Journal ArticleDOI
Indomethacin-responsive mononuclear cell dysfunction in “atypical” mycobacteriosis
TLDR
The hypothesis that some patients with “atypical” mycobacterial disease have abnormal immunoregulation which may be mediated by an imbalance of the metabolic products of arachidonic acid, an abnormality similar to that noted in Hodgkin's disease and chronic coccidioidomycosis is supported.About:
This article is published in Cellular Immunology.The article was published on 1982-07-15. It has received 29 citations till now. The article focuses on the topics: Cellular immunity & Phenidone.read more
Citations
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Regulation of the immune response by prostaglandins
James S. Goodwin,Jan Ceuppens +1 more
TL;DR: Of all the arachidonic acid metabolites, only prostaglandin E (PGE) has been shown to have a clear role in the regulation of cellular and humoral immune responses.
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Current concepts: immunology. Monocytes and macrophages.
TL;DR: Macrophages play a central and essential part in the immune response by presenting antigen to lymphocytes during the development of specific immunity and by serving as supportive, "accessory" cells...
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The immunology of mycobacterial diseases.
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Disease due to Mycobacterium avium-intracellulare.
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Macrophage-T cell interaction in experimental mycobacterial infection. Selective regulation of co-stimulatory molecules on Mycobacterium-infected macrophages and its implication in the suppression of cell-mediated immune response.
TL;DR: The results demonstrate that upon mycobacterial infection, the macrophages are rendered incapable of delivering the co‐stimulatory signals to T helper cells, possibly due to the involvement of prostaglandin, as inhibition of its biosynthesis by indomethacin reversed the defect.
References
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Journal ArticleDOI
Suppression of human T-cell mitogenesis by prostaglandin. Existence of a prostaglandin-producing suppressor cell.
TL;DR: PGE inhibits PHA- and Con A-stimulated cultures much better than PWM cultures, suggesting a differential effect of PGE on T-cell vs. B-cell function.
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Prostaglandins, arachidonic acid, and inflammation
TL;DR: The discovery and biological activities of thromboxane A2 and prostacyclin as well as a destructive oxygen-centered radical as additional products of this biosynthetic pathway now require these to be considered as potential inflammatory mediators.
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Prostaglandin-Producing Suppressor Cells in Hodgkin's Disease
James S. Goodwin,Ronald P. Messner,Arthur D. Bankhurst,Glenn T. Peake,John H. Saiki,Ralph C. Williams +5 more
TL;DR: A glass-adherent, prostaglandin-producing suppressor cell is responsible for the hyporesponsiveness to phytohemagglutinin seen with Hodgkin-disease lymphocytes.
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Lipoxygenation of arachidonic acid as a source of polymorphonuclear leukocyte chemotactic factors in synovial fluid and tissue in rheumatoid arthritis and spondyloarthritis.
TL;DR: An involvement of the potent chemotactic factors 5-HETE and leukotriene B4 in human inflammatory disease is suggested.