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)

The purpose of this study was to determine whether human tissue macrophages (M phi s) in various inflammatory/reactive conditions express different immunophenotypes. Using a large panel of monoclonal antibodies to monocyte/M phi-related antigens and a frozen-section immunoperoxidase technique, the following conditions were studied: granulomatous inflammation of unknown etiology, sarcoidosis, cat-scratch fever, toxoplasmosis, Gaucher's disease, and juvenile xanthogranulomas. The results show that there is immunophenotypic variation of the M phi s among the various inflammatory/reactive conditions. For example, the M phi s in cat-scratch fever are nearly unique in the expression of the "early inflammation" antigen identified by antibody 27E10, and the M phi s in juvenile xanthogranulomas, unlike those in most of the other conditions, lacked the antigen detected by antibody 25F9. The M phi s in Gaucher's disease differed from those in the other disorders by the combined absence of CD11b, CD14, G16/1, CD1a, CD25, and CD30. The inflammatory/reactive M phi s also exhibited differences from those in "normal" tissues, namely, a tendency toward acquisition of the antigens identified by antibodies Mac 387 and G16/1 and the more uniform expression of the "activation" antigens CD25, CD30, and CD71. The antigenic variations described here probably reflect differences in antigenic stimuli and M phi function. In addition to the possible biologic implications, this M phi immunophenotypic diversity may have practical diagnostic applications.
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PMID:Macrophages (histiocytes) in various reactive and inflammatory conditions express different antigenic phenotypes. 133 45

A detailed immunologic study of three cases of sinus histiocytosis with massive lymphadenopathy (SHML) was performed to better characterize this rare disorder. One patient had prominent cervical lymphadenopathy that regressed spontaneously, whereas the other two patients had persistent cervical lymphadenopathy and recurrent infections. The first patient was otherwise healthy and had normal immunologic studies. One of the latter patients had a relative increase in blood B cells, a decreased level of serum immunoglobulin A (IgA), decreased blood lymphocyte mitogenic responses to multiple mitogens (37-42% of controls), and cutaneous anergy. The other patient with persistent disease also had a relative increase in blood B cells, polyclonal hypergammaglobulinemia, and circulating immune complexes, as well as decreased blood T cells and markedly decreased blood lymphocyte responses to mitogens (12-37% of controls). Immunohistochemical stains of the lymph nodes of the three patients revealed a characteristic phenotype for the sinus histiocytes: S-100 protein, 3/3; CD14 (Leu M3) 3/3; CD11c (Leu M5), 1/1; CD71 (OKT9), 3/3; CD4 (Leu 3a), 2/3; CD1a (OKT6), 1/3; alpha-1-antitrypsin, 3/3; alpha-1-antichymotrypsin, 3/3; CD35 (C3b), 1/1; CD11b (Mo1), 0/3; CD15 (Leu M1), 0/3; HLA-DR, 0/3; and lysozyme, 0/3. This phenotype suggests that the cells of SHML have features of both the Langerhans/interdigitating cell and mononuclear phagocyte lineages. Emperipolesis by the histiocytes of B cells, T cells, and natural killer cells was demonstrated by a double-staining technique. Our findings indicate that patients with SHML may have a variably expressed immunodeficiency that predisposes them to recurrent infections.
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PMID:Sinus histiocytosis with massive lymphadenopathy: a spectrum of disease associated with immune dysfunction. 171 75

