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)

Fc gamma-receptors (FcR) in cryostat sections of normal human skin were detected with soluble immune complexes of horseradish peroxidase (HRP) and rabbit IgG anti-HRP (HRP-anti-HRP). The binding of HRP-anti-HRP to Langerhans' cells (LC) was demonstrated using a double immunofluorescence staining in which LC were identified with a CD1a specific monoclonal antibody (Leu 6). The immune complexes gave granular staining of CD1a+ epidermal cells in sections of all specimens from normal skin. The mean percentage of CD1a+ cells that were FcR+ was 49 +/- 11 (n = 8). The FcR+/CD1a+ cells had a clearly defined dendritic pattern. The staining intensity of LC with HRP-anti-HRP was weaker than the intense staining of CD1a-macrophages in the dermis. Results of inhibition experiments indicate that human epidermal LC express low affinity FcR, but the presence of high affinity FcR as well cannot be excluded. The demonstration of FcR expression on normal LC clarifies previous uncertainty on LC membrane receptors, though the functional significance of these receptors is still not well understood.
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PMID:Fc gamma-receptor as a functional marker on epidermal Langerhans' cells in situ. 248 27

The immunoreactivity of a CD1a monoclonal antibody (MAb), denoted 010, was investigated by means of the streptavidin-biotin-peroxidase method in formalin-fixed and paraffin-embedded tissues from 47 cases. The samples comprised reactive lymphoid proliferations of skin, tonsil, and lymph node including dermatopathic lymphadenopathy and Langerhans' cell histiocytosis, Hodgkin's and non-Hodgkin's lymphomas, and thymomas. Interdigitating and dermal dendritic cells, veiled cells, Langerhans' cells, and also cortical thymocytes and their neoplastic counterparts displayed immunostaining with MAb 010 in paraffin sections. These results are identical to previous ones reported for other CD1a MAbs in fresh or frozen specimens. The findings suggest that the binding site of 010 is a fixation-resistant epitope of CD1a antigen which has not been previously identified.
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PMID:Immunohistochemical detection of CD1A antigen in formalin-fixed and paraffin-embedded tissue sections with monoclonal antibody 010. 750 72

The epidermal Langerhans' cells are dendritic cells of the skin capable of triggering cutaneous immune responses. They possess the membrane antigens required to this effect: class II histocompatibility antigen, CD1a and CD4; the latter acts as receptor for the human immunodeficiency virus. The skin is the organ primarily affected by Kaposi's sarcoma (KS). In epidemic KS, the local immunologic conditions of the skin are little known. We therefore studied 12 patients with AIDS-associated KS, evaluating the density and phenotypic expression in KS-affected and unaffected skin of the following antigens: CD1a, HLA-DR, CD4 in dendritic epidermal cells and dermis, and CD3, CD4 and CD8 in cells of the inflammatory infiltrate, using monoclonal antibodies applied to frozen sections with the avidin-biotin-peroxidase technique. Langerhans' cells in the AIDS-KS skin lesions were found to be decreased in number. This decrease was even more pronounced in the case of cells expressing HLA-DR antigen. A number of them were also revealed with CD4. The tumour lymphocytic infiltrate was almost exclusively composed of CD3+ CD8+ phenotype lymphocytes. The dermis also revealed CD4+ dendritic cells. The basal keratinocytes focally expressed HLA-DR. These phenotypical alterations of the Langerhans' cells and the local immunological imbalance observed may contribute to the growth and continuity of the KS lesions.
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PMID:Langerhans' cells and lymphocytic infiltrate in AIDS-associated Kaposi's sarcoma. An immunohistochemical study. 752 Nov 2

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

CD34+ precursors in normal human bone marrow (BM) generate large numbers of dendritic cells alongside macrophages and granulocytic precursors when cultured for 12 to 14 days in c-kit ligand, granulocyte-macrophage colony-stimulating factor (GM-CSF), and tumor necrosis factor-alpha (TNF-alpha). This study reports an intermediate cell type that develops by day 6, and has the potential to differentiate into either macrophages or dendritic cells. When the d6 progeny are depleted of mature macrophages and residual CD34+ precursors, a discrete CD14+ HLA-DR+ population persists in addition to immunostimulatory CD14- HLA-DR() dendritic cells. Half of the CD14+ HLA-DR+ population is in cell cycle (Ki-67+), but colony-forming units (CFUs) are no longer detectable. The calls are c-fms+, but lack myeloperoxidase and nonspecific esterase. They also possess substantial phagocytic and allostimulatory activity. These post-CFU, CD14+ HLA-DR+ intermediates develop into typical macrophages when recultured in the absence of exogenous cytokines. M-CSF supports up to approximately 2.5-fold expansion of macrophage progeny. In contrast, the combination of GM-CSF and TNF-alpha supports quantitative differentiation into dendritic cells, lacking c-fms, CD14, and other macrophage properties, and expressing HLA-DR, CD1a, CD83, CD80, CD86, and potent allostimulatory activity. Therefore, normal CD34+ BM precursors can generate a post-CFU bipotential intermediate in the presence of c-kit ligand, GM-CSF, and TNF-alpha. This intermediate cell type will develop along the dendritic cell pathway when macrophages are removed and GM-CSF and TNF-alpha are provided. Alternatively, it can differentiate along a macrophage pathway when recultured with or without M-CSF.
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PMID:Dendritic cells and macrophages can mature independently from a human bone marrow-derived, post-colony-forming unit intermediate. 863 19

