Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06126 (CD1a)
 2,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunomodulatory effects of retinoids may be part of their anti-carcinogenic and anti-inflammatory properties. We studied the in vivo effects of retinoic acid (RA) on antigen-presenting activity of human epidermal Langerhans cells and on accessory cell activity of keratinocytes. Two skin sites from each volunteer were treated in vivo with 0.1% RA or vehicle, respectively, once a day for 4 d. RA-treated epidermal cell (RA-EC) alloantigen presentation to CD4+ T cells in each volunteer tested was consistently greater than that induced by vehicle EC. However, this increased antigen-presenting activity did not lead to autoreactive CD4+ T-lymphocyte proliferation. Elevated unfractionated epidermal antigen-presenting activity of RA-EC was not due to increased keratinocyte major histocompatibility complex (MHC) or intercellular adhesion molecule expression or to other keratinocyte accessory signaling, because incubation of CD1a-fluoroscence-activated cell sorter (FACS)-purified RA-EC inhibited alloantigen presentation, presumably through increased keratinocyte transforming growth factor-beta. By contrast, Langerhans cell function was upregulated; FACS-purified CD1a+ Langerhans cells derived from RA-EC displayed a markedly increased ability, relative to Langerhans cells from vehicle EC, to present alloantigen to T cells. Triple color flow-cytometric analysis of RA-EC and vehicle EC suspensions revealed that RA treatment did not modify the number of DR+ and CD1a+DR+EC, but did result in statistically significant increases in Langerhans cells expression of HLA-DR, CD11c, and CD1c. Another novel finding was that HLA-DR-dependent Langerhans cells antigen-presenting activity in both normal and RA-treated skin was completely blocked by anti-CD11c antibody. Thus, retinoid upregulation of antigen-presenting activity may be due to upregulation of Langerhans cell CD11c, as well as class II MHC. Upregulation of cutaneous immune responsiveness in human skin without autoreactivity has not (to our knowledge) been reported previously, and the Langerhans cell phenotypic and functional state achieved is distinct from previously reported states of Langerhans cell activation.
J Invest Dermatol 1994 Dec
PMID:Retinoic acid upregulates human Langerhans cell antigen presentation and surface expression of HLA-DR and CD11c, a beta 2 integrin critically involved in T-cell activation. 779 14

Birbeck granules (BG) are cytoplasmic organelles that are only found in Langerhans cells (LC). The function of BG is still unclear, although it has been claimed that they are actively involved in receptor-mediated endocytosis and participate in the antigen-processing/presenting function of LC. We have identified a healthy white 29-year-old man whose LC completely lack the presence of BG as determined by electronmicroscopic studies. This was observed repeatedly using skin biopsy specimens taken from several places on the body during a period of 2.5 years. The absence of BG in these LG was documented further by the lack of staining with a BG-specific monoclonal antibody. Despite the complete lack of BG, LC were present in normal numbers, had all the usual morphologic characteristics, and were CD1a and human leukocyte antigen (HLA) class II positive. Two observations indicate that these BG-negative LC display normal antigen-presenting capacity. First, the individual could be sensitized by the hapten diphenylcyclopropenone. This was accompanied by a strong increase in the cell surface expression of HLA class II antigens on his LC, suggesting LC activation. Second, his epidermal cells elicited a normal positive response in an allogeneic mixed epidermal cell lymphocyte reaction. Together these observations strongly suggest that BG are not a prerequisite for normal LC function in vivo and in vitro.
J Invest Dermatol 1994 Dec
PMID:Functional human epidermal Langerhans cells that lack Birbeck granules. 779 19

We describe papular xanthomatosis that progressively developed in a patient with long-standing erythrodermic atopic dermatitis and normal lipid metabolism and without an associated systemic disease. Light microscopy showed a lobulated aggregate of sometimes foamy histiocytes. Ultrastructurally, these histiocytes contained lipid inclusions and lacked features of Langerhans or epithelioid cells. Other granulomatous skin diseases such as tuberculosis, sarcoidosis, or foreign body granuloma were excluded by histologic study, polarizing microscopic examination, electron microscopy, and microbiologic investigations. Nevertheless, these xanthomas showed an antigen expression pattern similar to that found in noninfectious granulomas (CD1a-, MS-1-, CD11c+, MRP-8/-14+, 25F9+, RM 3/1+/-, CD36(+), indicating that normolipemic papular xanthomatosis may be reactive process and should not be included among the true cutaneous non-Langerhans cell histiocytoses.
J Am Acad Dermatol 1995 Feb
PMID:Normolipemic papular xanthomatosis in erythrodermic atopic dermatitis. 782 34

