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Autor     Jefferey A. Bluestone, Abul K Abbas
Titel    Natural v Adaptive Regulatory T-Cells
Zeitschrift    Nature Reviews
Jahr    2003
Jahrgang    5
Seiten    253-257
ISSN    1474-1733
URL    http://www.nature.com/nri/journal/v3/n3/full/nri1032.html

Literaturverz.   

yes
Fußnoten    yes
Fragmente    7


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[1.] Mag/Fragment 027 21 - Diskussion
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Bluestone Abbas 2003, Fragment, Gesichtet, Mag, SMWFragment, Schutzlevel sysop, Verschleierung

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The two subsets of regulatory T cells might function in different immunological settings, depending on the context of antigen exposure, the nature of the inflammatory response and the T cell receptor (TCR) repertoires of the individual cells. The natural Treg cells are probably most effective at suppressing autoreactive T cell responses locally, in non-inflammatory settings – circumstances in which antigen specific, self limiting reactions are required to achieve a fine homeostatic balance. In contrast, during self-damaging inflammatory reactions to microbes or transplanted tissue, or settings (for example inflammatory bowel disease), adaptive Treg cells might be induced to suppress the pathological immune responses. The two TReg-cell subsets might function in different immunological settings, depending on the context of antigen exposure, the nature of the inflammatory response and the TCR repertoires of the individual cells. We argue that natural TReg cells would be most effective at suppressing autoreactive T-cell responses locally, in non-inflammatory settings — circumstances in which antigen-specific, self-limiting reactions are required to achieve a fine homeostatic balance. By contrast, during self-damaging inflammatory reactions to microbes or transplanted tissue, or in settings of inflammatory autoimmune disease that are more similar to the infectious setting (for example, inflammatory bowel disease), adaptive TReg cells might be induced to suppress the pathological immune responses.
Anmerkungen

No indication of the source.

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Schumann

[2.] Mag/Fragment 028 23 - Diskussion
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The resident regulatory cells that develop in the thymus are generated in a burst of activity during the early stages of fetal and neonatal T cell development (Sakaguchi et al., 2001). They are polyclonal on the basis of diverse TCR usage (Shevach, 2002), and they are potentially capable of recognizing diverse self-antigens.

The promiscuous gene expression of many self tissue-specific proteins in the medullar epithelial cells of the thymus is described as a potential mechanism to ensure central tolerance to peripheral self-antigens, because this self-antigen expression in the thymus might lead, among other things, to the deletion of immature autoreactive T cells (Derbinski et al., 2001). 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.]

[page 253]

The resident regulatory cells that develop in the thymus are generated in a burst of activity during the early stages of fetal and neonatal T-cell

[page 254]

development7. They are polyclonal on the basis of diverse TCR usage3, and they are potentially capable of recognizing diverse self-antigens. Kyewski and colleagues8, have shown that messenger RNA transcripts encoding many tissue-specific proteins are expressed by ‘islands’of medullary epithelial cells in the thymus. It has been proposed that this promiscuous gene expression might be a mechanism to ensure central tolerance to peripheral self-antigens. Self-antigens that are expressed by these medullary epithelial cells in the thymus might delete immature self-reactive T cells. 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.


7. Sakaguchi, S. et al. Immunologic tolerance maintained by CD25+CD4+ regulatory T cells: their common role in controlling autoimmunity, tumor immunity and transplantation tolerance. Immunol. Rev. 182, 18–32 (2001).

3. Shevach, E. M. CD4+CD25+ suppressor T cells: more questions than answers. Nature Rev. Immunol. 2, 389–400 (2002)

8. Derbinski, J., Schulte, A., Kyewski, B. & Klein, L. Promiscuous gene expression in medullary thymic epithelial cells mirrors the peripheral self. Nature Immunol. 2, 1032–1039 (2001).

Anmerkungen

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[3.] Mag/Fragment 029 01 - Diskussion
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[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).

Anmerkungen

No indication of the source.

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Schumann

[4.] Mag/Fragment 030 01 - Diskussion
Zuletzt bearbeitet: 2014-03-10 13:36:04 Hindemith
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4.2 Adaptive regulatory T cells

These cells are generated from mature T cell populations under certain conditions of antigenic stimulation, and they can be induced ex vivo by culturing mature CD4+ T cells with antigen or polyclonal activators in the presence of immunosuppressive cytokines, namely IL-10 (Barrat et al., 2002; Levings et al., 2001). Similar to natural Treg cells, adaptive Treg cells originate from thymus, but they might be derived from classical T cell subsets or natural Treg cells. The level of expression of CD25 by adaptive Treg cell is variable, depending on the disease setting and the site of regulatory activity. Of note, adaptive Treg cells function in vivo in a cytokine dependent manner (Barrat et al., 2002; Chatenoud et al., 1997; Maloy and Powrie, 2001), so that these regulatory T cells are distinguished from natural Treg cells not by their origin (the thymus), but by their requirement for further differentiation as a consequence of exposure to antigen in a distinct immunological context.


