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)

The simultaneous demonstration of three surface antigens of Langerhans cells (LC) within LC-enriched fresh epidermal cell suspensions from normal human skin was achieved, by means of a triple immunogold (IG) staining, using commercially available monoclonal antibodies (moAb) and immunoreagents, in a simple pre-embedding immunoelectronmicroscopy (IEM) procedure. As a result, suspended LC were triple-stained as follows: gold particles of 40 nm revealed the CD1 a antigen; gold particles of 20 nm revealed the HLA-DR antigen; and gold particles of 5 nm revealed the CD4 antigen. All the observed epidermal Birbeck granule-bearing LC were triple IG stained, thus simultaneously expressing the three surface differentiation antigens, which are therefore different from but coexisting with each other. The present investigation assesses the constant simultaneous expression by Birbeck granules bearing LC of not only CD1a and HLA-DR antigens, but also CD4 antigen. The occurrence is therefore excluded of both CD1a-positive HLA-DR-negative LC subpopulation and CD4-negative LC subpopulation, presumably due to the different sensitivity of the various procedures performed. The hypothetical occurrence of CD4-positive, CD1a-, and/or HLA-DR-negative LC subpopulations is ruled out. This study reaffirms indeed the high specificity and sensitivity of the IG-IEM method for a precise detection of the cell surface antigens of LC, and states the suitability of the IG labeling even for accurate multiple IEM stainings of LC.
J Invest Dermatol 1988 Dec
PMID:Simultaneous colloidal gold immunoelectronmicroscopy labeling of CD1a, HLA-DR, and CD4 surface antigens of human epidermal Langerhans cells. 326 98

Extensive immunophenotypic studies in a 2 1/2 month old girl with haemophagocytic lymphohistiocytosis were performed to characterise the proliferating histiocytes of the disease. The cells strongly expressed conventional macrophage antigens, but unexpectedly, there was a dissociated expression of the CD1a antigen (reacting with the monoclonal antibody NA1/34 but not with OKT6) and intracellular S-100 protein by the haemophagocytic lymphohistiocytosis histiocytes. These findings indicate that there is a "hybrid" phenotype between the two main arms of the mononuclear phagocyte system--namely, Langerhans' cells and phagocytic macrophages.
J Clin Pathol 1987 Dec
PMID:Unusual immunophenotype displayed by histiocytes in haemophagocytic lymphohistiocystosis. 332 48

Antigen-presenting (APC), suppressor T-cell-inducing macrophages infiltrate both human and murine epidermis after ultraviolet radiation (UVR) exposure. To determine their derivation, we prepared epidermal cell and dermal cell suspensions from human keratome biopsy specimens obtained from nonexposed skin and from UVB-irradiated sites (3 d after four times the minimal erythema dose). Simultaneous triple-marker flow cytometric analysis established the extended phenotype of macrophages infiltrating sunburned human epidermis (CD1a- CD1c- CD11b+ CD11c+ CD36+ Fc gamma RII+ DR+). This then enabled us to track dermal cells of this phenotype after UVR in relation to the heterogeneous DR+ populations in normal dermis. By both in situ immunohistology and cell suspension flow cytometry, UVR induced an expansion of bone marrow-derived DR+ cells in the perivasculature and sub-basement membrane zone of the papillary dermis. Despite an overall expansion of DR+ cells, the CD1a+ CD1c+ CD36- DR+ Langerhans-cell-like dendritic APC subset of dermal DR+ cells was depleted (p < 0.05), indicating that UVR-induced epidermal Langerhans cell loss (from 95% to 7% of DR+ epidermal cells) is not accounted for by Langerhans cell accumulation in the dermis. By contrast, UVR exposure induced a selective expansion of the dermal macrophage subset, which is phenotypically identical to the monocytic/macrophagic APCs that appear in the epidermis after UV injury (p < 0.01). Cell cycle analysis (to determine whether this expansion was accounted for entirely by infiltration) revealed no increase in the percentage of DR+ CD36+ UVR-exposed dermal cells in S/G2/M phase; however, the expanded DR+ CD36+ subset continued its already substantial level of proliferation unabated. Therefore, epidermal macrophages derive not only from transcapillary migration, but also from in situ proliferation of a dermal precursor. Taken together, these findings show that UVR creates an epidermal and dermal APC milieu which is dominated by monocytic/macrophagic cells, through depletion of cells of dentritic APC phenotype, and concomitant selective dermal expansion of a CD1a- CD1c- CD11b+ CD36+ Fc gamma RII+ DR+ (monocyte/macrophage) population.
J Invest Dermatol 1995 Dec
PMID:In human dermis, ultraviolet radiation induces expansion of a CD36+ CD11b+ CD1- macrophage subset by infiltration and proliferation; CD1+ Langerhans-like dendritic antigen-presenting cells are concomitantly depleted. 749 Apr 72