Murine Langerhans cells (LC) synthesize and express E-cadherin, a Ca(++)-dependent homophilic cell adhesion molecule that mediates LC-keratinocyte (KC) binding in vitro. In vivo, E-cadherin expression by LC may promote localization and persistence of LC within the epidermis through LC-KC adhesion. In addition, changes in LC E-cadherin expression or affinity may be an important factor in the egress of LC from the epidermis after exposure to antigen. The aim of the present study was to determine if human LC also express E-cadherin. Suction blister roofs were obtained from normal volunteers and epidermal cell (EC) suspensions were prepared by limited trypsinization in the presence of 1 mM Ca++. EC were then incubated with antibodies to E-cadherin and CD1a or HLA-DR, and examined by two-color analytical flow cytometry or immunofluorescence microscopy. Most (82.9% +/- 7.4% [mean +/- SD], range 67-89%, n = 7) freshly prepared human LC expressed E-cadherin, as did the majority of KC. The amount of E-cadherin (as determined by mean fluorescence intensity) expressed by LC and KC was similar. Trypsin/EDTA treatment of freshly prepared EC abrogated expression of E-cadherin by LC and KC, whereas E-cadherin was not degraded by trypsin in the presence of Ca++. LC expressed lower levels of E-cadherin after 3 d in culture. Thus, human LC, like murine LC, express the homophilic adhesion molecule E-cadherin, which may be important in establishing and maintaining interactions between LC and KC in mammalian epidermis.
J Invest Dermatol 1995 Feb
PMID:Human Langerhans cells express E-cadherin. 782 87

Ten patients with dermatitis herpetiformis had biopsies taken from involved and uninvolved skin. Monoclonal antibodies and the avidin-biotin peroxidase staining technique were used to stain for T cells and Langerhans cells in skin sections. A significant increase in the number of CD3-positive T cells was observed in the upper dermis of involved compared with uninvolved skin (P < 0.0005). Most of the T cells in involved skin were CD45RO-positive memory cells; CD4-positive T cells exceeded the number of CD8-positive T cells by a ratio of 4:1. In addition, CD1a-positive dendritic cells were observed within the clumps of T cells in involved dermis in nine of the 10 patients, but were absent from the dermis of uninvolved skin. Double immunofluorescent staining demonstrated that approximately 20-40% of the CD3-positive T cells were activated, and expressed the HLA-DR antigen. These findings suggest that activated T cells are involved in the pathogenesis of dermatitis herpetiformis skin lesions.
Br J Dermatol 1994 Dec
PMID:T lymphocytes in lesional skin of patients with dermatitis herpetiformis. 785 34

Confocal scanning laser microscopy (CSLM), when used in conjunction with computerized image processing systems, provides a powerful tool for morphological and quantitative analyses of biological tissues. In this study, normal human epidermal sheets were stained by an indirect immunofluorescence method using anti-CD1a monoclonal antibody. Positively stained epidermal Langerhans cells (LCs) were visualized using the Bio-Rad MRC-600 Confocal Imaging System. Images obtained from the confocal microscope were volumetrically rendered and quantitatively analysed using ANALYZE (Version 4.0) running on a Sun SPARC 2 Workstation. Normal epidermal LCs were shown to be large disc-like structures with five to nine long dendritic processes per cell, orientated with their flat surfaces parallel to the skin surface. LCs form a monolayer network of cells distributed evenly throughout the suprabasal layers of the epidermis, with no direct physical contact between dendritic processes. Mean LC density was estimated to be 582 per mm2 (95% confidence intervals, CI = 233-940), and mean cell volume was 612 microns3 (95% CI = 257-1020). LCs in sun-exposed sites were significantly lower in mean cell density, but larger in mean cell volume, than in covered sites. Mean surface area projected by LCs was estimated to be 26.8% (95% CI = 18.9-34.2), and this value did not show significant regional or individual variation. Our data support the notion that epidermal LCs are organized in such a way as to maximize their surface area for efficient trapping of antigens, and a reduction in LC density per unit area in sun-exposed sites is compensated for by an increase in the mean cell volume.
Br J Dermatol 1994 Dec
PMID:Morphological and quantitative analyses of normal epidermal Langerhans cells using confocal scanning laser microscopy. 785 37

