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

It is now well established that interactions of CD40 on the B cells, along with its ligand (CD40-L) on the T cells, regulate B cell proliferation and differentiation. However, the functional significance of CD40 expression on cells known for most efficient Ag-presenting function, i.e., dendritic cells, is not so clear. In this study, we demonstrate that CD40 is expressed on human dendritic Langerhans cells (LC) freshly isolated from epidermis. Using CD40-L transfected cells, CD40 triggering was found to enhance LC viability when cultured and to result in phenotypic alterations. Thus, a 2-day CD40 activation induced up-regulation of CD54 and CD86 at the LC surface, while it did not significantly affect the levels of HLA-DR, CD1a, CD58, and CD80 expression. These phenotypic changes correlate with enhanced LC allostimulatory property, as shown by the use of paraformaldehyde-fixed LC. Furthermore, mAbs against CD40, as well as CD40-L, strongly inhibit the primary T cell response to allogeneic LC. Collectively, these data support a role for CD40/CD40-L pair in the development of normal T cell functions.
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PMID:Functional expression of CD40 antigen on human epidermal Langerhans cells. 759 81

A 71-year-old Japanese woman had two dome-shaped tumors on her right buttock with several surrounding papules. Histological examination revealed that large anaplastic cells and atypical lymphoid cells densely infiltrated the entire dermis. On immunohistochemical examination, Ki-1, HLA-DR, CD25 (IL-2 receptor alpha), CD122 (IL-2 receptor beta), CD4, CD11c and CD68 were all positive in the tumor cells, whereas CD1a, CD3, CD5, CD8 and CD19 were negative. Neither rearrangement of the T-cell receptor beta, T-cell receptor gamma nor the immunoglobulin heavy-chain was seen. Ultrastructurally, most of the tumor cells contained thick bundles of intermediate filaments in the perinuclear cytoplasm. Thus, this patient was diagnosed as having Ki-1-positive lymphoma of non-T, non-B origin. No recurrence or metastasis of the tumor has been observed in the last 2 years, although surgical resection was required 3 times before control was achieved.
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PMID:Primary cutaneous CD30(Ki-1)-positive lymphoma of non-T, non-B origin. 759 89

The present paper deals with more precise characterization of Langerhans cells (LC) and accompanying lymphocytes in lung LC histiocytosis (LCH) and primary lung peripheral adenocarcinomas using immunohistochemical methods with various kinds of monoclonal antibodies against cell adhesion and activation markers and some cytokines. Tissue specimens were obtained from 4 patients with pulmonary LCH and from 29 patients with primary lung peripheral adenocarcinoma. In florid (exudative and granulomatous) nonfibrotic LCH lesions, LC, particularly those in contact with lymphocytes, were S100, CD1a, MHC Class II, CD11a and c, CD16, and CD54 positive. In this context, LC were CD4+ and CD25+. Lymphocytes around LC were CD3+ with a "memory" phenotype (CD45RO+) and, frequently, CD25+ and HLA-DR+. S100+ and CD1a+ LC were commonly observed in adenocarcinomas subclassified as papillary and as nonmucinous bronchioloalveolar, in both cases mainly where Clara cells and Type II pneumocytes were present. In carcinomas the vast majority of LC were HLA-DR+ and, rarely, weakly CD16+, CD25+, and CD54+. The infiltration of reactive cells in cancer tissue was mainly represented by T lymphocytes (CD3+CD45RO+). These T cells were HLA-DR- and CD25-. The presence of LC was associated with a strong reactivity of epithelial cells with antibodies PE-10 and 439-9B, both recognizing molecules mainly expressed by Type II alveolar cells. Several cells in LCH florid lesions showed immunoreactivity for both IL-1 alpha and beta. Immunostaining for IFN-gamma revealed the presence in the same areas of some positive cells showing lymphoid morphology. No IL-1 or IFN-gamma reactivity was found in adenocarcinomas.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Langerhans cells in Langerhans cell histiocytosis and peripheral adenocarcinomas of the lung. 769 Feb 10

