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)

Dermal dendritic cells from eleven cases of mycosis fungoides (MF) (six patch and five plaque stage), two cases of pre-MF, and five specimens of normal human skin, were characterized immunohistochemically using a panel of antibodies including anti-human Thy-1, intercellular adhesion molecule-1 (ICAM-1; CD54), endothelial leukocyte adhesion molecule-1 (ELAM-1), vascular cell adhesion molecule-1 (VCAM-1), CD1a, CD2, CD14, CD18, CD34, MAC387, KP-1, EBM-11, factor XIIIa, factor XIIIs, and S100. Thy-1 expression in normal skin was limited to the microvascular endothelium and perivascular dendritic cells. An extensive interstitial network of Thy-1+ dendritic cells was seen in the papillary dermis of all cases of MF, whereas no epidermal cells were Thy-1+. The mean +/- standard deviation of interstitial Thy-1+ cells per high power field in the dermis was: normal skin, 2.86 +/- 0.34; pre-MF, 15; patch stage MF, 13.4 +/- 7.08; plaque stage MF, 49.96 +/- 21.29. Thy-1+ dendritic cells morphologically resembled the factor XIIIa+ "dermal dendrocyte" (DD) and shared their VCAM-1+, ICAM-1+, CD1a, CD2-, CD14+, CD18+, EMB11+, factor XIIIa+, factor XI-IIs-, S100-, MAC387- and KP-1-immunophenotype in MF. Double labeling studies revealed up to 50% of Thy-1+DD were also factor XIIIa+ in MF. Immediately beneath these cells was a similar network of CD34+, Thy-1-, factor XIIIa- dendritic cells limited to the reticular dermis. Strong microvascular endothelial cell expression of Thy-1 and VCAM-1, and focal vascular ELAM-1 expression were also seen in MF. Distinct cellular compartmentalization (papillary dermis versus reticular dermis versus epidermis) of dendritic cells is demonstrated by the differential expression of Thy-1, factor XIIIa, and CD34 antigens. The extensive number and prominent dermal dendritic network in the papillary dermis juxtaposed between epidermal keratinocytes (KC) and dermal/epidermal T cells, suggests an important pathophysiologic role for this newly recognized and immunophenotypically distinctive cell population in MF.
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PMID:Cutaneous expression of Thy-1 in mycosis fungoides. 128 18

The changes in the number of Langerhans cells within the gingiva during a 21 day experimental gingivitis episode were investigated immunohistochemically. Monoclonal antibodies to CD1a (specific for Langerhans cells and thymocytes) and HLA-DR (class II major histocompatibility antigens - (MHC)) were used to identify Langerhans cells within gingival biopsies taken on days 0, 7, 14 and 21. HLA-DR antibody stained dendritic cells within the oral epithelium which were morphologically identical to the CD1a+ Langerhans cells. Class II MHC LC numbers rose and plateaued between day 7 and 14 then decreased to baseline by day 21. As plaque accumulated and initial inflammation developed there was an increase in the number of CD1a+ Langerhans cells which peaked at day 7 and stayed high (day 14). As inflammation developed there was a statistically significant decrease in the number of CD1a+ Langerhans cells by day 21 (p = 0.028). The initial increase, followed by a decrease in CD1a+ Langerhans cells as inflammation developed, suggests that migration of Langerhans cells occurs within the gingival epithelium and this may represent an important early event in the gingival immune response to plaque.
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PMID:Langerhans cell dynamics in human gingiva during experimentally induced inflammation. 128 8

The population of CD1a+ cells and the quantity of Birbeck granules were evaluated in comparison with the population of T lymphocytes in a variety of clinical lesions of mycosis fungoides. Anti-CD1a and Lag antibodies that specifically react with Birbeck granules and related structures of human Langerhans cells were used immunohistochemically. CD1a+ cells in the dermis of lesions of mycosis fungoides significantly increased in plaques of the plaque stage and in plaques of the tumor stage. They were most frequent in lesions with CD4+ cells ranging in number from 100 to 150/mm2. These lesions were suspected to be progressing from the plaque to the tumor stage. During the course of the disease, most of the dermal CD1a+ cells had few Lag antigens. These results suggest that dermal CD1a+Lag- cells may promote the progression of mycosis fungoides from the plaque to the tumor stage.
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PMID:A subpopulation of Langerhans cells (CD1a+Lag-) increased in the dermis of plaque lesions of mycosis fungoides. 171 24