Keratinocytes express the macrophage/monocyte antigen CD36 in a variety of inflammatory cutaneous diseases characterised by a T lymphocyte rich infiltrate. Since cell-mediated immune mechanisms also play a role in host responses to skin tumours, we investigated the presence of CD36 antigen on keratinocytes in a range of epidermal cell-derived benign and malignant tumours characterised by a peritumoural, dermal lymphocytic infiltrate. Frozen tissue sections of lesional tissue from a range of epidermally derived tumours were labelled with antibodies to CD1a, CD11b, CD36, and HLA-DR antigens. Benign and malignant squamoproliferative tumour cells exhibited a spectrum of CD36 expression, whereas those of basal cell origin were consistently CD36-. Suprabasal expression of CD36 was present in the normal perilesional epidermis of all tumours studied including basal cell carcinoma. Keratinocyte CD11b expression was not observed. The widespread presence of keratinocyte CD36 positivity in squamoproliferative, but not basal epidermal, tumours suggests its expression may be linked to the degree of keratinocyte differentiation. The stimulus for expression is unknown, but the fact that suprabasal perilesional epidermis expressed CD36 strongly in the absence of infiltrate suggests it may represent a non-specific response by keratinocytes to various stimuli.
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PMID:Keratinocyte expression of CD36 antigen in benign and malignant epidermal cell-derived tumours. 171 27

The immunophenotypic properties of the abnormal cells in routine specimens from 16 cases of Langerhans cell histiocytosis (LCH) were examined. In five cases, cryostat sections were also available. The abnormal cells expressed a similar phenotype and were positive for HLA-DR, S-100 protein, peanut agglutinin (PNA), CD1a, CD4 and several macrophage-associated markers, including CD11c, CDw32 and CD68 (the latter detectable in routine sections with antibody KP1). Staining with CD14, CD35 (C3b receptor), and CD11b (C3bi receptor) was negative with the exception of one of the cases in which a proportion of the cells showed faint positivity with CD11b. Staining for pan-T-cell (CD2, CD3, CD5) and pan-B-cell (CD19, CD22) antigens was negative in all lesions. It is concluded that LCH expresses a characteristic phenotype with some heterogeneity with regard to macrophage markers and that immunohistochemical methods in cryostat sections and routine specimens form a useful supplement to other techniques for the diagnosis of this condition.
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PMID:Immunohistochemical study of the abnormal cells in Langerhans cell histiocytosis (histiocytosis x). 210 27

Bone marrow cells of a patient with Letterer-Siwe disease were cultured for three weeks in long-term bone marrow culture (LTBMC) conditions and examined at one-week intervals with a large panel of monoclonal antibodies by immunohistochemistry and by the immunogold transmission electron microscopy (immunoTEM) technique. Although at diagnosis the bone marrow showed a slight increase of monocytes with a normal phenotype, a rapid expansion of cells expressing CD1a and CD1c was observed already after 1 week of culture. A progressive increase in CD4, CD11b and CD11c expression was also observed. ImmunoTEM of cultured cells demonstrated that CD1a+ cells had macrophage-like morphology, and did not contain Birbeck granules. These findings indicate that bone marrow monocytes acquire some phenotypical features of Langerhans cells in LTBMC and support the hypothesis that these cells may derive directly from a bone marrow monocytic precursor.
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PMID:Bone marrow monocytes in histiocytosis X acquire some phenotypic features of Langerhans cells in long term bone marrow cultures. 247 66

The distribution and immunophenotype of macrophages and interdigitating reticulum cells were investigated on frozen sections of seven normal thymuses and 10 thymomas. In normal thymus, macrophages were mainly located in the cortex, were markedly PAM-1+/MAC+, weakly Leu-M3+ (CD14), T4+ (CD4), T9+ and OKM-1+ (CD11b). Interdigitating reticulum cells were mainly located in the medulla and were pan-Leu+ (CD45), T4+(CD4+), HLA-DR+; furthermore, they were also often TAC+ (CD25) and T9+. Thymomas were composed of cytokeratin-containing epithelial cells admixed with variable proportions of T6+ (CD1a) lymphocytes. As defined by the histological features two thymomas were lymphocyte-rich, five were mixed type and three were epithelial-rich; eight thymomas were mainly composed of cortical epithelial cells and two were composed of spindle epithelial cells suggesting a medullary origin. In all cases, thymoma-associated macrophages were markedly PAM-1+/MAC+; they were numerous, and regularly distributed throughout the tumour. The density of macrophages per unit area was similar to that of the normal thymus, and was not influenced by the histological type or by the lymphocyte content of the tumour. Interdigitating reticulum cells were few and were confined to the areas of medullary differentiation.
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PMID:Macrophages and interdigitating reticulum cells in normal thymus and in thymoma: an immunohistochemical study. 292 78

