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)

The distribution of HLA class II (DR, DP, DQ) and Fc gamma R (I, II, III) was analyzed in the epithelia of patients with advanced marginal periodontitis using cryostat sections incubated with monoclonal antibodies (MoAb) against the Langerhans cell (LC) (CD1a) and various subtypes of HLA class II and Fc gamma R, and the indirect immunofluorescence technique. In the oral gingival epithelium (OGE), LC were concentrated subjacent to the connective tissue papillae, while in the pocket epithelium (PE), they were most abundant at the gingival margin. HLA-DP, DQ, and DR stained LC in both OGE and PE. HLA-DQ+ LC were significantly fewer than DP+ and DR+ LC. HLA-DR also stained keratinocytes (KC) in the whole extension of both OGE and PE. HLA-DP was also observed on KC, but not HLA-DQ. Fc gamma R II stained both LC and focal areas of KC. In PE FC gamma R II+ LC were concentrated near the bottom of the pocket, while in the OGE, they were concentrated at the gingival margin. Fc gamma R III was present only on KC, especially in the basal and suprabasal layer. The results indicate that the epithelial cells are actively involved in the development and maintenance of the inflammation of periodontal disease.
J Clin Periodontol 1994 Sep
PMID:Epithelial expression of HLA class II antigens and Fc gamma receptors in patients with adult periodontitis. 752 33

Conventional major histocompatibility complex class I molecules are highly polymorphic and present peptides to cytotoxic T cells. These peptides derive from the proteolytic degradation of endogenous proteins in the cytosol and are translocated into the endoplasmic reticulum by a peptide transporter consisting of two transporter associated with antigen processing (TAP) molecules. Absence of this transporter leads to the synthesis of unstable peptide free class I molecules that are weakly expressed on the cell surface. Mouse nonconventional class I molecules (class Ib) may also present TAP-dependent peptides. In humans, CD1 antigens are nonconventional class I molecules. Recently, we characterized a human HLA class I deficiency resulting from a homozygous TAP deficiency. We show here that CD1a and -c are normally expressed on epidermal Langerhans cells of the TAP-deficient patients, as are CD1a, -b, and -c on dendritic cells differentiated in vitro from monocytes. Moreover, the CD1a antigens present on the surface of the dendritic cells are functional, since they internalize by receptor-mediated endocytosis gold-labeled F(ab')2 fragments of an anti-CD1a mAb. This suggests either that CD1 molecules are empty molecules, that they are more stable than empty conventional class I proteins, or that CD1 molecules present TAP-independent peptides.
Hum Immunol 1994 Sep
PMID:CD1 expression is not affected by human peptide transporter deficiency. 753 Jun 99

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)
Am Rev Respir Dis 1993 Sep
PMID:Langerhans cells in Langerhans cell histiocytosis and peripheral adenocarcinomas of the lung. 769 Feb 10

Langerhans cells are characterized by specific markers, such as Birbeck granules and CD1a antigen. S100 protein and neuron-specific enolase are less specific but are expressed only on Langerhans cells among the cells of the phagocytic mononuclear system. In this study, the expression of these two antigens on many monocytic leukemic cells is shown. These cells could be precursors of Langerhans cells which have been transformed into malignant cells.
Eur J Haematol 1993 Sep
PMID:S100 protein and neuron-specific enolase on monocytic leukemic CD1+ cells, probable precursors of Langerhans cells. 769 52

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.
J Immunol 1994 Sep 01
PMID:Cytokine profile and ultrastructure of intraepithelial gamma delta T cells in chronically inflamed human gingiva suggest a cytotoxic effector function. 805 26

Langerhans cell histiocytosis is difficult to study because of its rarity. Although recent studies indicate that it may be a clonal proliferation this does not prove that it is a malignant tumour. New methods for culturing dendritic cells and their precursors provide the opportunity to resolve issues relating to clonality, underlying genetic lesions and functional abnormalities in LCH or other lesional cells. The expression of the CD1a antigen on LCH cells provides a target for therapy.
Br J Cancer Suppl 1994 Sep
PMID:The scientific challenge of Langerhans cell histiocytosis. 807 11

Human bronchoalveolar lavage (BAL) has been described to contain, besides a large number of alveolar macrophages (AM) (approximately 95%), small numbers of monocyte-like cells (approximately 2%) and dendritic cells (DC) (approximately 0.4%). To separate AM (high autofluorescence) from DC, we used a fluorescence activated cell sorter (FACS) to separate BAL cells into a low autofluorescent (LAF) fraction and a high autofluorescent (HAF) fraction. Immunocytologic and functional properties of these fractions were investigated. The LAF fraction was composed of acid phosphatase (APh)- and RFD9-negative cells, which were strongly positive for HLA-DR, L25, RFD1, and CD68. A portion of these cells expressed CD1a (22%) and My4 (60%). The marker pattern of these cells is reminiscent to that of intraepithelial bronchial DC and to that of blood DC. The majority of the LAF cells had a monocyte-like morphology, but after overnight culture the percentage of LAF cells with long cytoplasmic extensions (DC morphology) was strongly augmented (from 18 to 51%). The HAF fraction contained 100% AM, strongly positive for APh, HLA-DR, CD68, RFD7, and RFD9. In culture, the LAF cells formed clusters with T cells and vigorously stimulated the proliferation of allogeneic T cells and naive (CD45RO-negative) T cells. BAL and LAF cells produced higher responses in nonsmokers than in smokers. In contrast, HAF cells did not form clusters with T cells and did not stimulate allogeneic T cell proliferation. HAF cells even suppressed mitogen-driven T cell proliferation.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Respir Cell Mol Biol 1994 Sep
PMID:Dendritic cells and their precursors isolated from human bronchoalveolar lavage: immunocytologic and functional properties. 808 70