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

An unusual case of Langerhans cell histiocytosis in a 7-year-old female is presented. She had ultrastructural evidence of desmosomal biogenesis and formation of gland-like structures by lesional cells; their apical plasma membranes were folded into large numbers of microvilli. Despite the presence of these structures characteristic of epithelial cells, an infiltrated plaque on the abdominal skin of this patient was interpreted as cutaneous involvement of multiple system Langerhans cell histiocytosis because the immunohistochemical staining of the lesional cells for CD1a, S100, PNA, CD4, EN-4, and HLA-DR was positive, and numerous Birbeck granules were ultrastructurally identified in some lesional cells. Other clinical data included the presence of scaly erythematous skin lesions on the forehead and lytic osseous lesions in the maxilla, which were also histologically diagnosed as Langerhans cell histiocytosis. The absence of any internal malignancy in this patient readily ruled out the other diagnostic possibility of a metastatic adenocarcinoma showing glandular differentiation with brush border morphogenesis. The possibility that the desmosome-linked lesional epithelioid cells were actually cells of sweat glands entrapped in the histiocytic proliferation was also ruled out. The functional significance of the desmosomes and microvillous structures in the present case of Langerhans cell histiocytosis remains to be clarified. Awareness of this variant of Langerhans cell histiocytosis will be important for averting potential misdiagnosis in favor of epithelial tumors, especially metastatic adenocarcinomas.
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PMID:Langerhans cell histiocytosis (histiocytosis X) with morphologic expression of desmosomes and microvillous structures. 924 66

This study presents an immunohistochemical characterization of somatostatin-positive dendritic cells in psoriatic lesions. Somatostatin is a neuropeptide with inhibitory action on several neuropeptides and hormones, but also with immunomodulating properties, and has been used in several studies as treatment for psoriasis. The number of somatostatin-positive dendritic cells was found to be larger in psoriatic lesions than in normal skin of psoriasis patients and healthy controls. Colocalization of somatostatin and HLA-DR immunoreactivity was demonstrated in a subgroup of dendritic cells of psoriatic skin, whereas double-labelled cells were not found in uninvolved skin. The somatostatin-positive cells in the epidermis and dermis did not co-express CD1a, CD35, CD45RB, CD45RO, CD68, factor XIIIa or S-100. On the basis of these findings, the somatostatin-positive cells seem to represent a specific population of dermal dendritic cells, distinct from Langerhans' cells and factor XIIIa-positive cells, which are found in elevated amounts in chronic plaque psoriasis.
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PMID:Colocalization of somatostatin- and HLA-DR-like immunoreactivity in dendritic cells of psoriatic skin. 960 36

Calcipotriene is a synthetic analogue of 1,25-dihydroxyvitamin D3 established to be effective topically in the treatment of psoriasis. We investigated the early cellular and immunological events induced by calcipotriene in psoriasis. Thirty patients with moderate plaque-type psoriasis were randomly assigned to receive twice daily applications of either calcipotriene ointment 0.005% or matching vehicle for 6 weeks. Skin biopsies (6 mm) were performed from designated plaques at baseline and days 3 and 7. On these days and at weeks 2, 4 and 6, complete clinical evaluations were made in a double-blind fashion. Consistent with previous studies, significant clinical improvement (P < 0.05) in psoriasis was observed in patients receiving calcipotriene vs. those receiving vehicle by day 7 for scale and erythema, and by day 14 for thickness. No significant improvement, however, was seen on day 3. None of the immunohistological markers (CD1a, CD4, CD8, ICAM-1, VCAM-1, E-selectin, HLA-DR) semiquantitatively assessed in psoriatic plaques was significantly changed by calcipotriene treatment for 7 days. In the calcipotriene-treated group, interleukin (IL)-10 levels (pg/microgram of protein) increased by 57% from baseline (0.030 +/- 0.006; mean +/- SEM) to day 3 (0.047 +/- 0.011) (P = 0.05 vs. baseline; n = 10) and remained elevated at day 7 (0.046 +/- 0.012). IL-8 levels (pg/microgram of protein), however, declined by 70% from baseline (0.13 +/- 0.06) to day 3 (0.04 +/- 0.01), and remained low at day 7 (0.03 +/- 0.02) (P < 0.05 vs. baseline; n = 10). Both IL-8 and IL-10 were unaffected by vehicle treatment. Calcipotriene-induced clinical improvement of psoriasis is preceded by an increase in IL-10 and a concomitant decrease in IL-8 levels. The changes in the level of these two cytokines provide further evidence for immunological changes as a significant part of the mechanism of action of calcipotriene in psoriasis.
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PMID:Calcipotriene-induced improvement in psoriasis is associated with reduced interleukin-8 and increased interleukin-10 levels within lesions. 953 26

