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)

Juvenile xanthogranuloma (JXG) is considered to represent a lesion originating from histiocytes. Three cases of deeply located JXG and one case of cutaneous JXG were studied. One case with extensive mesenteric involvement presented with hypercalcemia and one case with liver involvement had hypergammaglobulinemia. Immunohistochemistry, electron microscopy, karyotyping, and DNA flow cytometry were used to determine the phenotype of the cells involved and to find further clues as to the histogenesis of these lesions. Immunohistochemically, all lesions studied expressed the CD1a antigen but showed no labeling for S-100 protein. The cells did not contain Birbeck granules. From these data it is suggested that the cells involved are of indeterminate dermal histiocyte lineage and that occurrence of deep located lesions of JXG may be due to migration of CD1 a-positive histiocytes.
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PMID:Deep juvenile xanthogranuloma: a lesion related to dermal indeterminate cells. 137 72

Increasing UVB radiation at the earth's surface might have adverse effects on in vivo immunologic responses in humans. We prospectively randomized subjects to test whether epicutaneous immunization is altered by prior administration of biologically equalized doses of UV radiation. Multiple doses of antigens on upper inner arm skin (UV protected) were used to elicit contact sensitivity responses, which were quantitated by measuring increases in skin thickness. If a dose of UVB sufficient to induce redness (erythemagenic) was administered to the immunization site prior to sensitization with dinitrochlorobenzene (DNCB), we noted a marked reduction in the degree of sensitization (P less than 0.0006) that was highly dose responsive (r = 0.98). Even suberythemagenic UV (less than a visible sunburn) resulted in a decreased frequency of strongly positive responses (32%) as compared to controls (73%) (P = 0.019). The rate of immunologic tolerance to DNCB (active suppression of a subsequent repeat immunization) in the groups that were initially sensitized on skin receiving erythemagenic doses of UV was 31% (P = 0.0003). In addition, a localized moderate sunburn appeared to modulate immunization with diphenylcyclopropenone through a distant, unirradiated site (41% weak responses) as compared to the control group (9%) (P = 0.05). Monitoring antigen presenting cell content in the epidermis revealed that erythemagenic regimens induced CD1a-DR+ macrophages and depleted Langerhans cells. In conclusion, relevant and even subclinical levels of UV exposure have significant down modulatory effects on the ability of humans to generate a T-cell-mediated response to antigens introduced through irradiated skin.
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PMID:UV exposure reduces immunization rates and promotes tolerance to epicutaneous antigens in humans: relationship to dose, CD1a-DR+ epidermal macrophage induction, and Langerhans cell depletion. 138 91

Depletion of Langerhans cells (LC) is known to follow bone marrow transplantation (BMT) and is thought to be mainly related to pretransplant radiation and chemotherapy conditioning regimens. We studied sequential biopsies of clinically normal skin of 22 thalassemic and leukemic patients undergoing allogeneic BMT who had received only chemotherapy (busulfan and cyclophosphamide) as conditioning regimen. LC were identified immunohistochemically using antibodies against CD1a and HLA-DR antigens, and their number expressed per square mm of epidermal vertical section, the latter measured by computerized image analysis. After the preparatory regimen, the number of LC decreased progressively in both leukemic and thalassemic patients. CD1a+ and HLA-DR+ epidermal cells were reduced, respectively, to 68.5% and 64.5% of their original number around Day 2, and to 23.1% and to 18.2% around Day 17. By this time, electron microscopic examination of selected biopsies confirmed the depletion of LC. Variable repopulation was observed between Days 40 and 60. Our results indicate that a conditioning regimen based exclusively on high dose chemotherapy depletes epidermal LC early after BMT, and that such depletion is not related to the development of acute graft-versus-host disease.
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PMID:Epidermal Langerhans cells after allogeneic bone marrow transplantation: depletion by chemotherapy conditioning regimen alone. 138 97

