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)

We examined the expression of various CD coded or not yet defined antigens in human thymus samples using indirect immunoperoxidase and immunoflourescent techniques. Data obtained are presented in concurrence with Clusters of Thymic Epithelial Staining (CTES) classification for various monoclonal antibodies recognizing CD antigens (CD1, CD1a, CD6, CD9, CD14, CD16, CD29, CD30, CD32, CD44, CD45RB, CD47, CD48, CD49a, CD49b, CD49c, CD49d, CD49e, CD49f, CD51, CD53, CD54, CD56, CD57, CD63, CD85, CD95, CD98, CD102, CD103, CD106, CD109, CD146, CD147, CD148, CD151, CD152, CD158a, CD158b, CD164, CD165, CD166) and for monoclonal antibodies 1B10, 5G7, A4, BD46, BLTZ, HP1C5, IND.64, M72, WU947 whose specifities are not yet defined. Some of the mAbs such as CD49f, IND.64 and BD46 are detected as good markers for specific cell types or compartments. Significance of the presence of these antigens on thymic epithelial cells at certain locations is briefly discussed.
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PMID:Antigenic profile of human thymus in concurrence with "Clusters of Thymic Epithelial Staining" classification. 1272 40

The role of endogenously produced cytokines and growth factors in the impaired healing of chronic leg ulcers remains uncertain. The aim of this study was to determine the functional capacity of skin cells in ulcer bed tissue compared to those in the edge of ulcers and skin distal to ulcers. Biopsies from leg ulcers of ten randomly selected patients were examined immunohistochemically for cytokines and growth factors produced by keratinocytes (KC) and vascular endothelial cells (EC). The phenotype of leukocytes infiltrating venous ulcers and the expression of vascular adhesion molecules responsible for extravasation were also studied. The expression of cytokines and growth factors by KC was similar in areas adjacent and remote from an ulcer. In the dermis adjacent to an ulcer, the expression of IL-1alpha, IL-1beta, IL-1Ra, EGF and PDGFa by EC was higher than the levels of expression in EC from the distant dermis. The expression of IL-6, TNFalpha and GM-CSF was comparable to that in cells from intact dermis. For all these factors staining was cytoplasmic, suggesting production in these areas. Ulcer bed tissue contained few fibroblasts and blood capillaries showing a high staining intensity for CD62E and CD106 EC adhesion molecules but no FGF2 expression (P<0.05). The intensity of staining for scavenging CD15+ elastase+ granulocytes and CD35+ (C3bR) activated macrophages in the ulcer bed was comparable to that in the margin but higher than that in the distant dermis (P<0.05), whereas staining for CD68+, HLA DR+, TGFbeta+ and CD54+ dermal macrophages was similar in all areas. There was reduced staining for CD4+ and CD8+ cells in the ulcer bed (P<0.05). There were no CD1a+ Langerhans cells in the epidermis encroaching upon the granulation tissue and there was reduced CD1a staining in the adjacent epidermis (P<0.05). In conclusion, there is chronic accumulation of scavenging cells with lack of remodeling of the granulation tissue and, at the same time, preserved cytokine and growth factor secretory potential of KC and dermal EC in non-healing venous leg ulcers.
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PMID:Keratinocyte and dermal vascular endothelial cell capacities remain unimpaired in the margin of chronic venous ulcer. 1556 1

At present only few biological data are available to indicate whether psoriatic arthritis (PsA) is part of the spondyloarthropathy (SpA) concept, whether it is a separate disease entity or a heterogeneous disease group with oligoarticular/axial forms belonging to SpA and polyarticular forms resembling rheumatoid arthritis (RA). To address this issue with regard to peripheral synovitis, we compared the synovial characteristics of PsA with those of ankylosing spondylitis (AS)/undifferentiated SpA (USpA) and RA, and compared the synovium of oligoarticular versus polyarticular PsA. Synovial biopsies were obtained from patients with RA, nonpsoriatic SpA (AS + USpA), and oligoarticular and polyarticular PsA. The histological analysis included examination(s) of the lining layer thickness, vascularity, cellular infiltration, lymphoid aggregates, plasma cells and neutrophils. Also, we performed immunohistochemical assessments of CD3, CD4, CD8, CD20, CD38, CD138, CD68, CD163, CD83, CD1a, CD146, alphaVbeta3, E-selectin, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, S100A12, intracellular citrullinated proteins and major histocompatibility complex (MHC)-human cartilage (HC) gp39 peptide complexes. Comparing SpA (PsA + AS + USpA) with RA, vascularity, and neutrophil and CD163+ macrophage counts were greater in SpA (P < 0.05), whereas lining layer thickness and the number of CD83+ dendritic cells were greater in RA (P < 0.05). In RA, 44% of samples exhibited positive staining for intracellular citrullinated proteins and 46% for MHC-HC gp39 peptide complexes, whereas no staining for these markers was observed in SpA samples. We excluded influences of disease-modifying antirheumatic drug and/or corticosteroid treatment by conducting systematic analyses of treated and untreated subgroups. Focusing on PsA, no significant differences were observed between PsA and nonpsoriatic SpA. In contrast, vascularity (P < 0.001) and neutrophils were increased in PsA as compared with RA (P = 0.010), whereas staining for intracellular citrullinated proteins and MHC-HC gp39 peptide complexes was exclusively observed in RA (both P = 0.001), indicating that the same discriminating features are found in PsA and other SpA subtypes compared with RA. Exploring synovial histopathology between oligoarticular and polyarticular PsA, no significant differences were noted. Moreover, intracellular citrullinated proteins and MHC-HC gp39 peptide complexes, which are specific markers for RA, were observed in neither oligoarticular nor polyarticular PsA. Taken together, these data indicate that the synovial histopathology of PsA, either oligoarticular or polyarticular, resembles that of other SpA subtypes, whereas both groups can be differentiated from RA on the basis of these same synovial features, suggesting that peripheral synovitis in PsA belongs to the SpA concept.
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PMID:Synovial histopathology of psoriatic arthritis, both oligo- and polyarticular, resembles spondyloarthropathy more than it does rheumatoid arthritis. 1589 64

Atherosclerosis is a lipid-related chronic inflammatory disease in which immune mechanisms play a pivotal role. The lesions are filled with large numbers of immune cells. During the last decade, dendritic cells have been identified in atherosclerotic plaques and are thought to play an important role in atherogenesis. Dendritic cells express major histocompatibility complex I and II, human leukocyte antigen-DR, CD1a, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and co-stimulatory molecule on their surfaces and this explains their unique ability to activate naive T cells. Factors such as oxidized low-density lipoprotein, hypoxia, nicotine, heat shock proteins, and altered nitric oxide synthase activity of the endothelium, all of which cause endothelial dysfunction, have a significant impact on dendritic cell adherence to endothelium and maturation. Mature dendritic cells are capable of presenting antigens to T cells, and activation of T cells leads to release of cytokines, which play an important role in the progression of disease. Drugs such as statins and diltiazem have been shown to protect endothelial function by inhibition of dendritic cell-endothelial cell interaction, and can be applied to delay the progression of cardiovascular diseases.
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PMID:Role of dendritic cells in atherosclerosis. 1655 30


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