Langerhans cells form a reticuloepithelial trap for external contact antigens

Shelley, Walter B.; Juhlin, Lennart

doi:10.1038/261046a0

Cited by 271 publications

(83 citation statements)

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“…Elegant studies of ultrastructural events in DTH have demonstrated the ability of LC to serve as a "messenger" between skin and lymph nodes (Silberberg et al, 1976). Uptake of antigens or haptens by LC is known to be an early event in this reaction, and occurs within 1-2 hours of challenge (Shelley and Juhlin, 1976).…”

Section: Mast Cells and The Neural-immune Networkmentioning

confidence: 99%

Mast Cells and Oral Inflammation

Walsh

2003

Critical Reviews in Oral Biology & Medicine

152

114

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Mast cells are mobile granule-containing secretory cells that are distributed preferentially about the microvascular endothelium in oral mucosa and dental pulp. The enzyme profile of mast cells in oral tissues resembles that of skin, with most mast cells expressing the serine proteases tryptase and chymase. Mast cells in oral tissues contain the pro-inflammatory cytokine tumour necrosis factor-␣ in their granules, and release of this promotes leukocyte infiltration during evolving inflammation in several conditions, including lichen planus, gingivitis, pulpitis, and periapical inflammation, through induction of endothelial-leukocyte adhesion molecules. Mast cell synthesis and release of other mediators exerts potent immunoregulatory effects on other cell types, while several T-lymphocyte-derived cytokines influence mast cell migration and mediator release. Mast cell proteases may contribute to alterations in basement membranes in inflammation in the oral cavity, such as the disruptions that allow cytotoxic lymphocytes to enter the epithelium in oral lichen planus. A close relationship exists among mast cells, neural elements, and laminin, and this explains the preferential distribution of mast cells in tissues. Mast cells are responsive to neuropeptides and, through their interaction with neural elements, form a neural immune network with Langerhans cells in mucosal tissues. This facilitates mast cell degranulation in response to a range of immunological and non-immunological stimuli. Because mast cells play a pivotal role in inflammation, therapies that target mast cell functions could have value in the treatment of chronic inflammatory disorders in the oral cavity.

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Section: Mast Cells and The Neural-immune Networkmentioning

confidence: 99%

Mast Cells and Oral Inflammation

Walsh

2003

Critical Reviews in Oral Biology & Medicine

152

114

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“…Currently, it is felt that Langerhans cells (LC) are critical to these responses. Investigators have shown that the outer layer of skin, the epidermis, is rather densely and uniformly populated (3-8% of the total population) with macrophage-like LC (5)(6)(7)(8)(9)(10). Evidence that LC represent a specialized subpopulation of macrophages includes (i) their synthesis and membrane expression of class II major histocompatibility complex (MHC) antigens (Ia) (11)(12)(13), (ii) their ability to present antigens in vitro and in vivo (14)(15)(16)(17), and (iii) the presence of receptors for the Fc component of IgG and the C3b component of complement on their cell surfaces (18,19 (22)(23)(24).…”

mentioning

confidence: 99%

Biology of Langerhans cells: Selective migration of Langerhans cells into allogeneic and xenogeneic grafts on nude mice

Krueger¹,

Daynes

Emam

1983

Proc. Natl. Acad. Sci. U.S.A.

