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)

In lymphoproliferative diseases of the skin, DC have a key role in T- and B-cell homing. Furthermore, DC alterations may have a pathogenic role in the natural history of specific disorders, either in the neoplastic lymphoid cell progression or in antitumoral lymphocyte reaction. Finally, the morphoantigenic and topographic features of DC may have diagnostic and histogenetic relevance in specific conditions. In CTCL, dermal CD1a+ DC ("indeterminate cells") seem to play a significant role in the neoplastic progression of MF, whereas the possible pathogenetic role of specific alterations of epidermal LC is yet to be proven. Recently, a possible implication of DD (resident, perivascular factor XIIIa+/CD1a- DC) in the pathogenesis of MF has been also suggested. The presence and possible significance of DC in CTCL non-MF are presently poorly studied. At present, DC number, distribution, and phenotype seem possibly useful in the differential diagnosis between CTCL and pseudo-CTCL, but this hypothesis has to be adequately confirmed. CBCL has been recently proposed as a unique type of clinically low-grade lymphoma, namely, skin-associated lymphoid tissue (SALT)-related B-cell lymphoma. Both SALT- and mucosa-associated lymphoid tissue (MALT)-related B-cell lymphoma share with a peculiar nodal lymphoma of follicle mantle origin (parafollicular-monocytoid lymphoma) the nonaggressive clinical behavior and the uniform phenotype (CD5-, CD10-) and genotype (lack of bcl-2 gene rearrangement) of neoplastic B cells, despite the wide variability of cytomorphologic appearances. The putative origin of CBCL is further supported by the typical CD14-, nerve growth factor receptor (NGFr)+ immunophenotype of DRC. Moreover, the immunophenotype and architectural fashion of DRC are interesting clues to the differentiation between neoplastic and true reactive folliclelike nodules and may be of help in the differential diagnosis between CBCL and B-cell pseudolymphoma as well as in the correct interpretation of lesions showing monoclonal proliferations of B cells accompanied by polyclonal follicular reactions.
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PMID:Dendritic cells in T- and B-cell proliferation in the skin. 804 37

We aimed to investigate the profile of the inflammatory infiltrate in lesional and nonlesional tissue in alopecia areata (AA) and look for possible associations between inflammatory mechanisms, neuropeptide expressions, and various clinical features. Twenty-four patch-type AA patients were included. Forty-eight lesional and nonlesional skin samples were stained immunohistochemically with antibodies for CD1a, CD3, CD4, CD8, CD20, CD57 (for natural killer cells), mast cell tryptase, nerve growth factor receptor (NGFR), and substance P (SP). Various clinical findings were recorded. Psychological distress levels and stress-related hormones were measured. Lesional skin showed statistically more CD3(+), CD8(+), and CD57(+) lymphocytes, mast cells, Langerhans cells, and more prominent immunoreactivities of NGFR and SP (P < 0.003). Most nonlesional skin showed CD3(+) and CD57(+) cells, mast cells, and NGFR(+) nerve fibers. NGFR and SP, and SP and perivascular mast cell infiltrates were correlated, whereas peribulbar mast cells and anagen follicle counts were inversely correlated in nonlesional skin (P < 0.05). Near half of the patients' distress levels were high. No relationship among biochemical, psychological, and clinical parameters could be shown. AA may involve the entire skin in which lesions occur as a result of local T cell-mediated cytotoxic inflammatory response initiated by Langerhans cells and mast cells activated via neuropeptides.
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PMID:Investigation of the inflammatory mechanisms in alopecia areata. 1915 26

An increase in S100 protein-positive cells has been reported in inflammatory bowel diseases, mainly Crohn disease. These cells were interpreted as myeloid-derived dendritic cells, chiefly in follicular areas. We were prompted to assess the nature of these cells in interfollicular areas of inflamed colonic mucosa in ulcerative colitis and study their involvement in tumor necrosis factor alpha production, the main inflammatory cytokine in ulcerative colitis. The number and distribution of cells expressing S100 protein, nerve growth factor receptor, CD68, CD1a, CD83, and calretinin were studied in samples from 16 patients with active ulcerative colitis using simple and double immunohistochemistry. Then, the localization in S100 protein-positive cells of (1) tumor necrosis factor alpha, (2) its sheddase A disintegrin and metalloprotease-17, and (3) the receptors TNFR1 was assessed using double immunofluorescence followed by confocal microscopy. In active ulcerative colitis, there was an increased number in S100 protein-positive cells in interfollicular areas of colonic mucosa compared with quiescent ulcerative colitis, nonulcerative colitis, or normal mucosa. All S100 protein-positive cells ensheathed calretinin-positive axons, indicating their Schwann cell origin. No CD1a- or CD83-positive dendritic cells were detected. Double immunofluorescence studies showed that in normal colon, Schwann cells of the mucosa and submucosal plexuses weakly expressed A disintegrin and metalloprotease-17 but did not express tumor necrosis factor alpha. By contrast, in active ulcerative colitis, they expressed both A disintegrin and metalloprotease-17 and tumor necrosis factor alpha. Schwann cells as well as calretinin-positive axons strongly expressed TNFR1. This study shows (1) a Schwann cell proliferation in the inflamed colonic mucosa during active ulcerative colitis and (2) that Schwann cells produce tumor necrosis factor alpha. Tumor necrosis factor alpha is thus likely to stimulate Schwann cell proliferation through an autocrine/paracrine mechanism.
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PMID:In situ evidence of involvement of Schwann cells in ulcerative colitis: autocrine and paracrine signaling by A disintegrin and metalloprotease-17-mediated tumor necrosis factor alpha production. 1937 60