nuclear transcription factor kB (NFkB), and has been shown to be protective against chemically induced oral cancer and leukoplakia. Alcohol-, tobacco-, and/or malnutrition-induced immunosuppression promotes impaired salivary gland function and oral mucosal immunity, a prominent reduction in the number of helper CD4 cells with less marked changes in number of suppressor T-cells, and depressed NK cell activity, among others. These suggest a breakdown in the capacity of the malnourished to mount effective tumor surveillance. This review article underscores the compounding but important roles of nutritional/dietary factors in the long-established causal link between abuse of alcohol and tobacco (smoking and smokeless) and oral cancer.

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Oral lichen planus: characterization of immunocompetent cells with hybridoma antibodies

Cited by 46 publications

References 25 publications

Oral lichen planus: immunohistology of mucosal lesions

Oral lichen planus: immunohistology of mucosal lesions

Immunoelectron microscopic study of distribution of T cell subsets in oral lichen planus

Bionutrition and Oral Cancer in Humans

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