In lymphoproliferative diseases of the skin, DC have a key role in T- and B-cell homing. Furthermore, DC alterations may have a pathogenic role in the natural history of specific disorders, either in the neoplastic lymphoid cell progression or in antitumoral lymphocyte reaction. Finally, the morphoantigenic and topographic features of DC may have diagnostic and histogenetic relevance in specific conditions. In CTCL, dermal CD1a+ DC ("indeterminate cells") seem to play a significant role in the neoplastic progression of MF, whereas the possible pathogenetic role of specific alterations of epidermal LC is yet to be proven. Recently, a possible implication of DD (resident, perivascular factor XIIIa+/CD1a- DC) in the pathogenesis of MF has been also suggested. The presence and possible significance of DC in CTCL non-MF are presently poorly studied. At present, DC number, distribution, and phenotype seem possibly useful in the differential diagnosis between CTCL and pseudo-CTCL, but this hypothesis has to be adequately confirmed. CBCL has been recently proposed as a unique type of clinically low-grade lymphoma, namely, skin-associated lymphoid tissue (SALT)-related B-cell lymphoma. Both SALT- and mucosa-associated lymphoid tissue (MALT)-related B-cell lymphoma share with a peculiar nodal lymphoma of follicle mantle origin (parafollicular-monocytoid lymphoma) the nonaggressive clinical behavior and the uniform phenotype (CD5-, CD10-) and genotype (lack of bcl-2 gene rearrangement) of neoplastic B cells, despite the wide variability of cytomorphologic appearances. The putative origin of CBCL is further supported by the typical CD14-, nerve growth factor receptor (NGFr)+ immunophenotype of DRC. Moreover, the immunophenotype and architectural fashion of DRC are interesting clues to the differentiation between neoplastic and true reactive folliclelike nodules and may be of help in the differential diagnosis between CBCL and B-cell pseudolymphoma as well as in the correct interpretation of lesions showing monoclonal proliferations of B cells accompanied by polyclonal follicular reactions.
Dermatol Clin 1994 Apr
PMID:Dendritic cells in T- and B-cell proliferation in the skin. 804 37

A 62-year-old female with histiocytosis X presented with a vulvar ulcer. Multiple osteolytic lesions were later detected. Histological examination of the ulcerated skin showed diffuse proliferation of histiocytic cells with folded nuclei and pale eosinophilic cytoplasm. Immunohistochemistry revealed S100 protein and vimentin as well as CD1a, CD4, and HLA-DR antigens in the proliferating cells. Electron microscopy demonstrated Birbeck granules in the cytoplasm of the cells. The patient was successfully treated by complete surgical excision of the ulcer followed by radiotherapy for recurrent vulvar erythema.
J Dermatol 1994 Apr
PMID:An adult case of histiocytosis X with a vulvar ulcer and multiple bone lesions. 805 99

Recently we reported that the high-affinity receptor for IgE, Fc epsilon RI, is constitutively expressed on normal epidermal Langerhans cells (LC) and on certain cells within the dermis. To study the nature of these cells we performed immunofluorescence double-labeling experiments using an anti-Fc epsilon RI reagent (MoAb 15-1) as well as monoclonal antibodies (MoAb) against leukocyte differentiation antigens expressed on LC, interdigitating cells and macrophages. Avidin-fluorescein isothiocyanate was used to distinguish mast cells. We found that dermal Fc epsilon RI+ cells are bone marrow derived (CD45+). Further, we found that a subset of 15-1+ dermal cells coexpresses antigens present on certain members of the LC/DC family: the majority of Fc epsilon RI+ cells reacted with MoAb anti-HLA-DR and RFD1, the latter recognizes an antigenic moiety on interdigitating cells, and a small subpopulation coexpressed CD1a. In reverse fashion, virtually all CD1a+ cells and most RFD1+ cells reacted with the anti-Fc epsilon RI reagent. Approximately one third of 15-1+ cells represented avidin-FITC+ mast cells whereas Fc epsilon RI expression was not detected on FXIIIa+ dermal dendrocytes or CD3+ lymphocytes. By immunoelectronmicroscopy, we found that perivascularly located 15-1-reactive cells exhibited pronounced dendrites, an indented nucleus, numerous mitochondria, and abundant endo-/lysosomal structures. However, Birbeck granules or granules specific for basophils or eosinophils were never detected in these cells. Collectively, our data suggest that the pool of dermal Fc epsilon RI+ cells consists mainly of cells of the LC (CD1a+)/DC(RFD1+) lineage and mast cells but does not include FXIIIa+ dermal macrophages.
J Invest Dermatol 1994 Mar
PMID:Immunomorphologic characterization of Fc epsilon RI-bearing cells within the human dermis. 812 Apr 15

By means of microsurgical lymph cannulation human skin lymph derived from the late phase of an elicitation reaction to diphenylcyclopropenone was sampled. Cells were isolated by centrifugation and then treated with mouse anti-CD1a monoclonal antibodies and sheep antimouse antibody-coated Dynabeads. Ultrastructural and immunocytochemical analyses revealed anti-CD1a/Dynabead-rosetted CD1a- and protein S-100-positive cells which did not express monocyte surface markers, but surface antigens such as HLA-DR, ICAM-1 and, in part, LFA-3. In comparison to freshly prepared human epidermal Langerhans cells (LC), a large fraction of these cells contained no or markedly fewer Birbeck granules and exhibited extensive ruffling of the surface. These data suggest that the phenotype of LC in skin lymph derived from the elicitation phase of allergic contact dermatitis is similar to LC cultured in vitro. In the functional concept of LC of our time, these cells correspond to the dendritic cells designated as "veiled".
Exp Dermatol 1993 Dec
PMID:Phenotype of Langerhans cells in human afferent skin lymph derived from allergic contact dermatitis. 816 48


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