Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0033036 (APC)
 10,214 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Undoubtedly, synovitis is a cell-mediated process involving various cell types, such as T cells, B cells, APC, monocytes/macrophages, synoviocytes, chondrocytes, and cytokines. Therefore, it is difficult to clarify the cell type that plays the central role in the inflammatory process. Despite this difficulty, there is strong evidence that T cells mediate the disease in collaboration with APC that bear specific antigenic peptides. The mediators released could perpetuate an ongoing inflammatory process in the joints irrespective of the nature of the initiating agents. Therefore, many approaches to a more specific immunotherapy for RA have been developed, directed toward the modulation of T cell function. Thus far, various forms of chemical and biologic treatment have been used, such as cyclosporin A and monoclonal antibodies directed against T-cell epitopes and IL-2 receptor, with some beneficial effects on the course of RA. The development of a more specific immunotherapy using reagents directed against the T-cell receptor and vaccination with specific T cells await further studies, since we still do not know the inciting antigen(s) in RA. Nevertheless, we are hopeful that the ongoing search for the still unknown antigen(s) will be successful, thus providing new and better treatment regimens for a still uncurable disease.
Adv Prostaglandin Thromboxane Leukot Res 1994
PMID:Basic mechanisms in rheumatoid arthritis: the role of T lymphocytes in rheumatoid synovitis. 777 43

We showed previously that dietary eicosapentaenoic acid [EPA, 20:5(n-3)] is antitumorigenic in the APC:(Min/+) mouse, a genetic model of intestinal tumorigenesis. Only a few studies have evaluated the effects of dietary fatty acids, including EPA and docosahexaenoic acid [DHA, 22:6(n-3)], in this animal model and none have evaluated the previously touted antitumorigenicity of alpha-linolenic acid [ALA, 18:3(n-3)], conjugated linoleic acid [CLA, 77% 18:2(n-7)], or gamma-linolenic acid [GLA, 18:3(n-6)]. Stearidonic acid [SDA, 18:4(n-3)], the Delta6-desaturase product of ALA, which is readily metabolized to EPA, has not been evaluated previously for antitumorigenic efficacy. This study was undertaken to evaluate the antitumorigenicity of these dietary fatty acids (ALA, SDA, EPA, DHA, CLA and GLA) compared with oleic acid [OA, 18:1(n-9)] at a level of 3 g/100 g in the diets of APC:(Min/+) mice and to determine whether any alterations in tumorigenesis correspond to alterations in prostaglandin biosynthesis. Tumor multiplicity was significantly lower by approximately 50% in mice fed SDA or EPA compared with controls, whereas less pronounced effects were observed in mice fed DHA (P: = 0.15). ALA, CLA and GLA were ineffective at the dose tested. Although lower tumor numbers coincided with significantly lower prostaglandin levels in SDA- and EPA-fed mice, ALA and DHA supplementation resulted in equally low prostaglandin levels, despite proving less efficacious with regard to tumor number. Prostaglandin levels did not differ significantly in the CLA and GLA groups compared with controls. These results suggest that SDA and EPA attenuate tumorigenesis in this model and that this effect may be related in part to alterations in prostaglandin biosynthesis.
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PMID:Highly unsaturated (n-3) fatty acids, but not alpha-linolenic, conjugated linoleic or gamma-linolenic acids, reduce tumorigenesis in Apc(Min/+) mice. 1101 69