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)

Adipose tissue is reported to contain monocyte-like pre-adipocytes, which may mature into macrophages, contributing to local inflammation. Dendritic cells (DC) can be derived from monocytes and initiate and regulate primary immune responses. We hypothesized, therefore, that adipose tissue may provide DC involved in local immune activity. To test this, we studied cells from human omental adipose tissue samples from 17 patients with benign gynecological disease. The hypothesis that adipose tissue DC are involved in inflammatory disease was tested by comparing these cells with those from 18 patients with Crohn's disease, where hypertrophy of adipose tissue suggests involvement in disease. A high proportion of the 1.33 +/- 0.12 x 10(5) CD45-positive cells/mg, obtained from control omenta, expressed CD11c, CD1a, and CD83; costimulatory molecules CD40, CD80, and CD86; and major histocompatibility complex (MHC) Class II but little CD14, CD16, or CD33. Omental cells showing morphological characteristics of DC were also observed. Metrizamide gradient-enriched DC from these populations were potent stimulators of primary proliferation of allogeneic T cells in mixed leukocyte reactions. Increased numbers of CD45+ cells from omentum of Crohn's patients (4.50+/-1.08 x 10(5) CD45+ cells/mg) contained higher percentages of CD11c+ and CD40+ cells (80.8+/-3.8% vs. 63.4+/-6, P=0.032; 77.9+/-4% vs. 58.8+/-6.5, P=0.029, respectively), but MHC Class II and stimulatory capacity were almost completely lost (P= <0.001), suggesting innate activation but lost capacity to stimulate adaptive immune responses. Granulocytes were also present amongst the omental cells from Crohn's patients. Results indicated that omentum may provide DC, which could "police" local infections and contribute to and/or reflect local inflammatory activity.
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PMID:Adipose tissue of human omentum is a major source of dendritic cells, which lose MHC Class II and stimulatory function in Crohn's disease. 1682 53

Dendritic cells (DCs) are key cells in innate and adaptive immune responses that determine the pathophysiology of Crohn's disease. Intestinal DCs migrate from the mucosa into mesenteric lymph nodes (MLNs). A number of different markers are described to define the DC populations. In this study we have identified the phenotype and localization of intestinal and MLN DCs in patients with Crohn's disease and non-IBD patients based on these markers. We used immunohistochemistry to demonstrate that all markers (S-100, CD83, DC-SIGN, BDCA1-4, and CD1a) showed a different staining pattern varying from localization in T-cell areas of lymph follicles around blood vessels or single cells in the lamina propria and in the MLN in the medullary cords and in the subcapsular sinuses around blood vessels and in the T-cell areas. In conclusion, all different DC markers give variable staining patterns so there is no marker for the DC.
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PMID:Dendritic cell populations in colon and mesenteric lymph nodes of patients with Crohn's disease. 1804 77

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