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)

Lyme arthritis synovial fluid contains a large proportion of gamma delta T cells that proliferates upon stimulation with the causative spirochete, Borrelia burgdorferi. A panel of Borrelia-reactive gamma delta T cell clones was derived from synovial fluid of two patients with Lyme arthritis. Each of six gamma delta clones from one patient used the V delta 1 TCR segment but had otherwise unique CDR3 sequences and diverse V gamma segment usage. Stimulation of the V delta 1 clones was optimal in the presence of Borrelia, dendritic cells, and exogenous IL-2, which was reflected by proliferation, TCR down-modulation, as well as induction of CD25 and Fas ligand expression. Stimulation by B. burgdorferi-pulsed dendritic cells withstood chemical fixation and was not restricted to class I or class II MHC, CD1a, CD1b, or CD1c. In contrast, anti-gamma delta antibody potently inhibited proliferation. Extraction of B. burgdorferi lipoproteins with Triton X-114 enriched for the stimulatory component. This was confirmed using lipidated vs nonlipidated hexapeptides of Borrelia outer surface proteins. These observations suggest that synovial V delta 1 T cells may mediate an innate immune response to common lipoprotein products of spirochetes.
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PMID:Lyme arthritis synovial gamma delta T cells respond to Borrelia burgdorferi lipoproteins and lipidated hexapeptides. 982 May 58

Previous reports of patients with Langerhans' cell histiocytosis have shown characteristics of osteolytic lesion, visceral involvement and organ dysfunction. We report a 2-year-old boy who was diagnosed as Langerhans' cell histiocytosis with a prominent hepatomegaly. X-Radiogram, computed tomography and magnetic resonance imaging revealed the osteolysis of the right iliac bone, the absence of the left eighth rib as well as the right mandible, and an enhancing mass in the left cerebellum. The data of radiography were highly suggestive of Langerhans' cell lineage. The presence of large CD1a-positive mononuclear cells associated with inflammatory cells in peripheral blood smear and bone marrow aspirate further confirmed the diagnosis. In addition, expressions of S100, CD25, CD68, CD80, CD86, and Fas ligand were identified on these cells by immunocytochemical staining. The results indicate that although these cells are activated Langerhans' cells, progression of the disease and the bone destruction could be mediated by the overt FasL expression of the cells.
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PMID:Expression of Fas ligand in Langerhans' cell histiocytosis: A case report of a boy with multisystem involvement. 1044 Sep 12

Mortality from measles virus (MV) infection is caused mostly by secondary infections associated with a pronounced immunosuppression. Dendritic cells (DCs) represent a major target of MV and could be involved in immunosuppression. In this study, human monocyte-derived DCs were used to demonstrate that DC apoptosis in MV-infected DC-T-cell cocultures is Fas mediated, whereas apoptotic T cells could not be rescued by blocking the Fas pathway. Two novel consequences of DC apoptosis after MV infection were demonstrated. (i) Fas-mediated apoptosis of DCs facilitates MV release, while CD40 activation enhances MV replication in DCs. Indeed, detailed studies of infectious MV release and intracellular MV nucleoprotein (NP) showed that inhibition of CD40-CD40L ligand interaction blocks NP synthesis. We conclude that the CD40 ligand expressed by activated T cells first enhances MV replication in DCs, and then Fas ligand produced by activated T cells induces Fas-mediated apoptosis of DCs, thus facilitating MV release. (ii) Not only MV-infected DCs but also bystander uninfected DCs undergo a maturation process confirmed by CD1a, CD40, CD80, CD86, CD83, and major histocompatibility complex type II labeling. The bystander maturation effect results from contact and/or engulfment of MV-induced apoptotic DCs by uninfected DCs. A model is proposed to explain how both a specific immune response and immunosuppression can simultaneously occur after MV infection through Fas-mediated apoptosis and CD40 activation of DCs.
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PMID:Consequences of Fas-mediated human dendritic cell apoptosis induced by measles virus. 1075 53

Decoy receptor 3 (DcR3), a soluble receptor belonging to the TNFR superfamily, is a receptor for both Fas ligand (FasL) and LIGHT. It has been demonstrated that DcR3 is up-regulated in lung and colon cancers, thus promoting tumor growth by neutralizing the cytotoxic effects of FasL and LIGHT. In this study, we found that DcR3.Fc profoundly modulated dendritic cell differentiation and maturation from CD14(+) monocytes, including the up-regulation of CD86/B7.2, and the down-regulation of CD40, CD54/ICAM-1, CD80/B7.1, CD1a, and HLA-DR. Moreover, DcR3-treated dendritic cells suppressed CD4(+) T cell proliferation in an allogeneic MLR and up-regulated IL-4 secretion of CD4(+)CD45RA(+) T cells. This suggests that DcR3.Fc may act not only as a decoy receptor to FasL and LIGHT, but also as an effector molecule to skew T cell response to the Th2 phenotype.
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PMID:Modulation of dendritic cell differentiation and maturation by decoy receptor 3. 1199 33

