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)

Using immunohistochemical techniques, we mapped and quantified the distribution of Langerhans cells (LCs) within the follicular epithelium of normal human skin in serial horizontal sections. Ten skin biopsies from disparate, disease-free sites from individuals of various skin types were stained with antibody to CD1a. LCs concentrated in the infundibular epithelium (x=16.16 cells), including the follicular bulge, and extended into the germinative sebaceous epithelium (x=8.84). In contrast, rare LCs (x=1.06) were observed in the follicular epithelium below the entry of sebaceous glands into the follicle. LCs were absent in bulbar epithelium. This infundibulocentric distribution of LCs corresponds to the pattern of follicular inflammation in the scarring folliculitides of lupus erythematosus and lichen planopilaris, as well as allogeneic graft versus host reaction and infundibulofolliculitis of atopy. Follicular LCs may act as the trigger and/or target for these T cell-mediated inflammatory processes.
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PMID:Distribution of Langerhans cells in human hair follicle. 944 91

Langerhans cell histiocytosis (LCH) is a pleomorphic disease entity characterized by local or disseminated atypical Langerhans cells found most commonly in bone, lungs, mucocutaneous structures, and endocrine organs. Cutaneous disease occurs in approximately one quarter of all cases. Cutaneous findings include soft-tissue swelling, eczematous changes, a seborrheic dermatitis-like appearance, and ulceration. We report a rare case of LCH confined to the scalp with folliculocentric infiltrates. This 32-year-old male patient presented with follicularly based erythema, scale, and pustules unresponsive to topicals and oral antibiotics. The patient's lesions mimicked lichen planopilaris and folliculitis decalvans during the disease process. On hematoxylin and eosin stain, scalp biopsy showed a perivascular interstitial patchy lichenoid mononuclear cell infiltrate that focally abutted follicular infundibula. Prominent mononuclear cells having reniform nuclei were present, and immunoperoxidase stains for CD1a confirmed Langerhans cell differentiation. Serological and imaging workup failed to display systemic involvement.
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PMID:Adult onset folliculocentric langerhans cell histiocytosis confined to the scalp. 1502 94

While the pathogenesis of most scarring alopecias is poorly understood, one recent study indicates destruction of follicular stem cells as a possible mechanism in lichen planopilaris, the prototypic scarring alopecia. The aim of this cross-sectional study was to ascertain the target of inflammation and to more precisely characterize the inflammatory infiltrate in various stages of primary scarring alopecias. Immunohistochemical studies were performed using a panel of antibodies that included anti-cytokeratin 15, an antibody that specifically targets follicular bulge stem cells and CD4, CD8, CD1a and human leukocyte antigen-DR to characterize the inflammatory infiltrate. Our data showing absence of follicular bulge stem cells in cases with moderate to heavy inflammation suggest involvement of the bulge region in 'early' active stages of primary scarring alopecia. The paucity of CD8+ T cells in the inflammatory infiltrate in the majority of these cases argues against a cell-mediated cytotoxic destruction of follicular bulge stem cells. Preservation of CK15+ cells in 'late' fibrotic stages of primary scarring alopecia further supports this and implies that the irreversible loss of hair follicles, the sine qua non of primary scarring alopecia, is not necessarily a consequence of T cell-mediated destruction of follicular bulge stem cells.
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PMID:Involvement of the bulge region in primary scarring alopecia. 1853 62

Folliculitis decalvans (FD) is a rare variant of primary cicatricial alopecia, for which the etiopathogenesis remains unclear. Our purpose was to evaluate whether certain immunologic mechanisms might have a significant role in the pathogenesis of FD. Lesional scalp biopsy specimens from 7 patients with FD, 7 with lichen planopilaris, and 4 with alopecia areata were studied immunohistochemically by using monoclonal antibodies to CD1a, CD3, CD4, CD8, CD20, CD25, HLA-DR, interleukin (IL)-1beta, IL-4, IL-8, interferon gamma, tumor necrosis factor alpha, basic fibroblast growth factor (b-FGF), transforming growth factor (TGF)-beta, endothelial leukocyte adhesion molecule 1, intercellular adhesion molecule (ICAM)-1, and vascular cell adhesion molecule. We showed that early FD lesions are characterized by an infiltration of activated T-helper cells, featuring mixed TH1/TH2 polarization. IL-8 and ICAM-1 may contribute to the infiltration of neutrophils, whereas b-FGF and TGF-beta may represent important mediators of the fibrosis that characterizes late-phase FD.
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PMID:Immunopathogenesis of folliculitis decalvans: clues in early lesions. 1879 44

Lichen planopilaris and long-standing traction alopecia are both traditionally classified as scarring alopecias. The etiology of lichen planopilaris has not been fully elucidated, although an autoimmune mechanism is generally accepted with Langerhans cell involvement implicated in previous studies. The etiology of traction alopecia is generally considered to be the result of mechanical force with subsequent inflammation without an autoimmune component. Langerhans cells in pure traction alopecia have not been previously evaluated nor have Langerhans cell concentrations been compared among the scarring alopecias. We performed double immunostaining with CD1a and CD3 to assess the ratio of Langerhans cells to T lymphocytes in lichen planopilaris and traction alopecia. Sixteen biopsies were evaluated including 9 biopsies of lichen planopilaris and 7 biopsies of traction alopecia. The mean ratio of the concentration of Langerhans cells to T lymphocytes was 1.28 for the lichen planopilaris group and 0.59 for the traction alopecia group. There is a significantly higher ratio of Langerhans cells to T lymphocytes in lichen planopilaris compared with that seen in traction alopecia. This supports previous data recognizing an immune component in lichen planopilaris mediated by Langerhans cells while emphasizing that most traction alopecias are not primarily immune related. Thus, the traditional classification systems for alopecia may need review and revision, especially when looking at etiopathogenesis. However, rare cases of traction alopecia demonstrated ratios similar to those seen in lichen planopilaris. These cases may represent the recently described "traction alopecia" condition, cicatricial marginal alopecia or changes seen in long-standing lesions, emphasizing the need for inclusion of distribution and duration within the clinical information.
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PMID:Comparison between Langerhans cell concentration in lichen planopilaris and traction alopecia with possible immunologic implications. 2151 39