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)

The CD45R and CDw29 antigens are expressed on naive and primed helper T cell populations which serve suppressor-inducer or helper-inducer functions, respectively. These antigens may also be expressed on epithelial cell subpopulations. In the present study, monoclonal antibodies reacting with T lymphocytes and Langerhans cells (LC) were used to characterize the expression of CD45R and CDw29 antigens in oral lichen planus. CDw29 was expressed by LC and lymphocytic cells whereas keratinocyte reactivity varied from negative through to full thickness staining. Expression of CD45R was confined to intraepithelial cells with either lymphocytic or dendritic morphology. A relatively constant ratio of CD1a + LC to CD45R + cells (2:1) was seen. These results demonstrate the existence of intraepithelial cells expressing antigens which are functionally important in T cell responses and which may provide local immunoregulatory influences.
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PMID:Expression of CDw29 and CD45R antigens on epithelial cells in oral lichen planus. 247 98

Interactions of CD28 (on T cells) with its recently identified ligand B7/BB1 (on antigen-presenting cells) have been shown to activate T cells via a major histocompatibility complex/Ag-independent "alternative" pathway, leading to an amplification of T-cell-mediated immune responses. The in vivo relevance of these molecules for cutaneous immunity is presently unknown. These findings prompted us to study the expression of B7/BB1 and CD28 in normal human skin and in selected T-cell-mediated inflammatory skin diseases. Biopsies were obtained from lesional skin of patients with allergic contact dermatitis, lichen planus, and, as control, from basal cell carcinoma and from healthy controls. Serial cryostat sections were stained with a panel of MoAbs directed against CD28, B7/BB1, CD3, CD1a, and KiM8 using immunohistochemistry (ABC technique). CD28 expression was observed in the majority of dermal and epidermal CD3+ T cells in contact dermatitis and lichen planus. In normal skin and basal cell carcinoma, CD28 was expressed only occasionally by perivascular T cells. In allergic contact dermatitis and lichen planus, B7/BB1-expression was found on dermal dendritic cells, on dermal macrophages, on Langerhans cells, focally on keratinocytes, and occasionally on dermal T cells. No B7/BB1 immunoreactivity was detected in normal skin and basal cell carcinoma. These findings indicate that T-cell-mediated skin diseases are accompanied by an influx of CD28+ T cells and an upregulation of B7/BB1 on cutaneous antigen-presenting cells, keratinocytes, and on some T cells. We speculate that "alternative" T cell-activation via the B7/CD28 pathway may contribute to the pathogenesis of these skin diseases.
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PMID:Expression of the B7/BB1 activation antigen and its ligand CD28 in T-cell-mediated skin diseases. 752 32

Expression of intercellular adhesion molecule-1 (ICAM-1, CD54) and vascular cell adhesion molecule-1 (VCAM-1, CD106) was examined in oral lichen planus (OLP) and normal oral mucosa (NOM). Immunoperoxidase staining showed ICAM-1 expression by vascular endothelium in all biopsies of OLP and NOM whereas endothelial VCAM-1 staining was found in 2/7 NOM and 8/9 OLP. In the lamina propria of NOM occasional cells were ICAM-1 or VCAM-1 positive, and virtually no staining of intraepithelial dendritic cells was seen for either marker. Intraepithelial dendritic cells stained for ICAM-1 in 7/9 and VCAM-1 in 4/9 OLP biopsies. Double immunofluorescence showed dual labelling of Langerhans cells (LC) with CD1a and VCAM-1 in a further 5/12 cases of OLP, but there was no such staining in four NOM. This is the first report of LC staining with VCAM-1. Induction of ICAM-1 and VCAM-1 on LC and macrophages in OLP suggests these cells are activated and may contribute to the pathogenesis of OLP by presenting antigen to infiltrating lymphocytes.
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PMID:VCAM-1 and ICAM-1 are expressed by Langerhans cells, macrophages and endothelial cells in oral lichen planus. 752 63

