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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 029 01 - Diskussion
Zuletzt bearbeitet: 2014-03-10 18:07:19 Graf Isolan
Bluestone Abbas 2003, Fragment, Gesichtet, Mag, SMWFragment, Schutzlevel sysop, Verschleierung

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Seite: 29, Zeilen: 1ff (entire page)
Quelle: Bluestone_Abbas_2003
Seite(n): 254, Zeilen: col. 1: 14-28, 42-46 - col 2: 1-2, 9-34, 38-44
[However, it is possible that these self proteins are expressed at low levels and, additionally, by only some of the epithelial] cells, making clonal deletion a rather ineffective means of inducing tolerance to peripheral antigens. An alternative mechanism of inducing self tolerance in the thymus might be the localized antigen presentation, resulting in a more robust regulation of autoreactivity. Once generated, the thymic Treg cells are exported in the peripheral tissues, where they may function normally to prevent the activation of other, self reactive T cells that have the potential of developing into effector cells (Salomon et al., 2000).

These regulatory T cells were described as a “normal” population of suppressor cells, because they are always present in normal individuals and carry out their regulatory function during normal surveillance of self-antigens. Furthermore, because of their development in the thymus, the natural regulatory T cells are expected to be specific for self-antigens.

Recent studies indicate that CD28 controls both thymic development and peripheral homeostasis of natural Treg cells. Ligation of CD28 is expected to act at two stages during Treg cell development (Boden et al., 2003). In addition, once the natural Treg cells emerge from the thymus, costimulation through CD28 is required to maintain a stable pool of these cells in the periphery by promoting their self renewal through homeostatic proliferation and by supporting their survival (Boden et al., 2003; Salomon et al., 2000). The development and maintenance functions of CD28 are not mediated through IL-2. It is possible that signalling through CD28 stimulates the production of a response to an yet unknown cytokine that functions as a growth and survival factor of these cells. The absence of CD80/CD86 or CD28 results in a reduction of the number of regulatory cells in peripheral lymphoid tissues and an unexpected exacerbation of natural Treg cells, which plays an important role controlling autoimmunity (Lenschow et al., 1996; Salomon et al., 2000).

However, it is probable that these self-proteins are expressed at low levels and by only some of the epithelial cells, making clonal deletion a rather ineffective means of inducing tolerance to peripheral antigens. An alternative mechanism of inducing self-tolerance in the thymus might be the generation of TReg cells in response to this localized antigen presentation, resulting in a more robust regulation of autoreactivity. Once generated, the thymic TReg cells are exported to peripheral tissues, where it is proposed that they function normally to prevent the activation of other, self-reactive T cells that have the potential of developing into effector cells9. [...] We refer to these regulatory cells as a ‘natural’ population, because they are always present in normal individuals and carry out their regulatory function during normal surveillance of self-antigens. Furthermore, because these TReg cells develop in the thymus, they are likely to be specific for self-antigens. [...]

Recent studies indicate that CD28 controls both thymic development and peripheral homeostasis of the natural TReg cells. Ligation of CD28 is likely to act at two stages during TReg-cell development13. Strong antigenic signals are required for the generation of natural TReg cells in the thymus14; therefore, a combination of TCR ligation and maximal co-stimulation might be required for these cells to develop from their immature precursors. In addition, once the natural TReg cells emerge from the thymus, co-stimulation through CD28 is required to maintain a stable pool of the cells in the periphery by promoting their self-renewal through homeostatic proliferation and by supporting their survival9,13. The development and maintenance functions of CD28 are not mediated through interleukin-2 (IL-2), IL-15 or its receptor (IL-15R), the anti-apoptotic molecule BCL-XL or OX40 (Q. Tang and J.A.B., unpublished observations). It is possible that signals through CD28 stimulate the production of and responses to an as yet unknown cytokine(s) that functions as a growth and survival factor for these cells. [...] The absence of CD80/CD86 or CD28 results in a reduction of the number of regulatory cells in peripheral lymphoid tissues and an unexpected exacerbation of autoimmunity owing to the absence of natural TReg cells, which are essential to control autoimmunity9,15.


9. Salomon, B. et al. B7/CD28 costimulation is essential for the homeostasis of the CD4+CD25+ immunoregulatory T cells that control autoimmune diabetes. Immunity 12, 431–440 (2000).

13. Boden, E., Tang, Q., Bour-Jordan, H. & Bluestone, J. A. in Novartis Foundation Symposium 252. Generation and Effector Functions of Regulatory Lymphocytes (Wiley, Europe) (in the press).

14. Bensinger, S. J., Bandeira, A., Jordan, M. S., Caton, A. J. & Laufer, T. M. Major histocompatibility complex class-IIpositive cortical epithelium mediates the selection of CD4+CD25+ immunoregulatory T cells. J. Exp. Med. 194, 427–438 (2001).

15. Lenschow, D. et al. CD28/B7 regulation of TH1 and TH2 subsets in the development of autoimmune diabetes. Immunity 5, 285–293 (1996).

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Sichter
Schumann


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