Barrat FJ, Cua DJ, Boonstra A, Richards DF, Crain C, Savelkoul HF, de Waal-Malefyt R, Coffman RL, Hawrylowicz CM, O'Garra A. In vitro generation of interleukin 10-producing regulatory CD4(+) T cells is induced by immunosuppressive drugs and inhibited by T helper type 1 (Th1)- and Th2-inducing cytokines. J Exp Med. 2002 Mar 4; 195 (5): 603-16.

Chatenoud L, Primo J, Bach JF. CD3 antibody-induced dominant self tolerance in overtly diabetic NOD mice. J Immunol. 1997 Mar 15 ; 158 (6): 2947-54.

Levings MK, Sangregorio R, Galbiati F, Squadrone S, de Waal Malefyt R, Roncarolo MG. IFN-alpha and IL-10 induce the differentiation of human type 1 T regulatory cells. J Immunol. 2001 May 1; 166 (9): 5530-9.

Maloy KJ, Powrie F. Regulatory T cells in the control of immune pathology. Nat Immunol. 2001 Sep; 2 (9): 816-22. Review.

Adaptive regulatory T cells. Additional populations of regulatory cells have been described in many settings of immunity18–21.These cells are generated from mature T-cell populations under certain conditions of antigenic stimulation, and they can be induced ex vivo by culturing mature CD4T+ T cells with antigen or polyclonal activators in the presence of immunosuppressive cytokines, notably IL-10 (REFS 5,22). Similar to natural TReg cells, adaptive TReg cells originate from the thymus, but they might be derived from classical T-cell subsets or natural TReg cells. The level of expression of CD25 by adaptive TReg cells is variable, depending on the disease setting and the site of regulatory activity23. Of note, adaptive TReg cells function in vivo in a cytokine-dependent manner5,6,18. So, we propose that adaptive TReg cells are distinguished from natural TReg cells not by their origin (the thymus), but rather by their requirement for further differentiation as a consequence of exposure to antigen in a distinct immunological context.

5. Barrat, F. J. et al. In vitro generation of interleukin-10-producing regulatory CD4+ T cells is induced by immunosuppressive drugs and inhibited by T helper type 1 (TH1)- and TH2-inducing cytokines. J. Exp. Med. 195, 603–616 (2002).

22. Levings, M. K., Sangregorio, R. & Roncarolo, M.-G. Human CD25+CD4+ T cells suppress naive and memory T-cell proliferation and can be expanded in vitro without loss of suppressor function. J. Exp. Med. 193, 1295–1302 (2001).

6. Chatenoud, L., Primo, J. & Bach, J. F. CD3 antibodyinduced dominant self-tolerance in overtly diabetic NOD mice. J. Immunol. 158, 2947–2954 (1997).

18. Maloy, K. J. & Powrie, F. Regulatory T cells in the control of immune pathology. Nature Immunol. 2, 816–822 (2001).

Anmerkungen

No mention of the source. Directly followed by Fragment_030_13.

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[5.] Mag/Fragment 030 29 - Diskussion
Zuletzt bearbeitet: 2014-03-10 18:11:03 Graf Isolan
Bluestone Abbas 2003, Fragment, Gesichtet, Mag, SMWFragment, Schutzlevel sysop, Verschleierung

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Another possibility to induce regulatory T cells is antigen exposure by certain routes, including intranasal or oral administration. This strategy seems to induce selectively the appearance of T cells with this regulatory phenotype (Chen et al., 1994). For example, antigen exposure by certain routes, including intranasal or oral administration, seems to induce selectively the appearance of T cells with this regulatory phenotype21.

21. Chen, Y., Kuchroo, V. K., Inobe, J.-I., Hafler, D. A. & Weiner, H. L. Regulatory T-cell clones induced by oral tolerance: suppression of autoimmune encephalomyelitis. Science 265, 1237–1240 (1994).

Anmerkungen

A short fragment, following directly after Fragment 030 13. Could alternatively be rated as "Keine Wertung".