The relative contribution of dermal-derived immunocompetent cells to the overall immunologic response in skin has been hampered by the lack of appropriate isolation techniques. In this report, we provide a purification schema that reliably yields highly purified populations of dermal dendritic cells (DDC). These cells are motile, express high levels of class II MHC antigens that decorate their cytoplasmic dendritic processes, and lack numerous B cell, T cell, and natural killer cell antigens. Using a broad panel of 45 different antibodies, an extensive phenotypic analysis was completed, revealing distinctive profiles for subsets of DDC. Despite homogeneous light scatter profile and cytologic appearance, three subsets of DDC could be distinguished by phenotypic and functional criteria. All DDC, but not epidermal Langerhans cells, express factor XIIIa. By triple color cell staining the relative distribution of factor XIIIa positive DDC is as follows: subset 1, 65% to 70% of total DDC express neither CD1a nor CD14; subset 2, 15% to 20% of total DDC express CD1a but not CD14; and subset 3, 10% to 15% of total DDC express CD14 but not CD1a. The CD14-negative subset of DDC were shown to be as potent stimulators of allogeneic mixed lymphocyte reactions as Langerhans cells or blood-derived dendritic cells. However, DDC subsets differed in their ability to support autologous T cell proliferation in response to the mitogenic lectin PHA or bacterial-derived superantigen. In these assays, subsets 1 and 2 were significantly more potent as antigen-presenting cells compared with subset 3. Thus, normal skin contains at least three separate populations of DDC, which have distinctive phenotypic markers and immunologic capabilities.
J Immunol 1993 Dec 01
PMID:Characterization of dermal dendritic cells obtained from normal human skin reveals phenotypic and functionally distinctive subsets. 750 23

We have examined the effects of low-dose monochromatic UVB irradiation (295 +/- 5 nm), biologically equivalent to that generally incident on the skin during a 12-session sun-bed course, on the expression of the CD1a epidermal Langerhans cell surface marker in human skin in vivo. In five subjects, 1.5 minimal erythema doses (MEDs) at 295 nm depleted its expression by 50%. In five further subjects, a single 1.5 MED dose, 1.5 MEDs in 10 equal fractions on alternate days, and a single 1.5 MED dose at one-tenth the previously used irradiance, delivered to separate sites, also led to variable but significant depletion of CD1a expression of around 30-50%. Thus, low-dose UVB irradiation, whether received rapidly or slowly, appears significantly and approximately equally to deplete human epidermal Langerhans cell numbers as measured by CD1a expression.
Br J Dermatol 1993 Dec
PMID:Low-dose ultraviolet-B irradiation depletes human epidermal Langerhans cells. 750 27

The CD1 gene family is composed of five distinct molecules: CD1a, b, c, d and e. CD1a, b and c are primarily expressed thymically with limited extrathymic expression. Preliminary studies have shown that CD1d is primarily expressed extrathymically in gastrointestinal epithelial cells, renal tubular epithelial cells and B cells. This report characterizes the expression of CD1d in a variety of human tissues by immunohistochemistry using two anti-human CD1d monoclonal antibodies (mAb). CD1d was found in a wide range of tissues including the intestine, liver, pancreas, skin, kidney, uterus, conjunctiva, epididymis, thymus and tonsil. Within those tissues CD1d was mainly present in epithelial cells, vascular smooth muscle cells and parenchymal cells. Therefore, the tissue distribution of CD1d is distinct from CD1a-c and classical major histocompatibility complex (MHC) proteins implicating a unique role for CD1d in the immune system.
Immunology 1993 Dec
PMID:Tissue distribution of the non-polymorphic major histocompatibility complex class I-like molecule, CD1d. 750 19

