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 cutaneous lymphocyte associated antigen (CLA) recognized by the monoclonal antibody (moAb) HECA-452 plays a major role in the homing of lymphocyte subpopulations to the skin by binding to E-selectin on dermal microvessels. The factors responsible for the immigration of Langerhans cells (LC) and their precursors into the skin are still unknown, but because normal resting LC are also capable of expressing CLA, the antigen was proposed as a candidate LC-homing structure. To gain insight into these mechanisms, the expression of HECA-452 on neoplastic LC within and outside the skin was investigated in paraffin-embedded sections from 44 patients with localized and disseminated forms of Langerhans cell histiocytosis (LCH) presenting with proliferating cells positive for CD45, CD1a, S100 and HLA-DR. Irrespective of the clinical presentation or the type of organ involved, HECA-452 positive LC were detected in all biopsies tested (range 5->90%). The most prominent HECA-452 reactivity was observed in skin lesions and in areas with accumulations of eosinophilic granulocytes. Our data provide evidence for heterogeneous expression of sLex/sLea structures in various stages of activated and/or differentiated LCH cells. Remarkably, CLA-antigen expression on LCH-cells was not restricted to cutaneous sites. In view of recent findings on the expression of HECA-452 on resting epidermal LC, our data are compatible with the view that local cytokine production by keratinocytes or cells from the surrounding infiltrate induce and/or modulate CLA expression on LC in both cutaneous and extra-cutaneous sites.
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PMID:Expression of the monoclonal antibody HECA-452 defined E-selectin ligands in Langerhans cell histiocytosis. 862 76

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

Evidence for the involvement of cellular immunity in the etiopathogenesis of the hypopigmentary disorder vitiligo is provided by rare cases of inflammatory vitiligo. Nonlesional, perilesional, and lesional skin biopsies from three inflammatory vitiligo patients were immunohistochemically analyzed. The composition of inflammatory infiltrates present in perilesional skin was analyzed by antibodies to T cells (CD2, CD3, CD4, and CD8), Langerhans cells (CD1a), and macrophages (CD36 and CD68). The presence of activation markers on inflammatory cells was evaluated by analysis of HLA-DR, interleukin-2 receptor, and HECA452 expression. The presence or absence of melanocytes was determined by the antibody NKI-beteb. Moreover, the abundance of matrix molecule tenascin was semi-quantified using T2H5. Results indicate that within perilesional skin, epidermis-infiltrating T cells exhibit an increased CD8/CD4 ratio and increased cutaneous lymphocyte antigen and interleukin-2 receptor expression. These cells are frequently juxtapositionally apposed to remaining melanocytes. In perilesional dermis, CD68+OKM5- macrophages were more numerous than in lesional or nonlesional skin. Keratinocytes as well as melanocytes consistently express major histocompatibility complex class II antigens along stretches of basal and suprabasal layers in perilesional epidermis. Moreover, inflammation is accompanied by increased tenascin content. Although these observations do not permit differentiation between the immune infiltrates being a result as opposed to the cause of the disease process, results presented in this study are very suggestive of involvement of local immune reactivity in melanocyte destruction.
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PMID:Presence of T cells and macrophages in inflammatory vitiligo skin parallels melanocyte disappearance. 864 62

We investigated epidermal cell suspensions prepared from lesional and nonlesional atopic eczema skin, other inflammatory skin conditions, and normal human skin for high-affinity IgE receptor (Fc epsilon RI) expression on dendritic CD1a cells by quantitative flow cytometric analysis. A single CD1a bright/CD1b neg/Fc epsilon RI dim/CD23 neg/CD32 dim/HLA-DR bright/CD36 neg population was found in normal skin. In contrast, lesional skin of atopic eczema and other inflammatory skin diseases harbored variable proportions of two distinct CD1a populations. Both populations exhibited typical ultrastructural features of Langerhans cells, but the second one lacked Birbeck granules and was unreactive to the Birbeck granule-specific LAG antibody. Both populations differed phenotypically: classical Langerhans cells were CD1a bright/CD1b neg/Fc epsilon RI dim/CD23 neg/CD32 dim/HLA-DR bright/CD36 dim, while the second population was CD1a dim/CD1b dim/Fc epsilon RI bright/CD23 dim/CD32 dim/HLA-DR bright/CD36 bright. The highest Fc epsilon RI expression was found on the second CD1a population in lesional atopic eczema skin. Furthermore, Fc epsilon RI expression on CD1a cells correlated significantly with the serum IgE level of the patients. Thus, a distinct population of CD1a inflammatory dendritic epidermal cells different from classical Langerhans cells appears in the epidermis of lesional skin and is subjected to specific signals leading to the upregulation of Fc epsilon RI in atopic eczema skin.
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PMID:Immunomorphological and ultrastructural characterization of Langerhans cells and a novel, inflammatory dendritic epidermal cell (IDEC) population in lesional skin of atopic eczema. 864 75