Colonies of CD1a+ HLA-DR+/DQ+ CD4+ cells with the functional and some of the structural attributes of Langerhans cells are observed in human bone marrow cultures in semi-solid media and are assumed to be the progeny of an early progenitor, the dendritic/Langerhans cell CFU (CFU-DL). The cytokine-regulated growth of these cells has been studied using a chemically defined serum-free system to culture both unfractionated and highly enriched bone marrow progenitor cell populations. Although unfractionated cell growth was optimal in serum replete cultures with PHA-stimulated leukocyte-conditioned medium (PHA-LCM) suboptimal proliferation of CFU-DL was observed in serum even in the absence of PHA-LCM. No colonies were observed under serum-free conditions when granulocyte-macrophage CSF (GM-CSF), IL-3, granulocyte CSF (G-CSF), and macrophage CSF (M-CSF) were present at levels optimal for granulocyte colony-forming unit (CFU-G) and macrophage colony-forming unit (CFU-M) growth. Addition of IL-1 alpha to these cytokines stimulated a small number of CFU-DL. However, in the presence of GM-CSF and IL-3, TNF-alpha or TNF-beta (5 U/ml) were both highly effective in promoting growth up to 82% of optimal and CFU-G growth was also enhanced at these concentrations. TNF was only active during the first 3 days of culture and higher concentrations of TNF-alpha but not TNF-beta were inhibitory for both CFU-DL and CFU-G. CD34+ cell-enriched populations were also enriched for both myeloid progenitors (CFU-G + CFU-M) and CFU-DL to 36- and 48-fold, respectively, and single cell cultures of CD34+ cells yielded single colonies containing both CD1a+ dendritic cells and CD1a- macrophages. Thus dendritic/Langerhans progenitors in the bone marrow expresses CD34, have a capacity for both macrophage and dendritic cell differentiation, and depend on hemopoietic growth factors and TNF for their further development in vitro.
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PMID:Interactions of tumor necrosis factor with granulocyte-macrophage colony-stimulating factor and other cytokines in the regulation of dendritic cell growth in vitro from early bipotent CD34+ progenitors in human bone marrow. 138 22

In this study we have analyzed, using immunoperoxidase (IPx) and indirect immunofluorescence (IIF), the intracellular and cell surface expression of CD1 antigens on PHA activated human T cells. By IIF, CD1 isotypes were not detected on the surface of 3 days PHA activated cells. Conversely, CD1a, CD1b and CD1c molecules were found by IPx in the cytoplasm of normal activated cells from 13 different donors. Kinetic studies showed that, while CD25 was already observed 24 h after activation, all 3 isotypes of CD1 molecules started to be detected 48 h after PHA activation, with a peak expression at 72 h.
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PMID:Intracellular expression of CD1 molecules on PHA-activated normal T lymphocytes. 138 19

CD1 antigens are classified into at least three groups, CD1a, CD1b, and CD1c. In order to delineate the localization of epitopes of CD1 antigens in human skin, we examined the immunoreactivity of fourteen different CD1 antibodies (seven CD1a, five CD1b, and two CD1c antibodies). The epitopes for CD1a, CD1b, and CD1c are differentially localized on epidermal Langerhans cells, dermal dendritic cells, keratinocytes, the luminal portion of eccrine gland ducts, and the basement membrane zone in normal human skin.
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PMID:Epitope mapping of CD1a, CD1b, and CD1c antigens in human skin: differential localization on Langerhans cells, keratinocytes, and basement membrane zone. 138 41

Epidermal Langerhans cells (LC) are Birbeck granule-containing bone-marrow-derived cells, which are located mainly in the suprabasal layer of the epidermis. They can be readily identified by their strong expression of CD1a and MHC class II molecules. In addition to these 'classical' properties, an extensive phenotypic profile of normal human LC, summarized in this review, is now available. The powerful capacity of LC to activate T lymphocytes is clearly documented and, to date, LC are recognized as the prominent antigen-presenting cells of the skin immune system. They are generally believed to pick up antigens encountered in the epidermis and to migrate subsequently from the epidermis to the skin-draining lymph nodes. Upon arrival in the paracortex of lymph nodes, the antigen-laden LC transform into interdigitating cells and they present antigen to naive T lymphocytes in a MHC class II-restricted fashion; this results in the generation of antigen-specific immune responses. It has also been demonstrated that transformation of LC into interdigitating cells occurs when LC are cultured in vitro. Both in vivo and in vitro studies have indicated that properties of LC, such as phenotype, morphology and the stimulatory potential to activate T lymphocytes, are dependent on the local microenvironment in which the LC reside. The essential role of LC in the induction of contact allergic skin reactions and skin transplant rejection is well established.
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PMID:Dynamic nature and function of epidermal Langerhans cells in vivo and in vitro: a review, with emphasis on human Langerhans cells. 142 96