In human epidermis, expression of CD1a is confined to Langerhans cells (LC), whereas CD1c expression has been observed in dendritic cells of the dermis, as well as the epidermis. In transfected fibroblasts, expression of CD1c at the cell surface appears to exclude expression of either CD1b or CD1a, despite continued transcription of the latter genes. In order to determine whether this mechanism might be operative in human skin, we have compared the expression of CD1a and CD1c on the surface of dermal and epidermal dendritic cells to their expression at the level of mRNA using a combination of dual-label immunofluorescence microscopy, northern blot hybridization, and reverse transcriptase-polymerase chain reaction (RT-PCR). By both immunofluorescence and Northern blotting, CD1c expression was observed in both dermal and epidermal cells, whereas expression of CD1a was confined largely to the epidermis. Moreover, as shown by immunomagnetic bead selection and RT-PCR, CD1a and CD1c were both expressed on epidermal LC, but were absent from other epidermal cell types. These results argue against cell surface exclusion as a mechanism for selective expression of CD1c in human dermis.
J Dermatol Sci 1993 Dec
PMID:CD1 gene expression in human skin. 751 Sep 98

Macrophages play important roles in immunity and inflammation, and in allergic, granulomatous and neoplastic diseases. Here, we present the indepth results of an ongoing study of macrophage differentiation pathways in cutaneous macrophage disorders and in vitro. Up to now, a total of 40 cases of cutaneous macrophage disorders (histiocytoses and granulomas) and related diseases were examined using a panel of monoclonal and polyclonal antibodies to macrophage differentiation antigens (mAb MS-1, mAb alpha CD1a, mAb alpha CD34, mAb RM 3/1, mAb alpha CD11c, mAb alpha CD36, mAb MAC 387, mAb 27E10, polyclonal antibodies alpha MRP-8 and -14, mAb alpha CD68, mAb 25F9, mAb DRC1-R4/23, and mAb 1F10). Of these, MS-1 high molecular weight protein, synthesized by non-continuous sinusoidal endothelial cells and highly dendritic perivascular macrophages in normal human organs, is the most specific macrophage differentiation marker. MS-1 high molecular weight protein is selectively expressed by cutaneous non-Langerhans cell histocytoses, and proves to be a valuable diagnostic tool for these diseases. MS-1 high molecular weight protein is not found in Langerhans cell histiocytosis cells, epithelioid cells in sarcoidosis, and palisading histiocytes in granuloma annulare. MS-1+ macrophages may be found intermingled in cellular type dermatofibroma and in foreign body granulomas; they differ from MS-1+ non-Langerhans cell histiocytosis cells by their highly dendritic morphology, and thus rather resemble the MS-1+ macrophages in normal skin. RM 3/1 antigen shows a similar, but broader expression pattern including non-Langerhans cell histiocytoses, xanthelasmata palpebrarum, foreign body granulomas, granuloma annulare, and cellular type dermatofibroma. Moreover, xanthelasmata palpebrarum paradigmatically represent a class of macrophage lesions with strong RM 3/1, but little MS-1 antigen expression. In sarcoidosis, RM 3/1+ macrophages are only found at the very periphery of epithelioid cell granulomas. In contrast, 25F9 antigen is strongly and consistently expressed in epithelioid cells of sarcoidosis, and in foreign body granulomas. In cultured human monocytes/macrophages, RM 3/1 antigen is expressed early on, while MS-1 high molecular weight protein and 25F9 antigen are late and very late macrophage differentiation antigens, respectively. Expression of RM 3/1 antigen and MS-1 high molecular weight protein is inducible by glucocorticoid and interleukin-4, and less so by interleukin-13 and interleukin-10, and combinations thereof, while 25F9 antigen seems to be less influenced by these agents. Interferon-gamma (and less so tumor necrosis factor-alpha) inhibit expression of all three antigens in cultured human monocytes/macrophages.(ABSTRACT TRUNCATED AT 400 WORDS)
Exp Dermatol 1994 Dec
PMID:Dissection of macrophage differentiation pathways in cutaneous macrophage disorders and in vitro. 774 70

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


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