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Crosstalk between autoreactive T cells and alveolar type II epithelial cells in inflammation and tolerance

von Dr. Marcus Gereke

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[1.] Mag/Fragment 012 01 - Diskussion
Zuletzt bearbeitet: 2014-03-16 20:38:16 WiseWoman
BauernOpfer, Fehrenbach 2001, Fragment, Gesichtet, Mag, SMWFragment, Schutzlevel sysop

Typus
BauernOpfer
Bearbeiter
Hindemith
Gesichtet
Yes
Untersuchte Arbeit:
Seite: 12, Zeilen: 1-19
Quelle: Fehrenbach 2001
Seite(n): 33, 38, 39, 40, Zeilen: 33: 18-19; 38: r.col: last lines; 39: 1ff: 40: l.col: 26ff
The alveolar epithelium can be classified as a continuously renewing tissue since it comprises a population of alveolar type II epithelial cells that are characterized by almost unlimited potential to proliferate. It is still a matter of debate whether all AECII or only a small population act as the alveolar epithelial stem cell population (Uhal, 1997). The concept of AECII as stem cells of the adult alveolar epithelium was proposed by Kapanci and colleagues, and is widely accepted today (Kapanci et al., 1969). During ontogenesis, the AECII may derive from precursor cell common to AECII and Clara cells (Wuenschell et al., 1996). Furthermore AECII proliferate and differentiate to AECI to repair the damaged alveolar epithelium after lung injury or during fetal lung development, thus contributing to epithelial repair, whereas AECI are terminally differentiated, lack mitotic activity, and are easily injured. The programmed cell death or apoptosis is an important mechanism of cell removal or renewing of tissue. AECII are known to express the membrane receptor Fas (CD95, APO-1), the ligation of which may initiate the apoptotic cascade (Fine et al., 1997). This can be achieved by binding of Fas-ligand or the Fas-stimulating antibodies. There is some evidence that apoptosis of AECII is an integral mechanism of alveolar septal modelling in lung morphogenesis (Scavo et al., 1998; Schittny et al., 1998). Notably, apoptotic AECII appeared to be removed not only by alveolar macrophages but also by AECII cell neighbours (Fehrenbach et al., 2001).

Fehrenbach H. Alveolar epithelial type II cell: defender of the alveolus revisited. Respir Res. 2001; 2 (1): 33-46. Epub 2001 Jan 15. Review.

Fine A, Anderson NL, Rothstein TL, Williams MC, Gochuico BR. Fas expression in pulmonary alveolar type II cells. Am J Physiol. 1997 Jul; 273 (1Pt1): L64-71.

Kapanci Y, Weibel ER, Kaplan HP, Robinson FR. Pathogenesis and reversibility of the pulmonary lesions of oxygen toxicity in monkeys. II. Ultrastructural and morphometric studies. Lab Invest. 1969 Jan; 20 (1): 101-18.

Scavo LM, Ertsey R, Chapin CJ, Allen L, Kitterman JA. Apoptosis in the development of rat and human fetal lungs.Am J Respir Cell Mol Biol. 1998 Jan; 18 (1): 21-31.

Schittny JC, Djonov V, Fine A, Burri PH. Programmed cell death contributes to postnatal lung development. Am J Respir Cell Mol Biol. 1998 Jun; 18 (6): 786-93.

Uhal BD. Cell cycle kinetics in the alveolar epithelium. Am J Physiol. 1997 Jun; 272 (6Pt1): L1031-45. Review.

Wuenschell CW, Sunday ME, Singh G, Minoo P, Slavkin HC, Warburton D. Embryonic mouse lung epithelial progenitor cells co-express immunohistochemical markers of diverse mature cell lineages. J Histochem Cytochem. 1996 Feb; 44 (2): 113-23.

[page 33, Abstract]

AE2 cells proliferate, differentiate into AE1 cells, and remove apoptotic AE2 cells by phagocytosis, thus contributing to epithelial repair.

[page 38]

The alveolar epithelium can be classified as a continuously renewing tissue since it comprises a population of cells

[page 39]

(AE2) that are characterised by the almost unlimited potential to proliferate. [...] It is still a matter of debate whether all AE2 cells or only a subpopulation act as the alveolar epithelial stem cell population (for review, see [103]).

[...]

The concept of the AE2 cell as a stem cell of the adult alveolar epithelium was proposed by Kapanci and coworkers [108], and is widely accepted today (for review, see [103]). During ontogenesis, the AE2 cell may derive from a precursor cell common to AE2 and Clara cells [109].

[page 40]

One important mechanism of cell removal that was recognised almost a century ago [129] is programmed cell death or apoptosis [130]. [...] AE2 cells are known to express the membrane receptor Fas (CD95, APO-1), ligation of which may initiate the apoptotic cascade [134]. This can be achieved by binding of Fasligand or the Fas-stimulating antibodies. There is some evidence that apoptosis of AE2 cells is an integral mechanism of alveolar septal modelling in lung morphogenesis [135,136].

[...]

Notably, apoptotic AE2 cells (Fig. 6) appeared to be removed not only by alveolar macrophages but also by AE2 cell neighbours [138].


103. Uhal BD: Cell cycle kinetics in the alveolar epithelium. Am J Physiol 1997, 272:L1031–1045.

108. Kapanci Y, Weibel ER, Kaplan HP, Robinson FR: Pathogenesis and reversibility of the pulmonary lesions of oxygen toxicity in monkeys. II. Ultrastructural and morphometric studies. Lab Invest 1969, 20:101–117.

109. Wuenschell CW, Sunday ME, Singh G, Minoo P, Slavkin HC, Warburton D: Embryonic mouse lung epithelial progenitor cells coexpress immunohistochemical markers of diverse mature cell lineages. J Histochem Cytochem 1996, 44:113–123.

129. Gräper L: A new point of view regarding the physiological elimination of cells [in German]. Arch Zellforsch 1914, 12:373–394.

130. Rich T, Watson CJ, Wyllie A: Apoptosis: the germs of death. Nat Cell Biol 1999, 1:E69–71.

134. Fine A, Anderson NL, Rothstein TL, Williams MC, Gochuico BR: Fas expression in pulmonary alveolar type II cells. Am J Physiol 1997, 273:L64–71.

135. Scavo LM, Ertsey R, Chapin CJ, Allen L, Kitterman JA: Apoptosis in the development of rat and human fetal lungs. Am J Respir Cell Mol Biol 1998, 18:21–31.

136. Schittny JC, Djonov V, Fine A, Burri PH: Programmed cell death contributes to postnatal lung development. Am J Respir Cell Mol Biol 1998, 18:786–793.

138. Fehrenbach H, Kasper M, Koslowski R, Tan P, Schuh D, Müller M, Mason RJ: Alveolar epithelial type II cell apoptosis in vivo during resolution of keratinocyte growth factor-induced hyperplasia in the rat. Histochem Cell Biol 2000, 114:49–61.

Anmerkungen

On the last line the author gives "Fehrenbach et al., 2001" for the statement "Notably, apoptotic AECII appeared to be removed not only by alveolar macrophages but also by AECII cell neighbours". The author might either mean Fehrenbach et al. (2000), which is the reference for this statement in the source, or he means Fehrenbach (2001), which is the only publication with Fehrenbach as first author listed in the bibliography. In either case, it does not become clear to the reader that the whole passage is adapted from the source.

Sichter
(Hindemith), WiseWoman



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