Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

T-cell subsets extracted from chronically inflamed periodontal tissues were identified using monoclonal antibodies, and their functional activity was analysed using the autologous mixed lymphocyte reaction (AMLR). Tissue was obtained from a total of 33 adult periodontitis (AP) patients and 6 normal/marginal gingivitis (N/MG) patients. All AP patients had received repeated oral hygiene instruction and root planing prior to the surgery, and the majority (30 out of 33) had at least one site with greater than 6 mm loss of attachment from the cementoenamel junction within the surgical field. The N/MG patients had no loss of attachment, and probing depths were less than 3 mm. Single cell suspensions were obtained following collagenase digestion (90 minutes at 37 degrees C) and mechanical disruption of the tissue. T-cell subsets were identified using an indirect immunofluorescence assay on cells obtained from 19 AP patients and the 6 N/MG patients. The mean (+/- standard error) helper:suppressor (T4:T8) ratio for the AP patients was found to be 0.94 +/- 0.48 compared with 1.65 +/- 0.16 for the N/MG group and 1.51 +/- 0.12 for peripheral blood controls. HLA-DR positive macrophages were identified and were found to include both acid phosphatase (AcP) positive and adenosine triphosphatase (ATPase) positive populations. Functional analysis was carried out using cells extracted from the remaining 14 AP patients. Cells from six of these 14 patients were found to be capable of spontaneous proliferation. Co-culture experiments using autologous T and non-T populations revealed that cells from only four patients were able to respond in an AMLR while those from only one of the 14 patients were able to stimulate the AMLR.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phenotypic and functional analysis of T cells extracted from chronically inflamed human periodontal tissues. 295 90

Immunohistological analysis of experimental gingivitis in humans was carried out to provide a baseline for the study of immunoregulatory mechanisms in chronic inflammatory periodontal disease. Using a panel of monoclonal antibodies in an avidin biotin immunoperoxidase technique, T cell subsets were identified and the pattern of Class II major histocompatibility complex (MHC) antigens determined. Twenty third-year dental students took part in the study. Following the cessation of oral hygiene procedures, gingival biopsies were taken from each of five students at days 0, 4, 8 and 21 during the development of the inflammatory lesion. Each student had one biopsy which healed uneventfully. The T4:T8 ratio showed only slight variation over the time course of the lesion varying from 2.18:1 at day 0 to 2.48:1 at day 4. At all stages the T cells displayed both HLA-DR and HLA-DQ antigens, but less than 10% had detectable IL-2 receptors. The predominant macrophage population was acid phosphatase + ve, adenosine triphosphatase -ve, HLA-DR+ and HLA-DQ+ antigens suggesting an activated phagocytic population. During the development of the lesion, the number of intraepithelial Langerhans cells (T6+) increased but there appeared to be a discrepancy between HLA-DR and HLA-DQ expression on these cells. Similarly, the keratinocytes expressed HLA-DR but failed to express HLA-DQ at any stage. These results suggest that the developing gingival lesion is a well controlled lesion and follows a similar pattern to a controlled delayed type hypersensitivity (DTH) response.
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PMID:Immunohistological analysis of experimental gingivitis in humans. 328 Jan 78