Both activation and repression have been implicated in the cell cycle-regulated transcription of the histone HTA1-HTB1 locus in Saccharomyces cerevisiae. Transcriptional repressors have been identified through the isolation of recessive mutations in the HIR1, HIR2 and HIR3 genes. These three regulatory genes encode proteins that act at a negative site in the HTA1-HTB1 promoter, and their inactivation results in cell cycle-independent transcription. We report here on the characterization of a fourth HIR mutant. The HIR4-1 mutation is dominant, and the phenotypes that it confers suggest that the mutant gene encodes an altered transcriptional activator. The function of this activator is very specific: it uniquely regulates transcription of the HTA1-HTB1 locus, and it may antagonize repressors that act through the HTA1-HTB1 negative site.
Genetics 1993 Sep
PMID:The HIR4-1 mutation defines a new class of histone regulatory genes in Saccharomyces cerevisiae. 822 24

A better understanding of the pathophysiological role of Langerhans cells (LC) in atopic diseases is dictated by the characterization of the structures involved in immunoglobulin (IgE)-binding on their cell surface. We previously reported that human LC express the high affinity receptor for IgE (Fc epsilon RI), as well as the low affinity receptor for IgE (Fc epsilon RII/CD23). In the present study, we document the presence of a third IgE-binding structure on human LC, the IgE-binding protein (epsilon BP), an endogenous soluble beta-galactoside binding lectin. Immunohistochemical studies performed on normal human skin revealed an anti-epsilon BP reactivity in the cytoplasm of keratinocytes and in that of acinous cells of eccrine sweat glands. epsilon BP was also found on the cell surface of LC, as shown by anti-epsilon BP/anti-CD1a double labeling and flow cytometric analysis. Anti-epsilon BP binding to the surface of LC was completely abolished by preincubation with lactose and restored by addition of recombinant human epsilon BP, indicating that epsilon BP binds to LC surface by virtue of its lectin property. Immunoblot analysis of anti-epsilon BP-reactive material in keratinocytes and purified LC disclosed a protein with an apparent molecular weight of 33,000 consistent with epsilon BP. Interestingly, mRNA transcripts for epsilon BP were detected only in keratinocytes but not in purified LC isolated from normal skin. epsilon BP was found to be released in culture supernatants of keratinocytes. Incubation of LC with these supernatants resulted in epsilon BP-binding to LC surface via protein-carbohydrate interaction. Most importantly, we could show that binding of human myeloma IgE to LC was inhibited by epsilon BP. In contrast, neuraminidase-treated human myeloma IgE binds to LC only in the presence of epsilon BP. In situ binding studies revealed that keratinocytes, although containing epsilon BP intracytoplasmatically, failed to exhibit any IgE-binding properties. Collectively, our results suggest that human keratinocytes produce the beta-galactoside-binding lectin epsilon BP, which subsequently binds to the surface of LC where it is functional in modulating their binding capacity for IgE glycoforms.
J Exp Med 1993 Sep 01
PMID:Human keratinocytes release the endogenous beta-galactoside-binding soluble lectin immunoglobulin E (IgE-binding protein) which binds to Langerhans cells where it modulates their binding capacity for IgE glycoforms. 835 53

In a pilot study designed to investigate immunopathologic events in the evolution of cutaneous lesions in pemphigus foliaceus, we found that in this condition the epidermis is replete with CD68+ dendritic cells. The present study was designed to investigate the nature of this novel intraepidermal CD68+ cell population. For that purpose lesional skin of five patients with PF and, for comparison, of patients with another acantholytic autoimmune disease, pemphigus vulgaris, were examined using a panel of monoclonal antibodies in a three-step immunoperoxidase technique, in an immunofluorescence double-labeling technique, and by immunoelectron microscopy. We found epidermal CD1a+ Langerhans cells significantly decreased in pemphigus foliaceus compared to pemphigus vulgaris, but pemphigus foliaceus and not pemphigus vulgaris epidermis harbored large amounts of bone marrow-derived (CD45+) cells that expressed CD68, HLA-DR, and beta 2-integrin antigens, the most pronounced expression being observed for CD11c and CD18. These epidermal CD68+ cells were of dendritic shape, were CD1a-, and lacked Birbeck granules (BG); however, a small portion of CD68+ cells was also CD1a+ and exhibited BG as revealed by immunoelectron microscopy. These findings demonstrate that in certain conditions, i.e., in pemphigus foliaceus but not in pemphigus vulgaris, there is a shift from CD1a+/CD68- epidermal Langerhans cells towards CD1a-/CD68+ dendritic epidermal cells. The detection of a small number of CD1a+/CD68+/BG+ dendritic epidermal cells may identify these cells as a link between the CD1a+/CD68+/BG+ Langerhans cells and the CD1a-/CD68+/BG- cell population and suggests that these cells represent a transitional form of myelomonocytic cells during their phenotypic and morphologic transformation into resident epidermal Langerhans cells.
J Invest Dermatol 1993 Sep
PMID:CD68 positive epidermal dendritic cells. 837 Sep 61


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