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)

Dermal dendritic cells from eleven cases of mycosis fungoides (MF) (six patch and five plaque stage), two cases of pre-MF, and five specimens of normal human skin, were characterized immunohistochemically using a panel of antibodies including anti-human Thy-1, intercellular adhesion molecule-1 (ICAM-1; CD54), endothelial leukocyte adhesion molecule-1 (ELAM-1), vascular cell adhesion molecule-1 (VCAM-1), CD1a, CD2, CD14, CD18, CD34, MAC387, KP-1, EBM-11, factor XIIIa, factor XIIIs, and S100. Thy-1 expression in normal skin was limited to the microvascular endothelium and perivascular dendritic cells. An extensive interstitial network of Thy-1+ dendritic cells was seen in the papillary dermis of all cases of MF, whereas no epidermal cells were Thy-1+. The mean +/- standard deviation of interstitial Thy-1+ cells per high power field in the dermis was: normal skin, 2.86 +/- 0.34; pre-MF, 15; patch stage MF, 13.4 +/- 7.08; plaque stage MF, 49.96 +/- 21.29. Thy-1+ dendritic cells morphologically resembled the factor XIIIa+ "dermal dendrocyte" (DD) and shared their VCAM-1+, ICAM-1+, CD1a, CD2-, CD14+, CD18+, EMB11+, factor XIIIa+, factor XI-IIs-, S100-, MAC387- and KP-1-immunophenotype in MF. Double labeling studies revealed up to 50% of Thy-1+DD were also factor XIIIa+ in MF. Immediately beneath these cells was a similar network of CD34+, Thy-1-, factor XIIIa- dendritic cells limited to the reticular dermis. Strong microvascular endothelial cell expression of Thy-1 and VCAM-1, and focal vascular ELAM-1 expression were also seen in MF. Distinct cellular compartmentalization (papillary dermis versus reticular dermis versus epidermis) of dendritic cells is demonstrated by the differential expression of Thy-1, factor XIIIa, and CD34 antigens. The extensive number and prominent dermal dendritic network in the papillary dermis juxtaposed between epidermal keratinocytes (KC) and dermal/epidermal T cells, suggests an important pathophysiologic role for this newly recognized and immunophenotypically distinctive cell population in MF.
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PMID:Cutaneous expression of Thy-1 in mycosis fungoides. 128 18

Although dithranol has been used for 75 years in the treatment of psoriasis, its working mechanism is still not resolved. In order to further define the mode of action of dithranol, the interference with normal skin was studied. The effect of dithranol on epidermal proliferation, keratinization and inflammation was examined using immunohistochemistry. Punch biopsies from 6 volunteers who applied dithranol 0.5% in petrolatum were taken before application, after 48 and 96 h. Biopsies were processed for assessing epidermal proliferation by Ki67 binding (cycling cells), for keratinization by Ks8.12 binding (keratin 13 and 16, keratin 16 is expressed by hyperproliferative keratinocytes) and RKSE60 binding (keratin 10). For assessing inflammation the antibodies antielastase (polymorphonuclear leukocytes (PMN)), T11 (T lymphocytes, CD2), T6 (Langerhans cells, CD1a) and WT14 (monocytes/macrophages, CD14) were used. Ki-67 staining started to increase between 48 and 96 h whereas Ks8.12 binding had increased already between 0 and 48 h. RKSE60 staining showed a decline between 48 and 96 h. Inflammation in the dermis showed an increase after 48 h, and continued to increase. In the inflammatory infiltrate, the accumulation of PMN was limited compared to the pronounced infiltration of T lymphocytes. Langerhans cell shape and epidermal position altered in 4 volunteers. Application of dithranol on normal skin produces analogies and discrepancies compared to application of dithranol on psoriatic lesions. Direct interference with epidermal growth and differentiation seems less likely as the antipsoriatic principle.
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PMID:Topical application of dithranol on normal skin induces epidermal hyperproliferation and increased Ks8.12 binding. 137 64