Determination was made of epidermal Langerhans cell (LC) distribution and infiltrating cellular events in lesional skin during varicella zoster virus (VZV) infection, and the results were compared with those for herpes simplex (HS), measles, and rubella by immunohistochemical staining with cell surface markers. CD1a positive epidermal LCs increased in number, particularly in measles and rubella. The number of LCs was within the normal range or slightly increased in the epidermis of VZV infection. In herpes zoster (HZ) and varicella, HLA-DR positive epidermal cells were present in the basal part of the epidermis. In measles, HLA-DR positive cells aggregated in papular lesions. In measles and rubella, the number of HLA-DQ positive epidermal cells appeared to increase. In HS cases, CD11b (OKM1) positivity of the upper epidermal keratinocytes was quite pronounced, but not in the basal layer. CD8 positive suppressor/cytotoxic cells extensively infiltrated the dermis of HZ and varicella. Dermal infiltrates were identified as CD8 positive cell dominant in measles, HZ, and varicella. These results provide a partial explanation as to why cellular events in skin lesions act immunosuppressively.
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PMID:Immunohistochemical study of cellular events in lesional skin during common virus infections. 872 Feb 54

CD1a positive cells of dendritic shape were detected in the intima of human arteries by immunohistochemical investigation. Analysis of contiguous parallel sections showed that the CD1a positive cells also stained with S-100 and expressed HLA-DR. The CD1a+/S-100+/HLA-DR+ vascular dendritic cell is a type of dendritic cell which participates in atherosclerotic lesion formation. This finding has important implications for understanding atherogenesis and offers a link between immune mechanisms and atherosclerotic lesion formation.
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PMID:Vascular dendritic cells and atherosclerosis. 883 51

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

The epidermal repopulation of Langerhans cells (LCs) during wound healing was examined using a human skin severe combined immunodeficient (SCID) mouse model. The experiments, were carried out after proving the human origin of keratinocytes repopulating the wound beds using the W6/32 monoclonal antibody. It was shown that CD1a- and HLA-DR-positive dendritic cells (mostly LCs) are already detectable 2 days after injury within the newly formed epithelium. In the excisional wounds investigated, neither HLA-DR nor ICAM-1 expression of human keratinocytes was observed. Our present data suggest that LC repopulation is an early event in the process of re-epithelization.
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PMID:Repopulation of Langerhans cells during wound healing in an experimental human skin/SCID mouse model. 890 6

Although it is known that dendritic cells (DC) migrate in response to inflammatory stimuli. There is little information about the expression of receptors for chemotactic factors on DC. The present study has demonstrated by double immunostaining and flow cytometry of Langerhan's cell (LC)-enriched epidermal cell suspensions that a small subpopulation (5-6%) of epidermal resident DC (rLC) expresses receptors for C5a (C5aR). Epidermal rLC positive for C5aR show a round-shape morphology, were located next to the basement membrane and express HLA-DR molecules higher than C5aR negative rLC. These observations suggest that rLC would express C5aR as part of their process of maturation during tissue trafficking. To investigate whether epidermal LC up-regulate C5aR along their differentiation pathway. LC were differentiated in vitro after culture in epidermal cell suspensions supplemented with granulocyte macrophage colony-stimulating factor (GM-CSF). As a result, in vitro differentiated LC increased the expression of C5aR up to 69% of the DC population. In accordance with this observation, interdigitating DC of secondary lymphoid organs (lymph node and tonsil) also expressed (5aR. Migratory CD1a positive DC that spontaneously migrated out of dermal or split-skin organ explants were also positive for C5aR and were used for chemotaxis and chemokinesis assays in response to human recombinant C5a (rC5a). Optimum migration to rC5a was observed at 10(-8)M with a sigmoidal dose response curve. Checkboard analysis demonstrated that locomotion in response to rC5a was chemotaxis and not chemokinesis.
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PMID:Expression and modulation of C5a receptor (CD88) on skin dendritic cells. Chemotactic effect of C5a on skin migratory dendritic cells. 891 Nov 50

The immunophenotype of 6 cases of Langerhans cell histiocytosis (LCH) of the hypothalamus and 3 cases of cranial bone manifestation of LCH was investigated by means of immunohistochemistry on paraffin sections. Antibodies against S 100 protein, lysozyme, CD68 (PG-M1), CD68 (KP1), HLA-DR, beta 2 microglobulin, placental alkaline phosphatase (PLAP), the monoclonal antibody MAC 387, and a monoclonal antibody against CD1a were used. All examined cases showed positive staining of lesional cells for S 100 protein, HLA-DR, beta 2 microglobulin, macrophage associated markers and CD1a. According to the "confidence levels" of the Writing Group of the Histiocyte Society [Chu et al. 1987], a "definite diagnosis" of LCH requires the demonstration either of Birbeck granules in lesional cells by electron microscopy, or of CD1a antigenic determinants on the surface of lesional cells. Since electron microscopy of these rare CNS lesions is not possible in many cases, we are now able to give a definite diagnosis of LCH of the hypothalamus by means of immunohistochemistry for CD1 a on routinely fixed and processed tissue.
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PMID:Langerhans cell histiocytosis of the hypothalamus: diagnostic value of immunohistochemistry. 892 2


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