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 have previously shown that tumor necrosis factor (TNF)alpha strongly potentiates the granulocyte-macrophage colony-stimulating factor (GM-CSF)/interleukin (IL)-3-dependent proliferation of CD34+ hematopoietic progenitor cells (HPC) through the recruitment of early progenitors with high proliferative potential. Furthermore, the combination of GM-CSF and TNFalpha allows the generation of large numbers of dendritic/Langerhans cells (D-Lc). Herein, we analyzed whether IL-3, when combined to TNFalpha would, as does GM-CSF, allow the generation of CD1a+ D-Lc. Accordingly, cultures of cord blood CD34+ HPC with IL-3 + TNFalpha yielded 20% to 60% CD14+ cells and 11% to 17% CD1a+ cells, while IL-3 alone did not generate significant numbers of CD1a+ cells. Although the percentage of CD1a+ cells detected in IL3 + TNFalpha was lower than that observed in GM-CSF + TNFalpha (42% to 78%), the strong growth induced by IL-3 + TNFalpha generated as many CD1a+ cells as did GM-CSF + TNFalpha. The CD14+ and CD1a+ cells generated with IL-3 + TNFalpha are similar to CD14+ and CD1a+ cells generated in GM-CSF alone and GM-CSF + TNFalpha, respectively. CD1a+ cells differed from CD14+ cells by (1) dendritic morphology, (2) higher expression of CD1a, CD1c, CD4, CD40, adhesion molecules (CD11c, CD54, CD58), major histocompatibility complex (MHC) class II molecules and CD28 ligands (CD80 and CD86), (3) lack of Fc receptor FcgammaRI (CD64) and complement receptor CR1 (CD35) expression, and (4) stronger induction of allogeneic T-cell proliferation. Thus, in combination with TNFalpha, IL-3 is as potent as GM-CSF for the generation of CD1a+ D-Lc from cord blood CD34+ HPC. The dendritic cell inducing ability of IL-3 may explain why mice with inactivated GM-CSF gene display dendritic cells.
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PMID:Interleukin-3 cooperates with tumor necrosis factor alpha for the development of human dendritic/Langerhans cells from cord blood CD34+ hematopoietic progenitor cells. 863 Apr 1

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

The human dermis contains a heterogeneous network of cells with a dendritic morphology, including factor XIIIa+ dermal dendrocytes and CD34+ dendritic cells located around epidermal adnexae. Whereas dermal dendrocytes have been immunohistochemically studied, CD34+ dermal cells have not yet been well characterized. We studied by simple and double immunolabeling techniques on tissue sections of normal human skin the phenotype of these cells and found them to express vimentin and Te7 but none of the remaining markers sought (factor XIIIa, von Willebrand factor, CD1a, CD3, CD4, CD8, CD14, CD25, CD36, CD45, CD54, CD56, LFA-1, EGF-R, S-100 protein, Mac 387, and muscle-specific actin). Rare CD34+ cells of the interstitial dermis expressed human leukocyte antigen (HLA)-DR antigens, but this was not the case for periadnexal CD34+ cells. These results show that CD34+ dendritic cells of human dermis are mesenchymal cells bearing a unique immunophenotype different from that of (myo)fibroblasts, monocytes-macrophages, Langerhans cells, and factor XIIIa+ dermal dendrocytes. Whereas the involvement of CD34+ cells in some cutaneous tumors is well known, their physiologic role in normal skin remains to be established. On the basis of our results, we speculate that these cells could represent uncommitted mesenchymal cells, unique by virtue of CD34 antigen expression.
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PMID:Immunohistochemical study of CD34-positive dendritic cells of human dermis. 979 Jan 22

The prevalence of anoperineal diseases, i.e. sexual transmitted infections, is increasing particularly in AIDS, a fact which is likely due to the alteration of mucosal immunity. However, no data were available on normal anal status. In order to study anal immunity in man, we characterized lymphocytes subtypes and Langerhans' cells (LC) using quantitative morphometric analysis and immunohistochemistry. Anal normal mucosal samples obtained from surgical specimens of 45 patients (30 suffering from hemorrhoids and 15 from fissurations) were analyzed. Immunohistochemistry was performed on frozen sections with antibodies recognizing CD1a (LC), CD3 (T lymphocytes), CD4 (T4), CD8 (T8) and CD22 (B-lymphocytes). Immunostained cells were counted per square millimeter of mucosal epithelium. The surface of CD1a cells was measured using a computerized software program and a percentage of CD1a immunostained area was calculated in comparison to the whole mucosal surface. LC and T-Lymphocytes were found in the squamous epithelium in all analyzed samples. The mean values of LC number were 84.13 +/- 9.6 and 64.77 +/- 9.8 in hemorroid- and fissure-patients, respectively. The mean values of LC area (% of CD1a stained area over total mucosal surface) were 3.89 +/- 0.44 and 4.84 +/- 0.64, respectively. In the two groups, the number of intraepithelial CD8 lymphocytes was higher than that of CD4 lymphocytes. These data suggest for the first time that anal mucosa could be considered as a part of MALT system.
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PMID:Quantitative analysis of the immune cells in the anal mucosa. 882 6