The pathological role played by T cells infiltrating hair follicles in lesions of alopecia areata (AA) is unknown. We examined the expression in cryostat sections of scalp skin obtained from a total of 28 patients with AA and from five normal control subjects of (1) molecules related to the induction of cell death including Fas, Fas ligand (FasL), perforin, granzyme B (GB), and TIA-1, (2) molecules related to antigen presentation including CD1a, CD40, CD54, CD80, and CD86, and (3) molecules induced by interferon gamma (IFN-gamma) including CD40, CD54, Fas, and HLA-DR. CD3(+) T cells infiltrated perifollicularly, perivascularly and in the hair structure and there was a predominance of CD4(+) over CD8(+) cells. Antigen-presenting cells expressing CD1a, CD40, CD54, or HLA-DR were also seen. Expression of CD40, CD54, HLA-DR and CD95 was also seen in the hair structure including the dermal papilla. Consistent with these observations, IFN-gamma-producing cells were also detected in the perifollicular infiltrate. In contrast, few Fas-L(+), perforin(+), GB(+) or TIA-1(+) cells were found adjacent to the follicles. Apoptotic cells were recognized only in the outer root sheath of catagen hairs. These findings suggest that infiltrating T cells interact with perifollicular or follicular antigen-presenting cells to produce IFN-gamma, which deprives dermal papilla cells of their ability to maintain anagen hair growth.
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PMID:Strong expression of CD40, CD54 and HLA-DR antigen and lack of evidence for direct cellular cytotoxicity are unique immunohistopathological features in alopecia areata. 1262 79

There is increasing evidence that ex vivo generated Langerhans cells (LCs) cannot fully substitute for their physiological counterparts in normal epidermis when studying the immunobiology of this prototype of a tissue-residing immature dendritic cell (DC). Here, we present CD1-based magnetic-activated cell-sorting (MACS) protocols for the effective isolation of human epidermal LCs. CD1c selection yielded a homogeneous population of pure and viable HLA-DR(+)/CD1a(+) DCs, with the ultrastructural features, surface antigen expression and cytokine profile, characteristic of epidermis-resident immature LCs. The immature state and functional integrity were established by allogeneic mixed lymphocyte reactions showing a weak stimulatory capacity of freshly isolated cells and upregulation upon stimulation. Characterizing the cells in more detail, we could demonstrate for the first time that normal human LCs express CXCR4, CD40 ligand (CD40L), and Fas and Fas ligand (FasL). The observed constitutive transcription of TGF-beta suggests that the viability and immature state of epidermal LCs are maintained not only by the TGF-beta production from the microenvironment, but also in an autocrine or paracrine manner. LPS and IFN-omega stimulated the expression of the inflammatory cytokines TNF-alpha and IL-1beta, and there was secretion of IL-12p70 after CD40 ligation. Remarkably, the CD1-sorted LCs showed no loss of their Birbeck granules and CD1a expression upon culturing and no spontaneous phenotypic and functional maturation into potent antigen-presenting cells (APCs). We conclude that human epidermal LCs obtained by the CD1c cell-sorting protocol are optimal candidates with which to elucidate the properties and capabilities of immature cells and to develop immunotherapeutic vaccines.
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PMID:CD1a and CD1c cell sorting yields a homogeneous population of immature human Langerhans cells. 1296 46

Mucin 1 (MUC1) forms a glycocalyx on the surface of decidual epithelial cells that needs to be removed for successful embryo attachment. We investigated whether MUC1 affects human early pregnancy decidual CD14(+) cells and their interactions with cognate decidual natural killer (NK) cells. FITC-dextran internalisation, surface and intracellular antigen levels, and proliferation of CD14(+) and/or CD56(+) cells were analysed by flow cytometry. Magnetic separation was used to purify CD56(+) and CD14(+) cells. Uncultured CD14(+) cells expressed a negligible percentage of CD1a and CD83 molecules. They expressed lower levels of CD16, and higher levels of endocytic mannose receptors (MR), dendritic cell-specific intercellular adhesion molecule grabbing non-integrin (DC-SIGN), proinflammatory chemokine CC receptor 5 (CCR5), and CD163 receptor, than their peripheral blood counterparts. Lipopolysaccharide stimulation did not affect FITC-dextran internalisation in CD14(+) cells. MUC1 bound and internalised, in a dose-dependent manner, the carbohydrate recognition domain of MR, increasing the decoy IL-1 receptor type II and decreasing IL-15 expression in CD14(+) cells. In the presence of MUC1-treated macrophages, the expression levels of the proliferation and cytotoxic mediators (perforin, Fas ligand and TNF-related activation-induced ligand or TRAIL) was attenuated, while that of the anti-inflammatory chemokine CCL17 was increased, in NK cells compared with untreated macrophages. In conclusion, MUC1 supports the alternative activation of tissue-specific CD14(+) cells, and may restrict proliferation of NK cells and regulate their content of cytotoxic mediators. Based on the experiments with first-trimester decidual cells in vitro, we conclude that removing MUC1 from decidual tissue might help control trophoblast invasion by NK cells.
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PMID:Specific decidual CD14(+) cells hamper cognate NK cell proliferation and cytolytic mediator expression after mucin 1 treatment in vitro. 2284 Nov 64