An immunoelectron-microscopic technique was applied to investigate the localization of molecules that are involved in the elicitation of allergic contact dermatitis in human epidermal cells in situ. Langerhans cells in the epidermis of lesions showed a strongly increased cell surface expression of HLA class II molecules as compared with normal skin. In addition, a high number of intracellularly located HLA class II molecules were present in Langerhans cells of lesional epidermis, suggesting increased biosynthesis of these molecules during the elicitation process. In contrast, no differences in the expression of CD1a by Langerhans cells was observed between normal and lesional skin. Frequently, the Langerhans cells were found in close apposition to mononuclear cells, which also exhibited a strong cell surface HLA class II expression. The number of Birbeck granules that are characteristic intracellular Langerhans cells organelles was increased in lesional Langerhans cells as compared with normal-skin Langerhans cells, which may correlate with the activated state of lesional Langerhans cells. These Birbeck granules were always HLA class II or CD1a negative. The increased synthesis and expression of HLA class II molecules on the cell surface of Langerhans cells suggests a direct role for these HLA class II molecules in the elicitation process of allergic contact dermatitis.
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PMID:HLA class II expression on human epidermal Langerhans cells in situ: upregulation during the elicitation of allergic contact dermatitis. 142 38

In a recent series of experiments, we observed that epidermal Langerhans cells (LC) of healthy, non-atopic individuals have the capacity of specifically binding monomeric serum or myeloma IgE. IgE-binding to LC could neither be prevented by pre-incubation of the cryostat sections with monoclonal antibodies (MoAb) against either Fc epsilon RII/CD23 or Fc gamma RII/CD32 nor by the addition of excess amounts of lactose, but could be entirely abrogated by pre-incubation with the anti-Fc epsilon RI MoAb 15-1. A direct testing of the anti-Fc epsilon RI MoAb 15-1 and 19-1 on cryostat sections in an indirect immuno-double-labeling technique showed that, in contrast to eight different anti-Fc epsilon RII/CD23 MoAb, these MoAb react with the majority of CD1a-bearing epidermal cells. At an ultrastructural level, 15-1 immunogold-labeling in the epidermis was confined to the surface of cells exhibiting Birbeck granules. In further experiments, we were able to amplify by polymerase chain reaction (PCR) technology transcripts for the alpha, beta, and gamma chains of Fc epsilon RI from LC-enriched epidermal cells and dermal cells, but not from LC-depleted epidermal cells. Transcripts for the mast cell enzyme tryptase were exclusively found in dermal cell-derived RNA preparations, thus excluding a contamination of the LC-enriched epidermal cell preparations by dermal mast cells. Collectively, these data show that epidermal LC, but not other epidermal cells, express Fc epsilon RI molecules.
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PMID:Fc epsilon RI mediates IgE binding to human epidermal Langerhans cells. 143 Dec 5

Immigration of Langerhans cell precursors from the peripheral blood to the skin was studied in human grafts placed on severe combined immunodeficient (SCID) mice. Monocyte fractions of human blood were injected intraperitoneally to SCID bearing either reconstituted (Langerhans cell free) epidermal sheets (E) or living skin equivalents (E/D) consisting of both epidermis and dermis. A range of immunocytochemical and ultrastructural markers was employed to monitor the colonization of the grafts, i.e., CD1a/c, Birbeck granules. In situ hybridization with probes against Alu sequences of human DNA were employed together with immunostaining for MHC class I mouse and human antigens to document graft survival. Although unequivocal LC were detected within E grafts, including both human (CD1a positive) and murine (NLDC-145 positive), no migration was achieved in the E/D situations.
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PMID:Comparative epidermal Langerhans cell migration studies in epidermal and epidermal/dermal equivalent grafts. 143 Dec 21


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