The purpose of our study was to investigate the role of immune mechanisms in the pathogenesis of pterygium using an immunohistochemical technique. Our material consisted of 35 surgically excised pterygia and 7 samples of normal conjunctiva obtained from an equal number of patients. HLA-DR antigen expression in epithelial cells, B-cells, suppressor and helper lymphocytes, Langerhans' cells, and monocytes/macrophages were studied immunohistochemically in frozen sections using anti-human HLA-DR, anti-CD22, anti-CD8, anti-CD4, anti-CD1a, and anti-LeuM5 monoclonal antibodies. Aberrant HLA-DR antigen expression in epithelial cells was detected in 30 of 35 cases of pterygium. Epithelial cells in samples of normal conjunctiva were found to be negative in HLA-DR antigen expression. HLA-DR antigen expression in pterygium was found to be closely related to the density of T4 cells and, especially, of CD4 lymphocytes. The present findings suggest that an immunopathologic mechanism plays a role in the pathogenesis of pterygium.
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PMID:HLA-DR antigen expression in pterygium epithelial cells and lymphocyte subpopulations: an immunohistochemistry study. 779 11

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.
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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

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.
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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.
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PMID:T lymphocytes in lesional skin of patients with dermatitis herpetiformis. 785 34

Cryostat sections of 20 clinical condylomata of the vulva induced by human papillomavirus and 5 normal control biopsies were examined using immunohistochemistry. The results indicated that in vulvar papillomavirus infection the intraepithelial Langerhans' cells showed abnormal morphology and a significantly lower density than controls. CD1a positive Langerhans' cells were also observed in dermis of condylomata, suggesting an abnormal epithelial traffic of dendritic cells. T lymphocytes with a mean CD4/CD8 ratio of 0.25 and a mean density of 267 +/- 59 cells/mm2 of epithelial section were the main cellular infiltrate in vulvar papillomavirus infection. Most of the T cells were HLA-DR negative. Those condylomata with moderate to severe mononuclear infiltrate showed leucocyte function antigen 1 positive T cells forming small clusters in the lower epithelial half around the ICAM-1 positive keratinocytes. Vulvar warts also showed epithelial areas with overlapped ICAM-1 and HLA-DR expression. Scattered T gamma-delta and B lymphocytes, macrophages and NK cells were observed among the cells of the dermal infiltrate of vulvar condylomata.
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PMID:Cellular subsets and epithelial ICAM-1 and HLA-DR expression in human papillomavirus infection of the vulva. 790 83

We have shown that gamma delta T cells in human gingiva have an intraepithelial location and, that in the chronic inflammatory disease periodontitis, the expression of CD45RO and CD8 or CD4 is induced on gamma delta T cells. To study the role of gamma delta T cells in local antibacterial responses, we determined the cytokine profiles of isolated human gingival cells. Different T cell subpopulations, isolated by positive selection with mAb-coated magnetic beads and macrophages, as well as epithelial cells, were analyzed for expression of mRNA for 15 cytokines by reverse transcriptase-PCR. The ultrastructure of gingival gamma delta T cells was also studied. The gamma delta T cells expressed mRNA for IFN-gamma, TNF-alpha, TGF-beta 1, and IL-6. Expression of IFN-gamma was a consequence of inflammation. CD4+ gamma delta T cells expressed IFN-gamma only, whereas CD8+ gamma delta T cells expressed all four cytokines. CD8+ cells expressing IFN-gamma, TNF-alpha, and IL-6 in combination suggest a cytotoxic effector function. Gingival gamma delta T cells contained cytoplasmic electron-dense membrane-bound granules and multivesicular bodies that are ultrastructural characteristics of cytotoxic cells. Epithelial cells from inflamed gingiva expressed HLA-DR, CD1a, CD1c, and heat shock protein 60 on the cell surface. They also expressed mRNA for IL-1 beta, IL-6, IL-8, TNF-alpha, and TGF-beta 1. Thus, epithelial cells may function as accessory cells in immune activation and, at the same time, be target cells for CD8+ gamma delta T cells reactive with CD1 Ag or heat shock protein. These results suggest that gamma delta T cells constitute a first line of defense in gingiva, preventing entrance of pathogens by cytotoxicity against infected and stressed epithelial cells, and by control of epithelial cell growth through secretion of regulatory cytokines.
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PMID:Cytokine profile and ultrastructure of intraepithelial gamma delta T cells in chronically inflamed human gingiva suggest a cytotoxic effector function. 805 26

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.
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PMID:An adult case of histiocytosis X with a vulvar ulcer and multiple bone lesions. 805 99


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