Sichter
(PlagProf:-)) Schumann

[6.] Mag/Fragment 031 01 - Diskussion
Zuletzt bearbeitet: 2014-03-10 12:23:47 Graf Isolan
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Moreover, in contrast to natural Treg cell, which are fully functional at the time of thymic export as a consequence of strong TCR engagement, the development of adaptive Treg cells in the periphery might be triggered by low-affinity antigen or altered TCR signal transduction. These antigen-stimulated adaptive Treg cells are not functional without activation by further exposure to antigens – such as during infection, organ transplantation under cover of certain immunomodulatory therapies, or ectopic expression of non-self-antigens (Apostolou et al., 2002; Belkaid et al., 2002; Fuss et al., 2002; Kingsley et al., 2002; Powrie, 2003). Concerning the antigen specificity of adaptive Treg cells, it is interesting to speculate that these cells have a diverse repertoire, which might be expanded as a consequence of fortuitous cross-reactivities with foreign proteins. It is possible that the TCR repertoire of adaptive Treg cells is self-antigen specific, but that these cells are triggered in an inflammatory environment to promote bystander suppression through the production of suppressive cytokines.

It is important to note that unlike natural Treg cells, adaptive Treg cells might not require costimulation through CD28 for their development or function (Taylor et al., 2002). Interestingly, IL-2 might promote the development and function of both types of Treg cells, on the basis of studies showing the total absence of Treg cells in IL-2 receptor-deficient mice (Malek et al., 2002; Furtado et al., 2002).

4.3 Mechanism of suppression

In addition to potential differences in terms of TCR repertoire and differentiation state, it is proposed that natural and adaptive subsets of Treg cells differ in their mechanism of action. Adaptive Treg cells mediate their inhibitory activities by producing immunosuppressive cytokines, such as TGF-ß and IL-10 (Kingsley et al., 2002; Nakamura et al., 2001). In contrast, natural Treg cells, at least in vitro, function by a cytokine-independent mechanism, which presumably involves direct interactions with responding T cells or antigen-presenting cells (Shevach, 2002). This contact-dependent mechanism of suppression has been shown most convincingly by CD4+CD25+ natural Treg cells employed in in vitro models of suppression, whereas cytokine-mediated suppression has been best established for peripheral adaptive Treg [cells in vivo.]

[page 254]

Moreover, in contrast to natural TReg cells, which are fully functional at the time of thymic export as a consequence of strong TCR engagement, the development of adaptive TReg cells in the periphery might be triggered by low-affinity antigen or altered TCR signal transduction. [...] These antigen-stimulated adaptive TReg cells are not functional without activation by further exposure to antigens — such as during infection, organ transplantation under the cover of certain immunomodulatory therapies, or ectopic expression of non-self antigens19,26–29. What remains unclear is the antigen specificity of the adaptive TReg cells. Given that they often seem to develop in the context of infection or organ transplantation, it is interesting to speculate that adaptive TReg cells have a diverse repertoire, which is perhaps

[page 255]

expanded as a consequence of fortuitous cross-reactivities with foreign proteins. However, as foreign-antigen-specific TReg cells have been described only rarely, it remains possible that the TCR repertoire of adaptive TReg-cell populations (in particular, the CD4+CD25+ subset) is self-antigen specific, but that these cells are triggered in an inflammatory environment to promote bystander suppression through the production of suppressive cytokines (see below). [...] However, it is important to note that unlike natural TReg cells, adaptive TReg cells might not require co-stimulation through CD28 for their development or function. [...] Interestingly, IL-2 might promote the development and function of both types of TReg cell, on the basis of studies showing the total absence of TReg cells in IL-2R-deficient mice11,31.

Mechanisms of suppression

In addition to potential differences in terms of TCR repertoire and differentiation state, we propose that the natural and adaptive subsets of TReg cells differ in their mechanism of action. Many studies have indicated that what we term adaptive TReg cells mediate their inhibitory activities by producing immunosuppressive cytokines, such as transforming growth factor-β (TGF-β) and IL-10 (REFS 19,32; L. Chatenoud, personal communication). By contrast, natural TReg cells, at least in vitro, function by a cytokine-independent mechanism, which presumably involves direct interactions with responding T cells or antigenpresenting cells3. This contact-dependent mechanism of suppression has been shown most convincingly by CD4+CD25+ natural TReg cells tested in in vitro models of suppression, whereas cytokine-mediated suppression has been best established for peripheral adaptive TReg cells in vivo33.


19. Kingsley, C. I., Karim, M., Bushell, A. R. & Wood, K. J. CD25+CD4+ regulatory T cells prevent graft rejection: CTLA-4- and IL-10-dependent immunoregulation of alloresponses. J. Immunol. 168, 1080–1086 (2002).