The morphological, ultrastructural and immunophenotypic properties of Histiocytosis-X (H-X) cells were investigated in a lymph node involved by Letterer-Siwe (L-S) disease. H-X cells were T6+ (CD1a), S-100+, T4+ (CD4) and HLA-DR+; in addition they were consistently T11+ (CD2) and were stained by antibodies directed against receptors for transferrin (T9), C3bi (OKM-1/CD11b), IgG-Fc (Leu-11/CD16) and Interleukin-2 (IL-2R/CD25). On immunostained cytosmears, T6+ cells were highly polymorphic and a prominent fraction (45%) showed immature morphology, characterized by lymphoid appearance. Cells expressing macrophage markers (ANAE, AACT, Leu-M3/CD14, PAM-1) were 10-fold fewer than T6+ cells and did not show a lymphoid morphology. At TEM level, H-X cells were characterized by poor content of LC granules and by the presence of myelin-like laminated bodies and of lysosome-like dense bodies. The immunophenotypic properties of H-X cells were compared to those of epidermal Langerhans cells (LCs) and of LCs present in lymph nodes of three cases of dermatophatic lymphadenitis. Epidermal LCs were T6+/HLA-DR+, and sometimes faintly T4+. Lymph node LCs were T6+, S-100+, T4+, HLA-DR+, and showed the same variety of surface receptors detected in H-X cells; furthermore, in a case with massive infiltration of the paracortex by T6+ cells, lymph node LCs were faintly T11+ and some of the T6+ cells had lymphoid aspect. Our findings suggest that the H-X cell population of L-S disease is not homogeneous, but is composed of discrete cell subsets with distinctive antigenic and morphological traits closely resembling those of cells of LC lineage at different maturational stages.
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PMID:Letterer-Siwe disease: immunohistochemical evidence for a proliferative disorder involving immature cells of Langerhans lineage. 313 61

To date no hematopoietic progenitors of dendritic Langerhans' cells (DLC), which represent an highly efficient class of antigen presenting cells, have been identified or the cytokines they elaborate have been defined. Here we describe an acute leukemia patient whose blasts (90-96% in peripheral blood and bone marrow) had a phenotype consistent with putative progenitors of DLC. The patient was treated with ara-C and VP-16 but did not achieve remission. The blasts had lobulated nuclei, no cytoplasmic vacuolation or Auer rods and were weakly positive for acid phosphatase and non-specific esterase and negative for PAS, granzyme A, dipeptidyl aminopeptidase IV, ATPase/ADPase and lysozyme production. The blasts were positive for CD1a, CD4, CD16, CD35, HLADR, HLADQ, CD11b, CD11c, CD14, CD33, CD34, CD11a, CD71, CD19, CD25, IL-2R beta and negative for CD2, CD7, CD8, CD10, CD22, CD56, CD57, surface or cytoplasmic CD3, TCR delta and TCR beta, HTLV-1p19 and P-glycoprotein. On liquid culture with or without 5 x 10(-9) M 12-O-tetradecanoylphorbol-13-acetate (TPA) for 3 days, the blasts formed aggregates of proliferating and elongating cells on the wall of the flasks with a decline in CD34, numerous dendritic processes appeared on the cells and there was strong positivity for ATPase/ADPase, but no other changes in phenotype. No macrophages were observed, indicating derivation from separate DLCs. Cytogenetic analysis showed chromosomal abnormalities and electron microscopy showed Birbeck granules. Southern blotting of DNA showed rearrangement of one allele for both JH and TCR beta but no HTLV-1 related sequences. Culture supernatants from blasts cultured with or without TPA showed the production of large amounts of IL-8, IL-6, TNF-alpha, MIP-1 alpha, IL-10 and interferon gamma and modest amounts of IL-1 alpha, GM-CSF and stem cell factor. The presence not only of CD1a, HLADR, HLADQ and many other characteristics including Birbeck granules, but also differentiation along the lines of DLC with appearance of dendritic processes on the cells and expression of ATPase/ADPase activity, indicate that the leukemic blasts in our patient represented a leukemic counterpart of normal progenitors of DLC and the leukemia a new entity which could possibly be classified as AML-M8. Lastly, many pro-inflammatory cytokines produced by DLC could contribute to inflammation and IL-10 to immunosuppression.
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PMID:Phenotype, genotype and cytokine production in acute leukemia involving progenitors of dendritic Langerhans' cells. 791 55

