Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P06126 (CD1a)
 2,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Langerhans cells (LC) are antigen-presenting cells which express high levels of Class II MHC antigens on their plasma membranes. While the expression of these antigens on gingival LC has been documented, their functional significance is unclear. In this study, the mixed epithelial cell-lymphocyte culture reaction (MECLR) between stimulator cells (LC) and allogenic lymphocytes was used as an in vitro model for investigating the role of the MHC Class II antigens HLA-DR, -DQ, and -DP in alloantigen presentation by gingival LC. In epithelial cell suspensions prepared from human gingiva, MHC Class II antigen expression (HLA-DR, -DP, -DQ) was confined to CD1a-positive LC. Depletion of Class II antigen-bearing LC from epithelial cells using monoclonal antibodies (L243, B7/21, and SK10) and complement inhibited the ability of epithelial cells to stimulate proliferation in the MECLR. Pre-treatment of epithelial cell suspensions with the same monoclonal antibodies suppressed proliferation in the MECLR, as did direct addition of these antibodies to co-cultures of epithelial cells and lymphocytes. These results indicate that HLA-DQ and -DP, together with DR antigens on gingival LC, are involved in LC-lymphocyte interactions. Since LC are potent antigen presenting cells, alterations in the expression of MHC Class II antigens on the surface of these cells will influence their ability to stimulate lymphocytes during the initiation of the cellular immune response to the accumulation of dental plaque.
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PMID:Human gingival Langerhans cells stimulate allogeneic lymphocytes: requirement for MHC class II antigens. 236 40

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

Employing a discontinuous Percoll gradient following Ficoll-Hypaque separation of peripheral blood mononuclear cells from normal subjects (n = 14) and patients with HIV-1 infection (n = 50), we separated a population of low-density cells consisting of monocytoid cells, lymphocytes, and some granulocytes. In cytospin preparations, less than 5% of the monocytoid cells were positive for nonspecific esterase and CD14. However, CD1a was positive in 5-20% of these cells. Ultrastructurally, CD1a-labeled immunogold particles were demonstrated on the monocytoid cells which bore some features of dendritic cells. Flow cytometry of the low-density cells identified a subset of buoyant, large cell population, which excluded lymphocytes. This large low-density cell (LLDC) population was significantly expanded in patients with HIV infection and comprised 32.3 +/- 21.3% of low-density cells compared to 7.0 +/- 2.8% in normal subjects (P < 0.0001). Of the LLDC population 45.2 +/- 23.4% were CD1a+ in patients compared to 17.5 +/- 13.3% in normal subjects (P < or = 0.0001). HLA-DR and HLA-DQ were coexpressed in approximately 70 and 50% of these CD1a+ LLDC, respectively. A simple nonculture assay method employed by us facilitates rapid screening of infected blood specimens for the CD1a+ large low-density cells with dendritic cell features, which could be an additional parameter to monitor HIV disease progression.
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PMID:The number of CD1a+ large low-density cells with dendritic cell features is increased in the peripheral blood of HIV+ patients. 750 34

The distribution of HLA class II (DR, DP, DQ) and Fc gamma R (I, II, III) was analyzed in the epithelia of patients with advanced marginal periodontitis using cryostat sections incubated with monoclonal antibodies (MoAb) against the Langerhans cell (LC) (CD1a) and various subtypes of HLA class II and Fc gamma R, and the indirect immunofluorescence technique. In the oral gingival epithelium (OGE), LC were concentrated subjacent to the connective tissue papillae, while in the pocket epithelium (PE), they were most abundant at the gingival margin. HLA-DP, DQ, and DR stained LC in both OGE and PE. HLA-DQ+ LC were significantly fewer than DP+ and DR+ LC. HLA-DR also stained keratinocytes (KC) in the whole extension of both OGE and PE. HLA-DP was also observed on KC, but not HLA-DQ. Fc gamma R II stained both LC and focal areas of KC. In PE FC gamma R II+ LC were concentrated near the bottom of the pocket, while in the OGE, they were concentrated at the gingival margin. Fc gamma R III was present only on KC, especially in the basal and suprabasal layer. The results indicate that the epithelial cells are actively involved in the development and maintenance of the inflammation of periodontal disease.
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PMID:Epithelial expression of HLA class II antigens and Fc gamma receptors in patients with adult periodontitis. 752 33

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

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 transitional stages in the relationship between sentinel monocytes and messenger dendritic cells that are active in adaptive immunity, are, as yet, unclear. To explore these events, 2-hr adherent peripheral blood mononuclear cells were used either as monocytes, or cultured for 7 days with granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4) to generate dendritic cells, and the phenotypic features and relationship of the two cell populations was investigated using an extensive panel of monoclonal antibodies (mAbs). The features of the shift from monocyte to dendritic cell were also examined by daily phenotyping during the 7-day culture period. Twenty-five mAbs, most of which recognized known CD molecules, bound both monocytes and dendritic cells equally, whereas 19 mAbs exhibited differential staining. Four molecules not previously reported on dendritic cells were documented: CD87, CD98, CD147 and CD148. Seven cell-surface molecules (HLA-DQ, CD1a, CD13, CD30, CD43, CD63 and CD86) were expressed either at very low levels or not at all on monocytes, but had a strikingly increased expression on dendritic cells, suggesting a role in antigen presentation. The kinetics of monocyte to dendritic cell transition revealed a rapid activation phase within the first 24 hr, with a considerable increase in expression of the activation markers HLA-DR, CD13, CD14 and CD98; this was followed by a down-regulation of CD14 and a more gradual development of the other dendritic cell features over the remaining 6 days, with steady increases in CD1a, CD18, CD43, CD86, HLA-DR and HLA-DQ. Thus, these studies have demonstrated four novel components of the dendritic cell, and have documented the dynamic multistep nature of the process whereby an antigen-presenting dendritic cell phenotype may emerge from a monocyte precursor.
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PMID:From sentinel to messenger: an extended phenotypic analysis of the monocyte to dendritic cell transition. 976 44