The CD1 family of proteins are structurally related to MHC class I proteins, but are only distantly related to the class I proteins or other MHC-linked class I-like proteins. Sequence comparisons indicate that the CD1 proteins have evolved into two subfamilies, those which are similar to human CD1a, b, and c and those which are similar to human CD1d. The CD1A-, B-, and C-like genes were deleted from rodents and the CD1D gene was duplicated. CD1a, b, and c are expressed by thymocytes, dendritic cells, activated monocytes, and B cells (CD1c), a tissue distribution which strongly suggests a role in antigen presentation. In contrast, CD1d and its murine homologues are expressed by many cells outside of the lymphoid and myeloid lineages. The CD1 proteins are in most cases expressed as beta 2mg-associated membrane glycoproteins, but may associate with additional proteins. CD1d is expressed on the surface of intestinal epithelial cells in a nonglycosylvated form without beta 2mg. Whether the CD1 proteins function as antigen-presenting molecules is unresolved, but it is unlikely that they present conventional peptide antigens. Strong evidence indicates that murine CD1 proteins are recognized by a population of NK1.1+, CD4+ or CD4-CD8- (double negative, DN) T cells which express an invariant TCR alpha chain. CD1d is most likely recognized by the homologous T cell population in humans. DN alpha beta T cells which recognize CD1a, b, or c have been isolated, including clones which recognize a lipid antigen from mycobacteria presented by CD1b. A third potential population of CD1 reactive cells are CD8+ T cells in the intestinal epithelium. Taken together, these observations indicate that CD1 proteins interact with several specialized populations of T cells. The precise biological functions mediated through these interactions remain to be determined.
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PMID:Structure and function of the CD1 family of MHC-like cell surface proteins. 884 79

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

Dendritic cells are potent stimulators of Ag-specific T cell responses and have been implicated in the pathogenesis of HIV-1 and other viral infections. Although cytokines may be involved in both of these processes, there is little information on the expression of cytokines by human blood dendritic cells. We characterized cytokine gene and protein expression in dendritic cells that were purified from normal human PBMC by flow cytometry and stimulated in vitro for up to 24 h with HIV-1 or herpes simplex virus (HSV). The unstimulated, uncultured dendritic cells were defined by their phenotype (HLA DR+ CD3- CD19- CD16- CD56- CD14-) and distinct morphology, lack of mRNA expression for CD3, CD14 and CD19, and presence of mRNA for CD4 and CD83. The purified dendritic cells also expressed CD4 (70-90%), CD33 (36-48%), and CD11c (44-54%); lacked CD1a expression (<1%); and were potent stimulators of an allogeneic MLR. The stimulated dendritic cells expressed mRNA for IFN-alpha, IL-1alpha, IL-1beta, IL-6, IL-10, IL-12, GM-CSF, and TNF-alpha within 4 to 12 h as determined by reverse transcription-PCR, with higher levels induced by HSV compared with HIV-1 strains IIIb or BaL. In contrast, the dendritic cells produced detectable protein only for IFN-alpha and IL-6 in response to HIV-1 or HSV, and IL-1beta in response to HSV within 24 h. There were no differences in expression of CD80 and CD86 surface molecules by dendritic cells that were either mock stimulated or stimulated with HIV-1 or HSV for 24 h. Production of IFN-alpha, IL-1beta, and IL-6 by dendritic cells may be important to the immunologic function of these cells and their role in the pathogenesis of HIV-1 and HSV infections.
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PMID:Cytokine expression by human peripheral blood dendritic cells stimulated in vitro with HIV-1 and herpes simplex virus. 889 36

