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)

Human epidermal Langerhans cells play an important role in the immunoregulation of the skin. We measured the numbers of CD(3+)-, CD(8+)-, CD1a(+)-, HLADR(+)-, IL2R(+)-, CD(4+)- and CD68 positive cells in the skin of 8 asymptomatic HIV-infected Persons, 3 Patients with AIDS and 11 healthy volunteers by suction blister technique. Our results indicate increased numbers of CD1a+ cells and increased numbers of CD4+ cells in the epidermis in asymptomatic HIV-infection. At the same time CD68+ cells are decreased already in an early stage of HIV-Infection. The number of CD1a/CD4+ cells is related to the degree of immunodeficiency. This fact might be caused by the activation of MPS.
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PMID:[Lymphocytes, Langerhans cells and CD68-positive monocytes/macrophages in the skin of HIV-infected patients and normal controls]. 172 11

Langerhans cells (LC) are dendritic epidermal antigen-presenting cells expressing the surface molecule CD4, which renders them theoretical cellular targets for direct infection by the human immunodeficiency virus (HIV). To date, somewhat conflicting results have been reported concerning the in vivo infection of LC by HIV as well as the numerical alteration of these cells in the course of HIV infection. In the present work we studied clinically normal skin of a group of 44 HIV-1-seropositive patients classified according to the Centers for Disease Control (CDC) stages II (n = 14), III (n = 9), and IV (n = 21). Monoclonal antibodies (MAb) to HIV p18, p24, and gp120 and to HLA-DR and CD1a antigens (specific for LC) were applied on frozen skin sections using an amplification biotin-streptavidin-fluorescein technique. The MAb to HIV p18 cross-reacted with a cytoplasmic antigen of epidermal basal keratinocytes also present on HIV-seronegative skin specimens. No other reactivity was observed with any of the three anti-HIV MAb. The quantitative study showed that no significant correlations could be established between the number of LC (evaluated independently by HLA-DR and CD1a antigens) and the number of peripheral blood CD4+ve lymphocytes or the CDC disease stage. These results cast some doubt on the previously reported in vivo infection and numerical decrease in LC in HIV infection. The precise involvement of LC in HIV infection awaits further investigation.
AIDS Res Hum Retroviruses 1989 Jun
PMID:Immunohistochemical study of normal skin of HIV-1-infected patients shows no evidence of infection of epidermal Langerhans cells by HIV. 247 43

Some infants infected with human immunodeficiency virus type 1 (HIV-1) rapidly develop a fatal disease characterized by a severe lymphopenia. To explain the immune dysfunction, we proposed a mechanism by which a nongeneration of CD4+ T cells is caused by HIV-1 infection of thymic cells. To examine this hypothesis, we infected primary triple-negative (TN; phenotypically CD3- CD4- CD8-), CD1a- TN, or CD1a+ TN thymic cell subsets. Our data indicate that by flow cytometry, TN, CD1a- TN, and CD1a+ TN cells remain CD4 negative throughout the culture period. We demonstrated that TN and CD1a+ TN thymic cell subsets are susceptible to HIV-1 as is the entire thymic cell population, whereas CD1a- TN cells are not. A limited number of infected TN cells are expressing HIV-1 but the level of transcription is very high in permissive cells, as detected by in situ hybridization. We then performed blocking experiments on TN cells to examine the mechanism of HIV-1 entry into these cells. CD4 (OKT4a) monoclonal antibody blocks their infection. Finally, infection experiments on two subpopulations of TN cells (CD2+ CD7+ and CD2- CD7-) indicate that infected TN cells may correspond to both immature thymocytes and thymic dendritic cells. These data are of particular interest since infection of thymic stromal cells might result in an impairment of T-cell differentiation, which may explain a nongeneration of functional CD4+ T-cell population in the thymus. This phenomenon may play a role in AIDS pathogenesis, in particular in infants born from seropositive mothers.
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PMID:Two subpopulations of human triple-negative thymic cells are susceptible to infection by human immunodeficiency virus type 1 in vitro. 751 58

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

Langerhans cells (LC) belong to the dendritic cell family and represent the principal antigen presenting cells populating squamous epithelia. We have reported the presence of human immunodeficiency virus Type 1 (HIV-1) proviral DNA and RNA in purified LC from the epidermis of seropositive patients. The aim of this study was to quantify HIV-1 proviral DNA in LC of infected patients using a competitive polymerase chain reaction (PCR) assay. Bulk epidermal cell (EC) suspensions were obtained from the skin of nine AIDS patients and six seronegative subjects. Purified LC and LC-depleted EC were prepared by immunomagnetic separation using an anti-CD1a monoclonal antibody. LC preparations did not contain T cells, as assessed by reverse transcription PCR analysis of the T cell receptor beta-chain gene (C region). In addition, no CD14+ cells could be detected in LC fractions by immunostaining of cytospin preparations. To quantify HIV-1 DNA, a new competitive PCR system was devised using SK145/150 as primers (gag) and a competitor plasmid DNA with a modified sequence (209 instead of 142 bp). The number of HIV-1 DNA copies found in the LC of AIDS patients ranged from 107 to 3,645/10(5) LC. In contrast, LC-depleted EC from the same subjects were all negative. The results indicate that in AIDS patients the frequency of infected LC is comparable to that reported for peripheral blood CD4+ T cells.
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PMID:Quantitation by competitive PCR of HIV-1 proviral DNA in epidermal Langerhans cells of HIV-infected patients. 810 64