Because activated human macrophages can be potent sources of IL-10, and because immunosuppressive tolerance-inducing macrophages populate the skin after UV exposure, we determined whether IL-10 is induced after UV exposure of human skin and whether it is related to the immigrating macrophages. Keratomes were obtained from control skin or from skin obtained 72 h after a single exposure to four minimal erythemal doses of UVB. Quantitative reverse-transcriptase PCR on total RNA extracted immediately from skin keratomes showed that IL-10 mRNA was elevated in UV-exposed skin. Epidermal cell suspensions from non-UV-exposed keratomes (C-EC) and UV-exposed keratomes (UV-EC) were fractionated by sequential immunobead selection. IL-10 mRNA was reproducibly 200- to 400-fold higher in CD11b+ UV-EC (macrophages) relative to CD11b- UV-EC (keratinocytes). IL-10 mRNA was not detected in C-EC that contained the CD1a+ population (Langerhans cells) nor in CD1a- C-EC keratinocytes from normal skin. As determined by ELISA, CD11b+ UV-EC IL-10 cell-associated protein was fivefold higher than that of CD11b- UV-EC; this was confirmed by flow cytometric visualization of IL-10 protein in permeabilized cells. CD11b+ UV-EC macrophages secreted IL-10 protein into the supernatant at a level of 333 +/- 51 pg/10(6) cells, whereas UV-EC keratinocytes did not secrete detectable levels of IL-10 (n = 3), although UV did induce low levels of IL-10 mRNA and cell-associated protein in keratinocytes. Therefore, although human keratinocytes accumulate intracellular IL-10 after in vivo UV exposure, the most potent production and secretion of IL-10 in the epidermis seems to be that of UV-induced macrophages. Skin-infiltrating macrophage secretion of such a potent immunoregulatory cytokine may account for the delayed immunosuppressive environment of sunburned skin and the altered APC activity of the infiltrating macrophages.
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PMID:CD11b+ macrophages that infiltrate human epidermis after in vivo ultraviolet exposure potently produce IL-10 and represent the major secretory source of epidermal IL-10 protein. 796 79

Langerhans' cell histiocytosis (LCH) is characterized by the presence of large mononucleated cells, associated with inflammatory cells. The Langerhans' cell (LC) lineage of the mononucleated cells is suggested by the presence of Birbeck granules and the expression of CD1a. We investigated the presence of 14 markers expressed by normal LCs in vitro. Nine skin and one lymph node frozen biopsies of LCH children were analysed by in situ immunohistochemistry. The data were compared with six skin and five lymph node frozen biopsies. LCH cells of the ten samples were positive for all 14 LC markers. We observed three different groups of markers, according to the respective staining of normal LCs and LCH cells. Group 1 included DR, DQ, CD1a, CD1c, and ICAM-3. Markers of group 1 were present on the majority of both normal LCs and LCH cells. Group 2 included CD1b, CD4, LFA-1, LFA-3, CD32, and CD68. Markers of group 2 were detected on the majority of LCH cells, but only on a fraction of normal LCs. Group 3 included CD11b, CD24, and B7/BB1. Markers of this group were detected on LCH cells, but not on normal LCs. This in situ immunohistochemical study confirms that LCH cells belong to the LC lineage. The different clinical LCH syndromes had the same immunohistochemical staining. The expression of some markers of groups 2 and 3 is known to be related to the activation of LCs in vitro. Our study suggests that LCH cells are activated LCs.
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PMID:Langerhans' cell histiocytosis cells are activated Langerhans' cells. 796 9


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