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)

We present an immunohistochemical study of accessory cells in acute appendicitis and ulcerative colitis (UC). By comparing these two diseases, it is possible to distinguish between changes associated with inflammatory bowel disease and those resulting from nonspecific intestinal inflammation. Nine total colectomy specimens from patients with UC, in which the appendix was also involved, were compared with nine cases of acute appendicitis. Accessory cells were stained for CD68 (PGMI), ACPI (acid cysteine proteinase inhibitor), S100 protein, MAC387 (calgranulin), CD1a, factor XIIIa, and WR18 (HLA class II). In ulcerative colitis, but not acute appendicitis, there was extension of a network of S100 positive dendritic cells into the crptal mucosa, and these S100-positive dendritic cells were closely aligned with the epithelium. The epithelium in UC, but not in acute appendicitis, showed intense upregulation of HLA class II, and this was particularly marked at the crypt bases. Dendritic, MAC387-positive cells were seen only in UC. In both diseases there were abundant ACPI-positive accessory cells in the cryptal areas, a population normally restricted to the dome areas. Factor XIIIa- and PGM1-positive cells, although abundant in both conditions, had distributions similar to those that we had previously shown in normal controls. No CD1a-positive cells were identified in either UC or acute appendicitis. We hypothesize that S100 identifies a subpopulation of activated macrophages. The concentration of this subpopulation, in close contact with the epithelium, which also shows altered expression of HLA class II antigens, suggests that a component of the immune response is targeting this area in UC. In addition, we also suggest that the identification of MAC387-positive dendritic cells in UC reflects increased macrophage turnover in inflammatory bowel disease.
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PMID:The accessory cell populations in ulcerative colitis: a comparison between the colon and appendix in colitis and acute appendicitis. 904 93

M cells are found in intestinal follicle associated epithelium. Studies into the physiological and pathological roles of human M cells have been hampered by the lack of well-substantiated, specific markers for these cells. A critical literature review suggests the following molecules may potentially serve as such markers: CK7, FcaR (CD89), S100, CD1a, CD21, CD23, sialyl Lewis A, and cathepsin E. Normal ileum, appendix and colorectum were studied using paraffin-embedded, formalin-fixed tissue and immunohistochemistry for these 8 markers. Cathepsin E immunohistochemistry was also performed on cases of colorectal adenocarcinoma, colorectal adenoma, colorectal hyperplastic/metaplastic polyp, lymphocytic colitis, collagenous colitis, pseudomembranous colitis and active ulcerative colitis. Of the 8 markers tested, only cathepsin E appeared to be specific to follicle associated epithelium (expressed by cells with and without M cell morphology) and follicular crypt epithelium; this specificity was limited to the colorectum. Focal epithelial expression of cathepsin E was seen in adenocarcinoma, adenoma, hyperplastic/metaplastic polyp, ulcerative colitis and pseudomembranous colitis. In conclusion, cathepsin E is a specific marker of normal colorectal follicle associated epithelium and follicular crypt epithelium though is not specific to M cells within these compartments. None of the other 7 markers studied is exclusively expressed by human M cells.
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PMID:An immunohistochemical study and review of potential markers of human intestinal M cells. 1277 11

The aim of this study was to evaluate the histological localization and phenotypic characteristics of infiltrating dendritic cells (DCs) and to examine the relationship between the degree of DC infiltration and the severity of inflammation in the colonic mucosa in ulcerative colitis (UC). Also explored was the expression of macrophage inflammatory protein-3alpha (MIP-3alpha), and its receptor CC-chemokine receptor 6 (CCR6), to evaluate the significance of immature DCs in the crypt inflammation evident in UC. There was a significant positive correlation between the number of infiltrating DCs and the degree of crypt inflammation, mononuclear cell infiltration, crypt atrophy, and comprehensive active inflammation. No significant correlation between the number of S-100 protein(+) cells and the severity of crypt atrophy was found. S-100 protein(+), MIP-3alpha(+), and CCR6(+) cells were frequently localized in or around the crypt with inflammation. MIP-3alpha(+) neutrophils and S-100 protein(+) CCR6(+) cells with dendritic morphology were detected in or around the crypt inflammation. Both S-100 protein(+) DCs and CCR6(+) cells were frequently clustered in the surface mucosa beneath the surface epithelium when the crypt was not inflamed. CD1a(+) Langerhans-cell-type DCs were not found in any of the tissues examined. These data indicate that DCs participate not only in chronic inflammation but also in active crypt inflammation.
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PMID:Correlation of dendritic cell infiltration with active crypt inflammation in ulcerative colitis. 1717 54

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