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A major question challenging immunobiologists relates to those mechanisms that control the selective movement of cells involved in immune and inflammatory processes at various tissue sites such as the skin. Little is known about those influences that control the selective migration of macrophage-like Langerhans cells (LC) to normal epidermis, where it is uniformly distributed. Mechanistically, this includes the interaction of blood-borne LC precursors with the vascular endothelium of the skin and those factors that control the migration of the LC into the avascular epidermal component of the skin. By using (i) monoclonal antibodies specific for I-region associated la antigens found on LC from various inbred strains of animals and (ii) the congenitally athymic (nude) mouse as an immunologically compromised recipient of allografts and selected xenografts, we developed a model system to study the factors that restrict LC migration into the epidermis. Using this model, which excludes the need to lethally x-irradiate graft recipients, we established that: (i) the ingress of LC does not show major histocompatibility complex restriction [LC of the nude host are capable of migrating into the epidermis of allogeneic and certain xenogeneic (rat) skin grafts]; (ii) host LC are incapable of migrating into the epidermis of guinea pig or human skin grafts; (iii) the ingress of host LC into the epidermis of the graft is not accompanied by an overgrowth of the graft by host epidermis; and (iv) LC or LC precursors are capable of dividing in the skin or, alternatively, represent an extremely long-lived cell population. The specificity of this model system provides a powerful tool to help understand many aspects of LC biology. Grafting human skin to the nude mouse not only provides a biologic support system for the graft but also is, by design, a system that is devoid of contaminating circulating precursor cell types. Manipulation of the experimental conditions is quite easy and provides a highly specific means to investigate many parameters of LC function.In addition to the well-recognized barrier function of skin, experimental observations have established that a complete immune response (antigen recognition through effector function) can occur in this organ (1-4). Currently, it is felt that Langerhans cells (LC) are critical to these responses. Investigators have shown that the outer layer of skin, the epidermis, is rather densely and uniformly populated (3-8% of the total population) with macrophage-like LC (5-10). Evidence that LC represent a specialized subpopulation of macrophages includes (i) their synthesis and membrane expression of class II major histocompatibility complex (MHC) antigens (Ia) (11)(12)(13), (ii) their ability to present antigens in vitro and in vivo (14-17), and (iii) the presence of receptors for the Fc component of IgG and the C3b component of complement on their cell surfaces (18,19 1650The publication costs of this article were defrayed in part by page charge payment. This article must ther...

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“…They are bone marrow derived dendritic cells (Stingl et al, 1980) which bind antigen (Shelley & Juhlin, 1976) and transport it to the local lymph nodes (Silberberg-Sinakin et al, 1977) for presentation to T cells, resulting in a specific immune response against the antigen.…”

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confidence: 99%

Carcinogen-induced depletion of cutaneous Langerhans cells

Muller¹,

Halliday²,

Knight³

1985

Br J Cancer

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Summary The chemical carcinogen 7,12-dimethylbenz (a) anthracene (DMBA) is a potent carcinogen which, when applied to the skin of BALB/c mice weekly for 7-8 weeks, causes the induction of macroscopically visible skin tumours. We report that DMBA also depletes Langerhans cells (LC) the chemical carcinogen 7,12-dimethylbenz (a) anthracene (DMBA) on LC numbers and morphology as assessed by adenosine triphosphatase (ATPase) staining during the induction and growth of DMBA-induced skin tumours. DMBA caused depletion of LC from skin surrounding the tumours, and the LC reappeared as the tumours ceased growing. The time scale of reappearance of LC suggests they were being repopulated from bone-marrow derived precursors. Materials and methodsCarcinogen treatment of mice Male BALB/c mice were obtained from Walter and Eliza Hall Institute, Melbourne; from 8-9 weeks of age they were treated with 7,12-dimethylbenz (a) anthracene (DMBA, Sigma, USA, Lot 24F-0052) as described by Muller & Flannery (1973). The dorsal trunk skin of the mice was shaved with electric clippers and painted with 1% DMBA dissolved in equal volumes of lanoline (Sigma, USA) and liquid paraffin (Supply and Tender, Hobart); control mice received solvent alone.To determine the early effects of DMBA on LC before tumours became apparent, groups of 4 mice were treated with DMBA. The first application of DMBA was designated as being on day 0, with weekly applications for up to 4 weeks; mice being killed 3 or 7 days following the last treatment. To determine the LC density in DMBA-treated skin during growth of DMBA-induced tumours, the DMBA was applied weekly for 7-8 weeks, the final application of DMBA was designated as being on day 0.(J The

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Langerhans cells form a reticuloepithelial trap for external contact antigens

Cited by 271 publications

References 5 publications

Mast Cells and Oral Inflammation

Mast Cells and Oral Inflammation

Biology of Langerhans cells: Selective migration of Langerhans cells into allogeneic and xenogeneic grafts on nude mice

Carcinogen-induced depletion of cutaneous Langerhans cells

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