CD1a+ dendritic cells (DC) differentiate from a major population of nonadherent CD13(hi)lin- cells that appear when human cord blood CD34+ hematopoietic progenitor cells are cultured with stem-cell factor, granulocyte/macrophage (MA) colony-stimulating factor, and tumor necrosis factor-alpha (TNF-alpha) for 5 days. CD13hilin- cells, which also comprise MA and granulocyte precursors, are CD4+ and can thus be targets of human immunodeficiency virus (HIV). Low replication was noted when these day 5 cells were infected with lymphotropic HIV-1LA1 (p24: < or = 4 ng/mL on day 8 postinfection [PI]), while high virus production occurred with MA-tropic HIV-1Ba-L, HIV-1Ada, or HIV-1-m-n. (p24: 50 to > or = 1,000 ng/mL). Strong cytopathicity (CPE) was then observed in nonadherent cells as in adherent MA. However, FACS analysis on day 7 PI showed that HIV did not affect differentiation of DC that survived CPE: apart from CD4 downmodulation related to HIV production, overall expression of CD40, CD80, and CD86 costimulatory molecules, and of HLA-DR, was unchanged relative to controls. At that time, the capacity of DC from HIV-infected cultures to stimulate the mixed leukocyte reaction was only altered less than 10-fold. Immunocytochemistry on day 7 PI showed that most HIV-infected cells were included in syncytia that were stained by anti-CD1a, anti-S100, and anti-CD14 antibodies, indicating that syncytia consisted of DC and cells of the MA lineage. Polymerase chain reaction analysis of FACS-sorted CD1a+ cells confirmed that they harbored then HIV DNA. Viral DNA was also detected in CD1a+ DC from noninfected cultures that had been exposed to HIV only after sorting. Therefore, we examined whether in infected cultures DC precursors were infected at the onset or if virus spread later from other infected cells to differentiated DC. This was answered by showing that, 24 hours postexposure to HIV, viral DNA was preferentially detected in day 5 sorted CD13hilin- versus CD13hilin- cells, and that it was found in the CD1a+ progeny of CD13(hi)lin- cells 48 hours later. In addition, HIV replication did not affect myeloid clonogenic progenitors in day 0 to day 7 PI cultures, although viral DNA was detected in colony-forming unit-granulocyte/macrophage (CFU-GM)/CFU-M colonies derived from day 3 and 7 PI cultures. Thus, precursors of DC and their progeny are susceptible to HIV in vitro, but, apart from CPE, the effect of virus production on DC differentiation or function is limited.
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PMID:The effect of in vitro human immunodeficiency virus infection on dendritic-cell differentiation and function. 894 57

The characteristics of a feline homologue of CD1, defined by a murine monoclonal antibody, Fe1.5F4 (IgG1), are described. This antibody precipitated a 49 kDa protein from biotinylated feline thymocyte extract in conjunction with a 14 kDa protein, consistent with beta 2 microglobulin subunit. The tissue distribution of this antigen was restricted to cortical thymocytes and antigen presenting cells of the thymic medulla, epidermis (Langerhans cells), dermis and occasional dendritic cells in the mantle and periarteriolar lymphoid areas of the spleen. Although flow cytometry demonstrated a continuous distribution of antigen expression on thymocytes, antigen density was found to decrease with age, consistent with physiological thymic involution. Thymocytes with high density expression of this antigen were predominantly restricted to cells with dual expression of CD4 and CD8 as defined by feline specific murine monoclonal antibodies Fe1.7B12 (IgG1) and Fe1.10E9 (IgG1) respectively. The tissue distribution of this CD1 homologue indicates that it is a member of the classic thymic CD1 family. This feline homologue of CD1 was distinct from CD1c by virtue of its lack of expression in peripheral blood and splenic mantle zone B cells. An unequivocal distinction could not be made between CD1a and CD1b based on tissue distribution due to species variation in expression of these CD1 molecules. Although the biochemical characteristics of this feline CD1 homologue more closely match with CD1a. The pattern of tissue expression and biochemical characteristics of the feline CD1 antigen appear largely similar to those described for human and other species.
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PMID:A feline homologue of CD1 is defined using a feline-specific monoclonal antibody. 909 31

Immunophenotyping of cells by flow cytometry has become a routine test to diagnose pulmonary and mediastinal diseases. Peripheral blood, extravascular fluids, bronchoalveolar lavage (BAL) and suspension of single cells obtained by fine-needle aspiration can be used. Peripheral blood (MOAb for immunophenotyping of lymphocytes: CD14, CD45, CD3, CD19, CD4, CD8, CD16/56, HLA DR, CD38, CD25) is the material of choice for detection and monitoring of immunodeficiences. BAL (MOAb for immunophenotyping of lymphocytes: CD14, CD45, CD3, CD19, CD4, CD8, CD16/56, HLA DR) is used mainly for differential diagnosis of extrinsic allergic alveolitis (low CD4/CD8 ratio) and sarcoidosis (high CD4/CD8 ratio). The enumeration of alveolar macrophage subsets is an important tool to establish diagnosis of histiocytosis X (CD1a > 3%). Extravascular fluids, suspension of single cells and BAL are preferred materials for detection and classification of non-Hodgkin lymphomas (MOAb for immunophenotyping of lymphocytes: CD14, CD45, CD3, CD19, CD4, CD8, CD16/56, HLA DR, CD38, CD25, CD23, CD5, CDl1c, CD30, light chain immunoglobulins).
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PMID:[Flow cytometry for extensive thoracic diagnosis]. 920 29


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