The roles of sialyl-Lewisx antigen were evaluated in the pathogenesis of psoriasis. Sialyl-Lewisx expression was investigated immunohistochemically in the epidermis of normal human skin and erythematous lesional skin of psoriasis vulgaris by avidin-biotin-peroxidase complex procedures. A few sialyl-Lewisx positive dendritic cells were detected in the epidermis of normal human skin. In 7 out of 9 cases of psoriasis vulgaris, the number of sialyl-Lewisx-positive epidermal dendritic cells increased in the erythematous lesion over the adjacent normal skin; there were no marked changes in the numbers of CD1a-positive cells in the epidermis between the two skin types. In the double immunofluorescence studies, more than half of the sialyl-Lewisx-positive epidermal cells in psoriatic erythema were stained with a monoclonal Lag antibody that specifically reacts with Birbeck granules and related structures of human Langerhans cells. Furthermore, we determined the changes in serum levels of sialyl-Lewisx antigens in patients with psoriasis. Although levels in the sera were not significantly elevated over those of controls, the increases correlated with the degree of disease activity. These findings suggest that sialyl-Lewisx antigen is possibly involved in the development of psoriasis.
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PMID:Evaluation of sialyl Lewisx antigen in the skin and the sera of patients with psoriasis vulgaris. 883 35

Dendritic cells (DC) are the most potent APCs within the immune system. We show here that highly purified CD14(bright) peripheral blood monocytes supplemented with granulocyte-monocyte (GM)-CSF plus IL-4 develop with high efficacy (>95% of input cells) into DC. They neo-expressed CD1a, CD1b, CD1c, CD80, and CD5; they massively up-regulated CD40 (109-fold) and HLA-DQ and DP (125- and 87-fold); and significantly (>5-fold) up-regulated HLA-DR, CD4, CD11b, CD11c, CD43, CD45, CD45R0, CD54, CD58, and CD59. CD14, CD15s, CD64, and CDw65 molecules were down-regulated to background levels, and no major changes were observed for HLA class I, CD11a, CD32, CD33, CD48, CD50, CD86, CDw92, CD93, or CD97. Monocytes cultured in parallel with GM-CSF plus TNF-alpha were more heterogeneous in expression densities but otherwise similar in their surface molecule repertoire. They clearly differed, however, in their accessory cell capacity. Only GM-CSF plus IL-4-cultured cells were found to be potent stimulators in allogeneic and autologous MLR and they presented tetanus toxoid 100- to 1000-fold more efficiently than other cell populations tested. Furthermore, only cytokine-treated monocytes formed clusters with resting T cells. At variance from all these similarities between in vitro-generated monocyte-derived DC and in vivo-developing DC, the DC populations generated by us contained significant amounts of myeloperoxidase and also expressed lysozyme. At least in this respect they, thus, differ from "classical" DC types.
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PMID:Molecular and functional characteristics of dendritic cells generated from highly purified CD14+ peripheral blood monocytes. 889 15