Human Langerhans cells (LC) are bone marrow-derived, HLA-DR+, CD1a+, and CD4+ dendritic antigen-presenting cells found in stratified squamous epithelia. As other members of the dendritic leukocyte family, to which they belong, LC have been reported as targets for HIV-1 infection. The aim of the present study was to investigate whether HIV-1 RNA is expressed in epidermal LC of HIV-1-infected patients. Bulk epidermal cell (EC) suspensions were prepared from skin of nine recently deceased AIDS patients and 11 seronegative controls. Purified LC (94 +/- 4% HLA-DR+ cells with no CD3+ cells, as assessed by flow microfluorimetry analysis) and LC-depleted EC were obtained by immunomagnetic separation using an anti-CD1a monoclonal antibody. Samples were analyzed for the presence of HIV-1 RNA by reverse transcription of a spliced mRNA region of the tat gene, followed by polymerase chain reaction amplification. HIV-1-spliced RNA was detected in LC from 6 of 9 patients examined, whereas LC-depleted EC fractions from the same patients were all negative. The results indicate that epidermal LC from HIV-seropositive patients actively transcribe HIV-1 proviral DNA, further supporting the hypothesis that HIV productively infected LC could serve as a reservoir of the virus in the epidermis and as a source for the infection of T lymphocytes.
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PMID:Direct detection of HIV-1 RNA in epidermal Langerhans cells of HIV-infected patients. 845 38

An in vitro culture system was developed that facilitates detailed studies of the interaction of Human Immunodeficiency Virus (HIV) with dendritic cells (DC). Cultured immature DC were generated from adherent peripheral blood mononuclear cells in the presence of GM-CSF and IL-4. These cells were non-adherent, non-phagocytic and had a veiled surface appearance. They expressed high levels of MHC class I and II proteins, CD1a, B7/BB1 and low levels of CD4, and were known to possess a potent soluble antigen presenting capacity. Upon infection with the HIV-1 strains Lai (lymphocytotropic) and BaL (monocytotropic), the viral RNA was reverse transcribed to complete DNA provirus. However the infection was non-productive as judged from measuring the activity of the virus encoded reverse transcriptase in the culture supernatant. Thus HIV infection was restricted at a step post entry.
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PMID:Infection of cultured immature dendritic cells with human immunodeficiency virus type 1. 852 22

The prevalence of anoperineal diseases, i.e. sexual transmitted infections, is increasing particularly in AIDS, a fact which is likely due to the alteration of mucosal immunity. However, no data were available on normal anal status. In order to study anal immunity in man, we characterized lymphocytes subtypes and Langerhans' cells (LC) using quantitative morphometric analysis and immunohistochemistry. Anal normal mucosal samples obtained from surgical specimens of 45 patients (30 suffering from hemorrhoids and 15 from fissurations) were analyzed. Immunohistochemistry was performed on frozen sections with antibodies recognizing CD1a (LC), CD3 (T lymphocytes), CD4 (T4), CD8 (T8) and CD22 (B-lymphocytes). Immunostained cells were counted per square millimeter of mucosal epithelium. The surface of CD1a cells was measured using a computerized software program and a percentage of CD1a immunostained area was calculated in comparison to the whole mucosal surface. LC and T-Lymphocytes were found in the squamous epithelium in all analyzed samples. The mean values of LC number were 84.13 +/- 9.6 and 64.77 +/- 9.8 in hemorroid- and fissure-patients, respectively. The mean values of LC area (% of CD1a stained area over total mucosal surface) were 3.89 +/- 0.44 and 4.84 +/- 0.64, respectively. In the two groups, the number of intraepithelial CD8 lymphocytes was higher than that of CD4 lymphocytes. These data suggest for the first time that anal mucosa could be considered as a part of MALT system.
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PMID:Quantitative analysis of the immune cells in the anal mucosa. 882 6

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

Human immunodeficiency virus (HIV)-1 Nef protein is an essential modulator of AIDS pathogenesis and we have previously demonstrated that rNef enters uninfected human monocytes and induces T cells bystander activation, up-regulating IL-15 production. Since dendritic cells (DCs) play a central role in HIV-1 primary infection we investigated whether rNef affects DCs phenotypic and functional maturation in order to define its role in the immunopathogenesis of AIDS. We found that rNef up-regulates the expression on immature DCs of surface molecules known to be critical for their APC function. These molecules include CD1a, HLA-DR, CD40, CD83, CXCR4, and to a lower extent CD80 and CD86. On the other hand, rNef down-regulates surface expression of HLA-ABC and mannose receptor. The functional consequence of rNef treatment of immature DCs is a decrease in their endocytic and phagocytic activities and an increase in cytokine (IL-1beta, IL-12, IL-15, TNF-alpha) and chemokine (MIP-1alpha, MIP-1beta, IL-8) production as well as in their stimulatory capacity. These results indicate that rNef induces a coordinate series of phenotypic and functional changes promoting DC differentiation and making them more competent APCs. Indeed, Nef induces CD4(+) T cell bystander activation by a novel mechanism involving DCs, thus promoting virus dissemination.
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PMID:HIV-1 Nef induces dendritic cell differentiation: a possible mechanism of uninfected CD4(+) T cell activation. 1196 93


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