Langerhans Cells of Human Mucosa

Fraissinette, Anne de Brugerolle de; Schmitt, Daniel; Thivolet, J

doi:10.1111/j.1346-8138.1989.tb01261.x

Cited by 34 publications

(19 citation statements)

References 55 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Langerhans cells are dendritic cells from bone marrow 22,36 and can be found in all squamous epithelia, 9 including the esophagus, were identified by electronic microscope 2 and immunoperoxidase 15 in 50% of the amount observed in the epidermis. 47 In the esophagus, the Langerhans cells have the same structure as the epidermis and are located in the suprabasal area and along the papillae of the lamina propria.…”

Section: Discussionmentioning

confidence: 99%

Immunophenotypic Characterization and Quantification of the Epithelial Inflammatory Infiltrate in Eosinophilic Esophagitis Through Stereology

Lucendo

Navarro

Comas

et al. 2007

American Journal of Surgical Pathology

155

166

View full text Add to dashboard Cite

Eosinophilic esophagitis (EE) is an emerging disease caused by dense infiltration of the esophageal epithelium by eosinophilic leucocytes. It is originated from local hypersensitivity to food or airborne allergens. Although the physiopathologic mechanisms of the illness have not been fully discovered, EE is a loss of immunologic tolerance by the esophagus, meaning that it should be considered as an active immunologic organ. In our study, we investigated the immunologic capacity of the epithelium using immunohistochemistry and stereology, to determine the cellular density of eosinophils, T and B lymphocytes, Langerhans cells, mast cells, and cells manufacturing immunoglobulin E in endoscopic biopsies of patients with EE (taken before and after topical treatment with fluticasone propionate) compared with normal individuals and patients suffering from gastroesophageal reflux disease (GERD). We have observed that the density of eosinophils in EE is 300 times greater than in normal conditions and it is only in this disease where eosinophils show signs of activation and degranulation (positivity to major basic protein immunostaining). The number of T intraepithelial lymphocytes also significantly rose in EE, compared with other entities, where CD8 cells were predominant. However, the human esophagus is deficient in B lymphocytes and we only found intraepithelial plasma cells that excreted immunoglobulin E in EE. Under normal conditions mast cells exist in the thickness of the epithelium that are slightly higher in GERD and multiply in density by 17 in EE. Langerhans cells did not show any significant variation in density under the different tested conditions. After topical treatment with steroids, the density of the different cell components fell to similar levels to GERD. Using our study, we can conclude that the human esophagus may contribute to the development of local immunologic responses as it contains all the necessary cell components. EE represents growth of this esophageal capacity and its pathogeny could respond to mixed cellular and humoral mechanisms.

show abstract

Section: Discussionmentioning

confidence: 99%

Immunophenotypic Characterization and Quantification of the Epithelial Inflammatory Infiltrate in Eosinophilic Esophagitis Through Stereology

Lucendo

Navarro

Comas

et al. 2007

American Journal of Surgical Pathology

155

166

View full text Add to dashboard Cite

show abstract

“…epidermis, appendages of the skin, and in mucosa, including buccal, oesophageal, pulmonary, vaginal and uterine cervical epithelium (reviewed by de Fraissinette et al, 1989). A major part of the LC population resides in the epidermis of the skin at a suprabasal level forming a regular and almost closed network with their dendritic protrusions (Fig.…”

Section: Origin Ontogeny and Distribution Of Langerhans Cellsmentioning

confidence: 99%

Dynamic nature and function of epidermal langerhans cellsin vivo andin vitro: a review, with emphasis on human Langerhans cells

Teunissen

1992

Histochem J

103

View full text Add to dashboard Cite

Epidermal Langerhans cells (LC) are Birbeck granule-containing bone-marrow-derived cells, which are located mainly in the suprabasal layer of the epidermis. They can be readily identified by their strong expression of CD1a and MHC class II molecules. In addition to these 'classical' properties, an extensive phenotypic profile of normal human LC, summarized in this review, is now available. The powerful capacity of LC to activate T lymphocytes is clearly documented and, to date, LC are recognized as the prominent antigen-presenting cells of the skin immune system. They are generally believed to pick up antigens encountered in the epidermis and to migrate subsequently from the epidermis to the skin-draining lymph nodes. Upon arrival in the paracortex of lymph nodes, the antigen-laden LC transform into interdigitating cells and they present antigen to naive T lymphocytes in a MHC class II-restricted fashion; this results in the generation of antigen-specific immune responses. It has also been demonstrated that transformation of LC into interdigitating cells occurs when LC are cultured in vitro. Both in vivo and in vitro studies have indicated that properties of LC, such as phenotype, morphology and the stimulatory potential to activate T lymphocytes, are dependent on the local microenvironment in which the LC reside. The essential role of LC in the induction of contact allergic skin reactions and skin transplant rejection is well established.

show abstract

“…The primary professional APC in the esophagus seems to be the Langerhans cell, a type of dendritic cell found in all squamous epithelia, 42 particularly the epidermis. Langerhans cells of the esophagus are structurally similar to those in the skin and are located along the papillae of the lamina propria and in the suprabasal region.…”

Section: Bodymentioning

confidence: 99%

Allergic Mechanisms in Eosinophilic Esophagitis

Wechsler

Bryce

2014

Gastroenterology Clinics of North America

View full text Add to dashboard Cite

Paralleling the overall trend in allergic diseases, Eosinophilic Esophagitis is rapidly increasing in incidence. It is associated with food antigen-triggered, eosinophil-predominant inflammation and the pathogenic mechanisms have many similarities to other chronic atopic diseases, such as eczema and allergic asthma. Studies in animal models and from patients over the last 15 years have suggested that allergic sensitization leads to food-specific IgE and T-helper lymphocyte type 2 cells, both of which appear to contribute to the pathogenesis along with basophils, mast cells, and antigen-presenting cells. This review will outline our current understandings of the allergic mechanisms that drive eosinophilic esophagitis, drawing from clinical and translational studies in humans as well as experimental animal models.

show abstract

Langerhans Cells of Human Mucosa

Cited by 34 publications

References 55 publications

Immunophenotypic Characterization and Quantification of the Epithelial Inflammatory Infiltrate in Eosinophilic Esophagitis Through Stereology

Immunophenotypic Characterization and Quantification of the Epithelial Inflammatory Infiltrate in Eosinophilic Esophagitis Through Stereology

Dynamic nature and function of epidermal langerhans cellsin vivo andin vitro: a review, with emphasis on human Langerhans cells

Allergic Mechanisms in Eosinophilic Esophagitis

Contact Info

Product

Resources

About