Using a recently described serum-free culture system of purified human CD34+ progenitor cells, we show here a critical cooperation of flt3 ligand (FL) with transforming growth factor-beta1 (TGF-beta1) in the induction of in vitro dendritic cell/Langerhans cell (DC/LC) development. The addition of FL to serum-free cultures of CD34+ cells supplemented with TGF-beta1, granulocyte-macrophage colony-stimulating factor, tumor necrosis factor alpha, and stem cell factor strongly increases both percentages (mean, 36% +/- 5% v 64% +/- 4%; P = .001) and total numbers (4.4- +/- 0.8-fold) of CD1a+ dendritic cells. These in vitro-generated CD1a+ cells molecularly closely resemble a particular type of DC known as an epidermal Langerhans cell. Generation of DC under serum-free conditions was found to strictly require supplementation of culture medium with TGF-beta1. Upon omission of TGF-beta1, percentages of CD1a+ DC decreased (to mean, 10% +/- 8%; P = .001) and, in turn, percentages of granulomonocytic cells (CD1a- cells that are lysozyme [LZ+]; myeloperoxidase [MPO+]; CD14+) increased approximately threefold (P < .05). Furthermore, in the absence of TGF-beta1, FL consistently promotes generation of LZ+, MPO+, and CD14+ cells, but not of CD1a+ cells. Serum-free single-cell cultures set up under identical TGF-beta1- and FL-supplemented culture conditions showed that high percentages of CD34+ cells (mean, 18% +/- 2%; n = 4) give rise to day-10 DC colony formation. The majority of cells in these DC-containing colonies expressed the Langerhans cell/Birbeck granule specific marker molecule Lag. Without TGF-beta1 supplementation, Lag+ colony formation is minimal and formation of monocyte/macrophage-containing colonies predominates. Total cloning efficiency in the absence and presence of TGF-beta1 is virtually identical (mean, 41% +/- 6% v 41% +/- 4%). Thus, FL has the potential to strongly stimulate DC/LC generation, but has a strict requirement for TGF-beta1 to show this costimulatory effect.
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PMID:flt3 ligand in cooperation with transforming growth factor-beta1 potentiates in vitro development of Langerhans-type dendritic cells and allows single-cell dendritic cell cluster formation under serum-free conditions. 926 60

In response to granulocyte-macrophage colony-stimulating factor plus tumor necrosis factor alpha, cord blood CD34+ hematopoietic progenitor cells differentiate along two unrelated dendritic cell (DC) pathways: (1) the Langerhans cells (LCs), which are characterized by the expression of CD1a, Birbeck granules, the Lag antigen, and E cadherin; and (2) CD14+ cell-derived DCs, characterized by the expression of CD1a, CD9, CD68, CD2, and factor XIIIa (Caux et al, J Exp Med 184:695, 1996). The present study investigates the functions of each population. Although the two populations are equally potent in stimulating naive CD45RA cord blood T cells through apparently identical mechanisms, each also displays specific activities. In particular CD14-derived DCs show a potent and long-lasting (from day 8 to day 13) antigen uptake activity (fluorescein isothiocyanate dextran or peroxidase) that is about 10-fold higher than that of CD1a+ cells, which is restricted to the immature stage (day 6). The antigen capture is exclusively mediated by receptors for mannose polymers. The high efficiency of antigen capture of CD14-derived cells is coregulated with the expression of nonspecific esterase activity, a tracer of lysosomial compartment. In contrast, the CD1a+ population never expresses nonspecific esterase activity. The most striking difference is the unique capacity of CD14-derived DCs to induce naive B cells to differentiate into IgM-secreting cells, in response to CD40 triggering and interleukin-2. Thus, although the two populations can allow T-cell priming, initiation of humoral responses might be preferentially regulated by the CD14-derived DCs. Altogether, those results show that different pathways of DC development might exist in vivo: (1) the LC type, which might be mainly involved in cellular immune responses, and (2) the CD14-derived DC related to dermal DCs or circulating blood DCs, which could be involved in humoral immune responses.
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PMID:CD34+ hematopoietic progenitors from human cord blood differentiate along two independent dendritic cell pathways in response to granulocyte-macrophage colony-stimulating factor plus tumor necrosis factor alpha: II. Functional analysis. 926 63

To carry out the characterization of feline Langerhans cells (LC), first described in 1994, we used a panel of monoclonal antibodies (MAb) known to react with human, canine and feline leukocyte membrane antigens (Ag). The immunolabeling was performed, at light microscope level, on frozen sections of feline skin and labial mucosa using an avidin-biotin-peroxidase technique, and at electron microscope level on epidermal cell suspensions using an immunogold technique. Out of the 52 MAb tested, six labeled basal or suprabasal DC cells in the frozen sections, either in epidermis or lip epithelium: MHM23 (anti-human CD18), CVS20 and vpg3 (respectively anti-canine and feline-major histocompatibility complex class II molecules), vpg5 (anti-feline leukocytes), vpg39 (anti-feline CD4) and Fel5F4 (anti-feline CD1a). These six MAb were used on suspensions, and labeled cells which showed no desmosomes or melanosomes, but contained 'zipper-like' structures similar to Birbeck granules (BG) in their cytoplasm, revealing they were LC. Consequently, feline LC are CD18-positive (CD18+), major histocompatibility complex class II-positive (Class II+), CD1a-positive (CD1a+), vpg5-positive (vg5+) and CD4-positive (CD4+). This immunophenotypic and ultrastructural characterization demonstrates that feline LC share many characteristics with their human counterparts, a fact that will allow us to study the role of feline LC in certain feline diseases such as Feline Immunodeficiency Virus (FIV) infection, since it has been shown that human LC cells are HIV-permissive, and to establish an animal model for human AIDS.
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PMID:Immunophenotypic characterization of feline Langerhans cells. 934 35


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