The diagnosis of post-transfusion graft-versus-host disease (GVHD) in early period is critical for the prognosis of the patients. Exanthema and fever are the earliest symptom of the post-transfusion GVHD and usually precede the disturbance of the liver and bone marrow. Snap-frozen, cryostat-sectioned specimens from the lesional and perilesional skin were labeled by monoclonal antibodies against HLA-ABC, HLA- DR, ICAM-1, CD1a and CD8. The reaction was visualized by indirect immunofluorescence. Graft-versus-host reaction (GVHR) was immunopathologically characterized by extensive expression of HLA-DR and ICAM-1 in the epidermal keratinocytes, exocytosis of CD8 positive cytotoxic T-cell and the reduction or disappearance of CD1a expression by epidermal dendritic cells. The other GVHRs such as erythema exudativum multiforme (EEM), fixed drug eruption, toxic epidermal necrolysis (TEN) and lichen planus could not be separated. Our protocol of the immunopathologic examination could be done quickly (within 3 hours) and provides more detailed and useful information for the diagnosis of GVHD in early period compared with conventional histopathology.
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PMID:[Differential diagnosis of post-transfusion graft-versus-host disease (GVHD) by rapid immunopathologic examination of the skin]. 930 Dec 87

Chronic graft versus host disease (cGVHD) of the oral mucosa, following allogeneic stem cell transplantation, and oral lichen planus (OLP) are both mucosal diseases where the immune system is involved in the pathogenesis. Although the aetiology of the two conditions is different, they present with a similar clinical appearance. This study compares the two diseases regarding the distribution of cells, which are expressing cell surface markers of interest for inflammatory responses. Monoclonal antibodies (MoAbs) were used in standard immunohistochemical procedures. CD1a+, CD80+ and CD86+ cells in the epithelium of OLP- and cGVHD lesions had the dendritic morphology of Langerhans cells (LC). Higher frequencies of CD1a+ LC as well as CD25+ cells were observed in the OLP epithelium than in the cGVHD epithelium. The OLP lesions showed higher frequencies of subepithelial cells expressing CD1a, CD86, CD4, CD8 and CD25 than the cGVHD lesions. Notably there was a significantly higher frequency of CD25+ cells in the epithelium and the connective tissue of OLP than in cGVHD. These cells might represent regulatory T cells. In conclusion, cGVHD and OLP show marked differences at the cellular level despite similar clinical appearance. Hence, the findings indicate differences in the regulation of the inflammatory response between the two conditions.
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PMID:Langerhans cells and T cells in oral graft versus host disease and oral lichen planus. 1169 4

To elucidate the pathogenesis of T cell-mediated inflammatory skin diseases, we examined the exact sites where CD8(+) T cells proliferate, correlating them with the localization of antigen-presenting dendritic cells. We performed CD8/Ki-67 double immunohistochemical staining and single staining for CD1a, CD68, and factor XIIIa on sections of paraffin-embedded tissue samples of inflammatory dermatoses in which T lymphocytes are thought to play a crucial role. The dermatoses were lichen planus (12 samples), acute graft-versus host disease (GVHD) (12 samples), chronic GVHD (10 samples), spongiotic dermatitis (8 samples) and psoriasis (7 samples). Labelling for Ki-67 among CD8(+) T cells was predominantly observed in the subepidermal lymphoid infiltrate, and was scanty in the epidermis. This suggested that proliferation of CD8(+) T cells occurred preferentially in the dermis. The labelling index for Ki-67 among dermal and epidermal CD8(+) cells was quite different among the different diseases studied (P < 0.05). They were rich in the subepidermal portion of the dermis of spongiotic dermatitis, acute GVHD and chronic GVHD, but rare in the dermis of psoriasis and lichen planus. A moderate infiltrate was also observed in lesional epidermis of spongiotic dermatitis, acute GVHD and chronic GVHD, whereas they was almost none in the epidermis of psoriasis and lichen planus. CD1a(+) dermal dendritic cells were densely distributed within the lymphoid infiltrate in the affected dermis of spongiotic dermatitis, psoriasis and lichen planus, whereas they were minimal in GVHD. These dermal dendritic cells are candidates as stimulators on T cells in the dermis. In conclusion, the proliferative status of T cells could be an important clue in the elucidation of the pathophysiology of T cell-mediated inflammatory dermatoses.
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PMID:Proliferative activity of CD8(+) T cells as an important clue to analyze T cell-mediated inflammatory dermatoses. 1175 86