Atherosclerotic plaques are chronic inflammatory lesions composed of dysfunctional endothelium, smooth muscle cells, lipid-laden macrophages, and T lymphocytes. This study analyzed atherosclerotic tissue specimens for expression of CD1 molecules, a family of cell surface proteins that present lipid antigens to T cells, and examined the possibility that CD1+ lipid-laden macrophages might present antigen to T cells. Immunohistochemical studies using a panel of specific monoclonal antibodies demonstrated expression of each of the four previously characterized human CD1 proteins (CD1a, -b, -c, and -d) in atherosclerotic plaques. Expression of CD1 was not observed in normal arterial specimens and appeared to be restricted to the CD68+ lipid-laden foam cells of atherosclerotic lesions. CD1 molecules colocalized in areas of the arterial wall that also contained abundant T lymphocytes, suggesting potential interactions between CD1+ cells and plaque-infiltrating lymphocytes in situ. Using CD1-expressing foam cells derived from macrophages in vitro, we demonstrated the ability of such cells to present lipid antigens to CD1 restricted T cells. Given the abundant T cells, CD1+ macrophages, and lipid accumulation in atherosclerotic plaques, we propose a potential role for lipid antigen presentation by CD1 proteins in the generation of the inflammatory component of these lesions.
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PMID:CD1 expression in human atherosclerosis. A potential mechanism for T cell activation by foam cells. 1075 21

Sinus histiocytosis with massive lymphadenopathy (SHML) is an idiopathic proliferation of unique histiocytes that have vesicular nuclei and voluminous pale cytoplasm, often with emperipolesis. Pure cutaneous involvement is very rare. We describe a patient with SHML limited to the skin whose lesion has spontaneously regressed. A 35-year-old Korean male visited the Department of Dermatology due to facial rash for 2 months. A 3 x 3.5 cm-sized well-demarcated dark erythematous nontender plaque was noted on the right cheek. Skin biopsy showed dense, nodular infiltrates of histiocytes with abundant cytoplasm and vesicular nuclei rimmed by lymphoplasma cell aggregates throughout the upper and mid-dermis. The histiocytes were immunohistochemically positive for S-100 protein and CD68, but negative for CD1a. Laboratory tests and a thorough physical examination revealed no abnormalities. These findings suggested that this was a case of SHML clinically limited to the skin. The skin lesion was initially resistant to steroid therapy, but began to regress 10 months after the onset without further treatment.
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PMID:Sinus histiocytosis (Rosai-Dorfman disease) clinically limited to the skin. 1049 12

Benign cephalic histiocytosis (BCH) is best understood as a form of non-Langerhans cell histiocytosis, specifically as an early mononuclear variant of juvenile xanthogranuloma (JXG). However, the progression of BCH into JXG in the same patient has only been reported once before. We describe the case of a 2-year-old girl with asymptomatic, large, ill-defined infiltrated flat plaques over both cheeks, in addition to isolated papules. A punch biopsy of a plaque revealed dermal infiltration by vacuolated and scalloped histiocytes positive for CD68 KP-1, and that lacked expression of CD1a and S-100 protein, favoring macrophages over Langerhans cells. Electron microscopy study showed comma-shaped intracytoplasmic bodies in the histiocytic cells leading to the diagnosis of BCH. One year later, after an episode of varicella-zoster infection, the flat plaques over the cheeks became large reddish-yellow nodules, and in a second biopsy appeared to progress to JXG. Virus-related mechanisms of progression are discussed.
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PMID:Benign cephalic histiocytosis progressing into juvenile xanthogranuloma: a non-Langerhans cell histiocytosis transforming under the influence of a virus? 1069 21


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