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| The factors involved in T cell and DC downmodulation by AM are partly known: In mice, nitric oxide (NO) produced by AM is the major source of this immunomodulation (Strickland et al., 1996). Several other immunomodulating factors produced by AM have been isolated, the most important being prostaglandins and cytokines. Prostaglandin E2 (PGE2) enhances interleukin (IL)-10 transcription and protein production by peripheral blood lymphocyte (Huang et al., 1996) which offers possibilities for potent immunomodulation. Finally, PGE2 has been ascribed as substance deactivating AM and T cell, and it is produced by AM (Kawano et al., 1999).
Huang M, Sharma S, Mao JT, Dubinett SM. Non-small cell lung cancer-derived soluble mediators and prostaglandin E2 enhance peripheral blood lymphocyte IL-10 transcription and protein production. J Immunol. 1996 Dec 15; 157 (12): 5512-20. Kawano T, Ogushi F, Tani K, Endo T, Ohmoto Y, Hayashi Y, Sone S. Comparison of suppressive effects of a new anti-inflammatory compound, FR167653, on production of PGE2 and inflammatory cytokines, human monocytes, and alveolar macrophages in response to endotoxin. J Leukoc Biol. 1999 Jan; 65 (1): 80-6. Strickland D, Kees UR, Holt PG. Regulation of T-cell activation in the lung: alveolar macrophages induce reversible T-cell anergy in vitro associated with inhibition of interleukin-2 receptor signal transduction. Immunology. 1996 Feb; 87 (2): 250-8. |
Nature of the immunomodulating mechanisms exerted by alveolar macrophages
The factors involved in T-cell and DC downmodulation by AM are partly known: In mice, nitric oxide (NO) produced by AM is the major source of this immunomodulation [3]. Several other immunomodulating factors produced by AM have been isolated, the most important being prostaglandins and cytokines. Prostaglandin E2 (PGE2) was the first macrophage-derived immunomodulator to be described. Increased production of PGE2 by monocytes appears to be a pivotal mechanism in post-trauma immunomodulation [13]. PGE2 enhances peripheral blood lymphocyte IL-10 transcription and protein production [14] which per se offers possibilities for potent immunomodulation (see below). Finally, PGE2 has been described as deactivating AM and T-cells, and it is produced by AM [15]. 3 Strickland D, Kees UR, Holt PG. Regulation of T-cell activation in the lung: isolated lung T cells exhibit surface phenotypic characteristics of recent activation including down-modulated T-cell receptors, but are locked into the G0/G1 phase of the cell cycle. Immunology 1996; 87:242–9. 13 Miller-Graziano CL, Szabo G, Griffey K, Mehta B, Kodys K, Catalano D. Role of elevated monocyte transforming growth factor beta (TGF beta) production in posttrauma immunosuppression. J Clin Immunol 1991;11:95–102. 14 Huang M, Sharma S, Mao JT, Dubinett SM. Non-small cell lung cancer-derived soluble mediators and prostaglandin E2 enhance peripheral blood lymphocyte IL-10 transcription and protein production. J Immunol 1996;157:5512–20. 15 Kawano T, Ogushi F, Tani K, Endo T, Ohmoto Y, Hayashi Y, et al. Comparison of suppressive effects of a new anti-inflammatory compound, FR167653, on production of PGE2 and inflammatory cytokines, human monocytes, and alveolar macrophages in response to endotoxin. J Leukoc Biol 1999; 65:80-6. |
No source given, nothing has been marked as a citation. Shortened but mostly identical (up to the references). These paragraphs are not part of the 2017 Erratum of Mag. |
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