Although dendritic cells (DC) can be cultured from cord blood (CB) CD34+ progenitor cells, the generation of DC from CB monocytes has not been reported. In this paper, we explored the generation of DC from CB monocytes to establish the simplest way to obtain a substantial number of DC from CB. We isolated monocytes from CB mononuclear cells (CB-MNC) by the plastic adherence method. These adherent cells (monocyte-rich cells) were cultured in RPMI 1640 medium supplemented with 10% fetal bovine serum (FBS) or in serum-free X-VIVO 15 medium (SFM) for 7 days, both of which contained 100 ng/ml granulocyte-macrophage colony-stimulating factor (GM-CSF) and 10 ng/ml interleukin-4 (IL-4) with or without 10 ng/ml tumor necrosis factor-alpha (TNF-alpha) (added at day 5). In the presence of GM-CSF and IL-4, CB-adherent cells became nonadherent, acquired DC morphology, and showed increased expression of CD1a, CD80, CD86, and HLA-DR; they lost membrane CD14 and some cells with the expression of CD83 and CMRF-44 were generated. With the addition of TNF-alpha to these cultures and culturing for further 2 days, the proportion of CD83+ cells was elevated in both the FBS and SFM culture systems, compared with the culture without TNF-alpha. In the culture with TNF-alpha, cells expressing CD1a, CD80, CD86, HLA-DR, and HLA-DQ were markedly increased. TNF-alpha-treated cells were demonstrated to be stronger stimulators for proliferation of both allogeneic CB lymphocytes and PB lymphocytes than were cells not treated with TNF-alpha. The yield of CD83+ DC at day 7 of cultures was 4.9 +/- 1.1 x 10(5) or 3.0 +/- 0.5 x 10(5) per 1.2 x 10(7) CB-MNC plated initially when cultured in FBS or SFM, respectively. These results have shown that a substantial number of mature DC could be generated from CB-adherent cells even by serum-free culture. We then compared these CB-adherent cell-derived DC (CB-DC) with peripheral blood (PB)-adherent cell-derived DC (PB-DC) in cell-surface phenotype and function. We found day 7 CB-DC have lower expression of CD80, CD1a, CD83, and CMRF-44 than day 7 PB-DC, but CB-DC have a similar capacity to stimulate the proliferation of both allo-CB lymphocytes and PB lymphocytes, compared with PB-DC. CB-DC cultured with GM-CSF and IL-4 have almost identical capacity of phagocytosis to take up fluorescein isothiocyanate (FITC)-dextran and Lucifer yellow (LY), compared with PB-DC. In summary, our findings suggest CB adherent cells, when cultured with GM-CSF, IL-4, and TNF-alpha, are a potent source of functional DC. Thus, CB-DC as well as PB-DC may become valuable tools for immunotherapy.
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PMID:Generation of dendritic cells from adherent cells of cord blood by culture with granulocyte-macrophage colony-stimulating factor, interleukin-4, and tumor necrosis factor-alpha. 1098 43

A subset of blood mononuclear cells from patients with chronic lymphocytic leukemia (CLL) can differentiate in vitro into "nurselike" cells (NLCs) that can protect CLL cells from apoptosis. NLCs express cytoplasmic vimentin and stromal-derived factor 1 (SDF-1). NLCs also express CD14, as well as CD11b, CD33, CD40, CD45RO, CD68, CD80, CD86, HLA-DQ, and HLA-DR, but not CD1a, CD2, CD3, CD11c, CD19, CD45RA, CD83, CD106, or CD154. Consistent with this phenotype, NLCs failed to differentiate from blood mononuclear cells that were depleted of CD14+ cells or from isolated CD19+ cells. CD14+ blood cells of healthy donors could differentiate into cells with the morphology and phenotype of NLCs when cultured in direct contact with CLL B cells, but not with normal B cells. Despite expressing antigens in common with blood monocytes, monocyte-derived dendritic cells, and macrophages, NLCs expressed significantly higher levels of CD68 than these other cell types. Consistent with the notion that NLCs are present in vivo, CD14+ splenocytes from CLL patients have NLC morphology and express significantly higher levels of CD68 than CD14+ splenocytes from persons without known B-cell malignancy. These findings indicate that although NLCs may differentiate from blood monocytes, they probably represent a distinctive hematopoietic cell type that exists in vivo, differentiates from hematopoietic CD14+ cells in the context of CLL, and in turn protect CLL cells from apoptosis via a mechanism that is independent of CD106 (vascular cell adhesion molecule-1). The interaction between CLL cells and NLCs may represent a novel target for therapy of patients with this disease.
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PMID:Distinctive features of "nurselike" cells that differentiate in the context of chronic lymphocytic leukemia. 1180 9