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3 ungesichtete Fragmente: Plagiat

[1.] Mag/Fragment 069 10 - Diskussion
Bearbeitet: 8. May 2017, 21:40 (Graf Isolan)
Erstellt: 8. May 2017, 21:39 Graf Isolan
Fragment, Holt 2000, KomplettPlagiat, Mag, SMWFragment, Schutzlevel, ZuSichten

Typus
KomplettPlagiat
Bearbeiter
Graf Isolan
Gesichtet
No.png
Untersuchte Arbeit:
Seite: 69, Zeilen: 10-24
Quelle: Holt 2000
Seite(n): S151, Zeilen: left col. 13-15, 20-27, 32-42
4.4 Antigen presentation in the lung

The epithelial surfaces of the lungs and conducting airways are continuously exposed to mixtures of antigens present in ambient air. The adaptive immune system in the lung is faced with the task of accurately categorizing these stimuli, such that T cell responses that are qualitatively appropriate for neutralization of each agent are selected. Secondarily, it must tightly control the intensity and duration of these responses, in order to preserve the integrity of the fragile, highly vascularized epithelial surfaces in the organ, particularly those at which gas exchange occurs.

The epithelial surfaces within the major conducting airways in which the majority of inhaled antigen is deposited are protected via the scrubbing action of the overlying mucociliary escalator, and the small proportion of inhaled antigen that escapes this mechanism and penetrates into the underlying epithelial layer is then dealt with via specialized antigen-presenting cells (APC), in particular Dendritic cell (DC) populations, within and below the epithelium. The alveolar surfaces in the deep lung are policed instead by macrophage populations, again backed up to APC population below the alveolar epithelium.

[page S151]

The epithelial surfaces of the lungs and conducting airways are continuously exposed to mixtures of antigens present in ambient air. [...] The adaptive immune system in the lung is faced with the task of accurately categorizing these stimuli, such that T cell responses that are qualitatively appropriate for neutralization of each agent are selected. Secondarily, it must tightly control the intensity and duration of these responses, in order to preserve the integrity of the fragile, highly vascularized epithelial surfaces in the organ, particularly those at which gas exchange occurs.

[...] The epithelial surfaces within the major conducting airways in which the bulk of inhaled antigen is deposited are protected via the scrubbing action of the overlying mucociliary escalator, and the small proportion of inhaled antigen that escapes this mechanism and penetrates into the underlying epithelial layer is then dealt with via specialized antigen-presenting cells (APCs), in particular dendritic cell (DC) populations, within and below the epithelium. The alveolar surfaces in the deep lung are policed instead by macrophage populations, again backed up by APC populations below the alveolar epithelium.

Anmerkungen

No source given, nothing has been marked as a citation.

These paragraphs are not part of the 2017 Erratum of Mag.

Sichter
(Graf Isolan)

[2.] Mag/Fragment 007 01 - Diskussion
Bearbeitet: 8. May 2017, 23:25 (Graf Isolan)
Erstellt: 8. May 2017, 23:09 Graf Isolan
Bingisser and Holt 2001, Fragment, Mag, SMWFragment, Schutzlevel, Verschleierung, ZuSichten

Typus
Verschleierung
Bearbeiter
Graf Isolan
Gesichtet
No.png
Untersuchte Arbeit:
Seite: 7, Zeilen: 1-9
Quelle: Bingisser and Holt 2001
Seite(n): 172, Zeilen: right col. 30-36, 41-46
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.

Anmerkungen

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.

Sichter
(Graf Isolan)

[3.] Mag/Fragment 006 12 - Diskussion
Bearbeitet: 18. May 2017, 22:18 (Graf Isolan)
Erstellt: 18. May 2017, 22:16 Graf Isolan
Bingisser and Holt 2001, Fragment, KomplettPlagiat, Mag, SMWFragment, Schutzlevel, ZuSichten

Typus
KomplettPlagiat
Bearbeiter
Graf Isolan
Gesichtet
No.png
Untersuchte Arbeit:
Seite: 6, Zeilen: 12-17
Quelle: Bingisser and Holt 2001
Seite(n): 172, Zeilen: left col. 5-7 - right col. 1-7
Most of the clearance of small inhaled particles and microorganisms reaching the periphery of the lung relies on the phagocytic system (Jonsson et al., 1985). Macrophages are the primary phagocytes in the healthy lung. The macrophages interact with other cells and molecules through the release of numerous secretory products and the expression of several surface receptors (Delacourt et al., 1997).

Delacourt C, Harf A, Lafuma C. Developmental aspects of alveolar macrophage functions involved in pulmonary defenses. Pediatr Pulmonol Suppl. 1997; 16: 211-2. Review.

Jonsson S, Musher DM, Chapman A, Goree A, Lawrence EC. Phagocytosis and killing of common bacterial pathogens of the lung by human alveolar macrophages. J Infect Dis. 1985 Jul; 152 (1): 4-13.

Most of the clearance of small inhaled particles and microorganisms reaching the periphery of the lung relies on the phagocytic system [6]. Macrophages are the primary phagocytes in the healthy lung. They reside in the interstitial spaces of the bronchi and alveoli, in the vascular compartment, and in the alveolus. Through the release of numerous secretory products and the expression of several surface receptors the macrophages interact with other cells and molecules [7].

6 Jonsson S, Musher DM, Chapman A, Goree A, Lawrence EC. Phagocytosis and killing of common bacterial pathogens of the lung by human alveolar macrophages. J Infect Dis 1985; 152:4–13.

7 Delacourt C, Harf A, Lafuma C. Developmental aspects of alveolar macrophage functions involved in pulmonary defenses. Pediatr Pulmonol Suppl 1997;16:211–2.

Anmerkungen

No source given, nothing has been marked as a citation though the paragraphs are mostly identical.

These paragraphs are not part of the 2017 Erratum of Mag.

Sichter
(Graf Isolan)

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