The Langerhans cell (LC) migrates between the epidermis and the regional lymph nodes to present antigens. This migration pattern requires the expression of a changing repertoire of cell-surface molecules. In this work, we have investigated the expression of the adhesion molecules CD 11/CD 18 and CD 58 on LCs. Human epidermal cell suspensions were enriched in LCs (mean enrichment 75%) using a two-step technique including a Ficoll-Hypaque gradient followed by Fc receptor panning with IgG-coated sheep erythrocytes. The number of cells obtained per experiment was 750,000 (extremes 280,000-1,800,000), and the following antibodies were tested on fresh suspensions and/or after 48 hours in culture: BB3 (antithyroglobulin negative control IgG2a), OKT6 (anti CD1a, Ortho), anti HLA-DR (Becton-Dickinson), MHM 24 (anti CD 11a, leukocyte typing workshop n(0)3), MO1 and 44 (anti CD 11b, leukocyte typing workshop n(0)3), anti CD 11c (Immunotech), 60.3 and MHM 23 (anti CD 18, leukocyte typing workshop n(0)2), TS2/9.1.1 (anti CD 58, leukocyte typing workshop n(0)3). We found that amongst CD 11 subunits, only CD 11c was expressed in fresh suspensions, but was weaker than CD 18, and disappeared with culture. CD 58 was not detected in fresh suspensions but appeared after 2 days of culture, confirming earlier work. Thus the LC exhibits cell surface characteristics similar to tissue macrophages (CD 18 and CD 11c) prior to culture. The expression of CD 58 after culture is in accordance with the interaction of LC with CD2 bearing T-lymphocytes during antigen presentation in peripheral lymph-nodes.
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PMID:Flow cytometry analysis of adhesion molecules on human Langerhans cells. 145 12

The effect of a battery of CD1 mAb on intracellular free Ca2+ concentration and IL-2 production has been examined on different T cell lines in this study. Both 0249F and NU-T2 two CD1b specific mAb tested, induced a rapid increase in the intracellular Ca2+ concentration on HPBALL T cells whereas only one (L161) among three different CD1c mAb (L161, 10C3, and M241) produced a similar effect. In contrast the addition of four different CD1a mAb directed against two different epitopic groups of this molecule were uneffective in modifying the intracellular Ca2+. Both L161 and 0249F also induced a comparable increase in the intracellular Ca2+ concentration on MOLT 4 and JURKAT, two other T cell lines of similar phenotype. The effect of L161 mAb on the IL-2 production of the IL-2 producing T cell line JURKAT was also examined. The association of the latter with PMA strongly induced the production of IL-2 on this cell model while either L161 or PMA alone had no effect. Although the natural ligand and the function of CD1 molecules are still unknown, the accumulation of these data strongly suggest that CD1b and CD1c might represent two activatory pathways for immature T cells operating before the classical CD2 and CD3 activation pathways.
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PMID:CD1 stimulation of human T cell lines induces a rapid increase in the intracellular free Ca2+ concentration and the production of IL-2. 169 Jul 69

We have investigated the role of the CD2 and the CD28 Ag-independent pathways of activation on CD3low thymocytes. We previously showed that anti-CD28 mAb synergized with anti-CD2 mAb directed against epitopes T11.1 and T11.2, in the activation of purified resting T cells or unseparated thymocytes. Proliferation induced via CD2 plus CD28 was mediated via an IL-2-dependent pathway and was not affected by prior modulation of the CD3-TCR complex. Here, we show that a subset of CD3low thymocytes, although unresponsive to CD3 activation, can be activated to proliferate through the CD2 or the CD28 pathways, in the presence of exogenous IL-2. The mitogenic combination of mAb to CD2 and CD28 induces a proliferation of thymocytes which, in absence of exogenous lymphokines, is restricted to the more mature intrathymic subpopulation, CD1a-. However, CD3low thymocytes can also be triggered through the CD2 plus CD28 activation pathways but require at least addition of exogenous IL-2 to proliferate. This study demonstrates that a fraction of immature CD3low thymocytes possesses functional CD2 and CD28 surface molecules at a time when CD3 is not yet functional.
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PMID:"CD3low" human thymocyte populations can readily be triggered via the CD2 and/or CD28 activation pathways whereas the CD3 pathway remains nonfunctional. 196 76

The immunophenotypic properties of the abnormal cells in routine specimens from 16 cases of Langerhans cell histiocytosis (LCH) were examined. In five cases, cryostat sections were also available. The abnormal cells expressed a similar phenotype and were positive for HLA-DR, S-100 protein, peanut agglutinin (PNA), CD1a, CD4 and several macrophage-associated markers, including CD11c, CDw32 and CD68 (the latter detectable in routine sections with antibody KP1). Staining with CD14, CD35 (C3b receptor), and CD11b (C3bi receptor) was negative with the exception of one of the cases in which a proportion of the cells showed faint positivity with CD11b. Staining for pan-T-cell (CD2, CD3, CD5) and pan-B-cell (CD19, CD22) antigens was negative in all lesions. It is concluded that LCH expresses a characteristic phenotype with some heterogeneity with regard to macrophage markers and that immunohistochemical methods in cryostat sections and routine specimens form a useful supplement to other techniques for the diagnosis of this condition.
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PMID:Immunohistochemical study of the abnormal cells in Langerhans cell histiocytosis (histiocytosis x). 210 27