Antigen-presenting cells (APCs) participate in the initiation of the inflammatory process in various immune-mediated dermatoses through the activation of antigen-specific T lymphocytes. The skin contains several different subsets of APCs. To investigate the role of these APCs in T-cell immune-mediated inflammation, we examined the distribution and numbers of epidermal and dermal CD1a(+) dendritic cells (DCs), factor XIIIa(+) dermal DCs, and CD68(+) macrophages in five T-cell-mediated inflammatory skin diseases. Immunohistochemistry of CD1a, factor XIIIa, and CD68 was performed using paraffin-embedded tissue obtained from a total of 51 patients with eczematous dermatitis (histologically spongiotic dermatitis), psoriasis, lichen planus, acute graft-versus-host disease (GVHD), and chronic GVHD. The numbers of positive cells for each staining were compared with those in site-matched normal skin control specimens from aged-matched subjects. In spongiotic dermatitis and lichen planus, the numbers of epidermal and dermal CD1a(+) cells and factor XIIIa(+) cells were significantly greater than in normal control skin, while in psoriasis only factor XIIIa(+) cells were significantly increased in number. Acute and chronic GVHD showed a reduced number of dermal CD1a(+) cells. Interestingly, factor XIIIa(+) cells were decreased in acute GVHD while they were increased in chronic GVHD. There was a significant reduction in epidermal CD1a(+) cells in acute GVHD, but not in chronic GVHD. The differences in the numbers of APCs in lesional skin appeared to reflect differences in the pathophysiology of these inflammatory skin diseases.
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PMID:Comparison of the distribution and numbers of antigen-presenting cells among T-lymphocyte-mediated dermatoses: CD1a+, factor XIIIa+, and CD68+ cells in eczematous dermatitis, psoriasis, lichen planus and graft-versus-host disease. 1237 34

Annular lichen planus is a rare, unique subtype of lichen planus. We report a 34-year-old Japanese male who had multiple, dark red to purple, annular macules with slightly raised borders. Histopathological examination of a skin biopsy specimen from the peripheral region of the macule showed the typical features of lichen planus. Immunohistochemical stainings revealed that a number of CD1a-positive, S-100-protein-positive Langerhans cells were present at the border zone of the annular lesion and most of the infiltrating cells were CD4-positive, CD8-negative lymphocytes. Conversely, inside the annular lesion, the number of Langerhans cells was decreased, and an equal number of CD4-positive cells and CD8-positive cells was present in the sparse infiltration. These results suggest that activation of Langerhans cells initiated a lichenoid tissue reaction but a subsequent depletion of Langerhans cells suppressed the lymphocyte infiltration. These sequential events might be involved in the formation of the unique annular structure in this condition.
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PMID:Annular lichen planus: study of the cellular mechanisms of annularity. 1517 17

Langerhans cell histiocytosis (LCH) is a rare histiocytic disorder characterized by clonal proliferation of neoplastic Langerhans cells (LCs). LC proliferation can also be seen in different reactive dermatosis. CyclinD1 is a downstream marker of mitogen-activated protein (MAP) kinase pathway, which is often activated in LCH. This study aimed to evaluate the role of cyclinD1 to differentiate reactive LC proliferation from LCH. All cases of cutaneous LCH diagnosed by biopsy in the past 3 years (n = 13) were immunostained with CD1a, p53, CD31, and cyclinD1. Seven cases each of discoid lupus erythematosus (DLE) and lichen planus (LP) were taken as control. Presence of p53, CD31, and cyclinD1-positive LCs (CD1a-positive) were compared in the dermis. In all LCH cases, dermal neoplastic LCs showed diffuse CD1a positivity and 12 cases (92.3%) showed variable (30%-70%) cyclinD1 expression. Weak p53 and CD31 expression were seen in 61.5% and 46.1% of LCH cases, respectively. In the control group, 5 cases of LP and 4 cases of DLE showed variable LC proliferation, highlighted by CD1a positivity. However, no case of reactive dermatosis showed cyclinD1 or p53 expression by the reactive LCs. Weak and patchy CD31 expression by the reactive LCs were found in 1 (25%) and 2 (40%) cases of DLE and LP, respectively. To conclude, cyclinD1 is frequently expressed in neoplastic LCs in LCH. It is an efficient marker to differentiate neoplastic from reactive LC proliferation, and can be used as a surrogate marker in LCH.
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PMID:CyclinD1 Is Useful to Differentiate Langerhans Cell Histiocytosis From Reactive Langerhans Cells. 3012 6