26. Apostolou, I., Sarukhan, A., Klein, L. & von Boehmer, H. Origin of regulatory T cells with known specificity for antigen. Nature Immunol. 3, 756–763 (2002).

27. Belkaid, Y., Piccirillo, C. A., Mendez, S., Shevach, E. M. & Sacks, D. L. CD4+CD25+ regulatory T cells control Leishmania major persistence and immunity. Nature 420, 502–507 (2002).

28. Fuss, I. J., Boirivant, M., Lacy, B. & Strober, W. The interrelated roles of TGF-β and IL-10 in the regulation of experimental colitis. J. Immunol. 168, 900–908 (2002).

29. Powrie, F. in Novartis Foundation Symposium 252. Generation and Effector Functions of Regulatory Lymphocytes (Wiley, Europe) (in the press).

11. Malek, T. R., Yu, A., Vincek, V., Scibelli, P. & Kong, L. CD4 regulatory T cells prevent lethal autoimmunity in IL-2Rβ- deficient mice. Implications for the nonredundant function of IL-2. Immunity 17, 167–178 (2002).

31. Furtado, G. C., de Lafaille, M. A., Kutchukhidze, N. & Lafaille, J. J. Interleukin-2 signaling is required for CD4+ regulatory T-cell function. J. Exp. Med. 196, 851–857 (2002).

19. Kingsley, C. I., Karim, M., Bushell, A. R. & Wood, K. J. CD25+CD4+ regulatory T cells prevent graft rejection: CTLA-4- and IL-10-dependent immunoregulation of alloresponses. J. Immunol. 168, 1080–1086 (2002).

32. Nakamura, K., Kitani, A. & Strober, W. Cell contactdependent immunosuppression by CD4+CD25+ regulatory T cells is mediated by cell surface-bound transforming growth factor-β. J. Exp. Med. 194, 629–644 (2001).

33. Bach, J. F. & Chatenoud, L. Tolerance to islet autoantigens and type I diabetes. Annu. Rev. Immunol. 19, 131–161 (2001).

Anmerkungen

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Schumann

[7.] Mag/Fragment 032 01 - Diskussion
Zuletzt bearbeitet: 2014-03-10 12:13:31 Graf Isolan
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[This contact-dependent mechanism of suppression has been shown most convincingly by CD4+CD25+ natural Treg cells employed in in vitro models of suppression, whereas cytokine-mediated suppression has been best established for peripheral adaptive Treg] cells in vivo. However, the adaptive Treg cell subset, although it suppresses in a cytokine-dependent manner, might still require direct cell-cell contact to initiate the suppressive cascade.

32a diss Mag.png

Figure 6: Two classes of regulatory T cells can be envisioned. a In this hypothetical model, the natural regulatory T (Treg) cells (blue) suppress immune response in a contact-dependent manner and function in general homeostasis to block the actions of autoimmune T cells (red) in noninflammatory settings. b The adaptive Treg cell subset enhances the robust nature of suppression in an inflammatory milieu. Importantly, adaptive Treg cells can develop either CD4+CD25+ natural Treg cells (blue striped) or by altering the activity of T helper (TH) cells (red striped). APC, antigen presenting cell; interleukin (IL)-10, transforming growth factor (TGF)-β, regulatory T cell (Treg) (adapted from Bluestone and Abbas, 2003).

This contact-dependent mechanism of suppression has been shown most convincingly by CD4+CD25+ natural TReg cells tested in in vitro models of suppression, whereas cytokine-mediated suppression has been best established for peripheral adaptive TReg cells in vivo33. However, the adaptive TReg-cell subset, although it suppresses in a cytokine-dependent manner, might still require direct cell-cell contact to initiate the suppressive cascade.

32a source Mag.png

Figure 1 Two classes of regulatory T cells can be envisioned. a In this hypothetical model, the natural regulatory T (TReg) cells (blue) suppress immune responses in a contact-dependent manner and function in general homeostasis to block the actions of autoimmune T cells (red) in non-inflammatory settings. b The adaptive TReg-cell subset enhances the robust nature of suppression in an inflammatory milieu. Importantly, adaptive TReg cells can develop either from CD4+CD25+ natural TReg cells (blue striped) or by altering the activity of T helper (TH) cells (red striped). APC, antigen-presenting cell; IL-10, interleukin-10; TGF-β, transforming growth factor-β.


33. Bach, J. F. & Chatenoud, L. Tolerance to islet autoantigens and type I diabetes. Annu. Rev. Immunol. 19, 131–161 (2001).

Anmerkungen

At the end of the caption one finds "adapted from Bluestone and Abbas, 2003".

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(Hindemith) Schumann

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