The morphological, ultrastructural and immunophenotypic properties of Histiocytosis-X (H-X) cells were investigated in a lymph node involved by Letterer-Siwe (L-S) disease. H-X cells were T6+ (CD1a), S-100+, T4+ (CD4) and HLA-DR+; in addition they were consistently T11+ (CD2) and were stained by antibodies directed against receptors for transferrin (T9), C3bi (OKM-1/CD11b), IgG-Fc (Leu-11/CD16) and Interleukin-2 (IL-2R/CD25). On immunostained cytosmears, T6+ cells were highly polymorphic and a prominent fraction (45%) showed immature morphology, characterized by lymphoid appearance. Cells expressing macrophage markers (ANAE, AACT, Leu-M3/CD14, PAM-1) were 10-fold fewer than T6+ cells and did not show a lymphoid morphology. At TEM level, H-X cells were characterized by poor content of LC granules and by the presence of myelin-like laminated bodies and of lysosome-like dense bodies. The immunophenotypic properties of H-X cells were compared to those of epidermal Langerhans cells (LCs) and of LCs present in lymph nodes of three cases of dermatophatic lymphadenitis. Epidermal LCs were T6+/HLA-DR+, and sometimes faintly T4+. Lymph node LCs were T6+, S-100+, T4+, HLA-DR+, and showed the same variety of surface receptors detected in H-X cells; furthermore, in a case with massive infiltration of the paracortex by T6+ cells, lymph node LCs were faintly T11+ and some of the T6+ cells had lymphoid aspect. Our findings suggest that the H-X cell population of L-S disease is not homogeneous, but is composed of discrete cell subsets with distinctive antigenic and morphological traits closely resembling those of cells of LC lineage at different maturational stages.
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PMID:Letterer-Siwe disease: immunohistochemical evidence for a proliferative disorder involving immature cells of Langerhans lineage. 313 61

We searched for the presence of human CD1-positive cells in bone marrow populations in order to characterize putative Langerhans cell precursors. Bone marrow progenitors were cultured in 0.8% methylcellulose supplemented with 10% granulocyte-macrophage (GM) colony-stimulating factor(s) GCT and HTB9. We compared the kinetics of these two factors and found that GCT was the more appropriate for our study. After 8 days of culture, colony-forming units of granulocyte-macrophages (CFU-GM) were tested for the presence of CD1-positive cells using the immunofluorescence technique. Positive cells were counted by cytofluorometric analysis: 9.4% CD1a (BL6), 13.4% CD1c (L161), 4.3% CD1b (NuT2), 4.6% CD2 (T11), and 25.5% CD33 (My9). Ultrastructural features and phenotype were then specified by the immunogold labeling technique using electron microscopy. A subpopulation of CD1-positive cells showed the ultrastructural morphology of bone marrow pro-monocyte/monocyte cells. By using well-characterized monoclonal antibodies, it was demonstrated that these cells expressed the following phenotype: CD14+, CD33+, CD4+, HLA-DR+, HLA-DP+, HLA-DQ-, OKT10-, CD2-. These data indicate that these bone marrow promonocyte/monocyte progenitors express a phenotype similar to that of epidermal Langerhans cells but the density of each antigen is much lower than that observed on mature skin dendritic cells.
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PMID:Culture of putative Langerhans cell bone marrow precursors: characterization of their phenotype. 316 59

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

Three colour flow cytometric analysis has been used to analyze the expression of a series of surface antigens on human thymic and peripheral T-cell populations. CD4, CD8 and CD3 were used to divide the populations into the conventional major categories, and the distribution of CD1a, CD2, CD7, CD34, CD44, class I MHC and class II MHC was then determined. Some characteristics of 'single positive' (CD4+8- and CD4-8+) T-lineage cells were unexpected. Amongst thymocytes, some 'immature single positives' were delineated as larger sized cells lacking cell surface CD3 and expressing low levels of class I MHC; however, in contrast with murine thymocytes, these were all CD4+8-, rather than being predominantly CD4-8+. Amongst peripheral T cells, a small proportion of CD7- cells were detected, within both the CD4+8-3+ and the CD4-8+3+ categories. Finally, in contrast to previous conclusions, CD1a was expressed at high levels on mature (CD4+8-3+ and CD4-8+3+) human thymocytes, although in agreement with previous reports it was absent from peripheral T cells. CD1a is therefore a useful marker of post-selection, post-thymic T-cell maturation.
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PMID:Surface antigens of human thymocyte populations defined by CD3, CD4 and CD8 expression: CD1a is expressed by mature thymocytes but not peripheral T cells. 768 45


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