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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 024 01 - Diskussion
Zuletzt bearbeitet: 2014-03-10 12:09:40 Graf Isolan
Bell Bird 2005, Fragment, Gesichtet, Mag, SMWFragment, Schutzlevel sysop, Verschleierung

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3 Autoimmunity

The concept of autoimmunity was first predicted by Paul Ehrlich at the beginning of the twentieth century, and he described it as “horror autotoxicus”. His experiments led him to conclude that the immune system is normally focused on responding to foreign materials and has an inbuilt tendency to avoid attacking self tissues. But when this process is disturbed, the immune system can attack self tissues resulting in autoimmune diseases.

Autoimmunity

The concept of autoimmunity was first predicted by Nobel Laureate Paul Ehrlich at the start of the twentieth century, and he described it as 'horror autotoxicus'. His experiments led him to conclude that the immune system is normally focused on responding to foreign materials and has an inbuilt tendency to avoid attacking self tissues. But when this process goes wrong, the immune system can attack self tissues resulting in autoimmune disease.

Anmerkungen

No source is indicated.

Sichter
Schumann

[2.] Mag/Fragment 024 08 - Diskussion
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Fragment, Gesichtet, Mag, Marrack et al 2001, SMWFragment, Schutzlevel sysop, Verschleierung

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Autoimmune diseases occur in up to 3-5% of the population (Jacobson et al., 1997). Many of these diseases are classified according to what organs and tissues are targeted by the damaging immune responses. There is an autoimmune disease specific for nearly every organ in the body, usually involving responses to an antigen expressed only in that specific organ. In other autoimmune diseases, such as systemic lupus erythematous [sic] (SLE), no particular cell type seems to be targeted; rather, the response seems to be directed against antigens that are widely expressed throughout the host. Nevertheless these diseases are antigen-specific; moreover, recognition of widely expressed antigens sometimes results unexpectedly in selective manifestations of the organ (Mathews et al., 1983; Yeaman et al., 1988). Autoimmune organ damage can be mediated by T cells, as in multiple sclerosis (MS) and type 1 diabetes (Steinman, 1996) and, furthermore, CD4+ and/or CD8+ T cells can have crucial roles (Haskins and McDuffie, 1990; Hutchings et al., 1992). In these diseases, autoantibodies are also produced and serve as markers of the antigen-specific T-cell responses, for example, antibodies to insulin or other pancreatic islet-cell antigens in type 1 diabetes (Yu et al., 1996). In other diseases, damage is actually mediated by autoantibodies and requires CD4+ T-helper cells. For example, nearly all SLE patients have elevated levels of autoantibodies to nuclear antigens.

Haskins K, McDuffie M. Acceleration of diabetes in young NOD mice with a CD4+ islet-specific T cell clone. Science. 1990 Sep 21; 249 (4975):1433-6.

Hutchings PR, Cooke A, Dawe K, Champion BR, Geysen M, Valerio R, Roitt IM. A thyroxine-containing peptide can induce murine experimental autoimmune thyroiditis. J Exp Med. 1992 Mar 1; 175 (3): 869-72.

Jacobson DL, Gange SJ, Rose NR, Graham NM. Epidemiology and estimated population burden of selected autoimmune diseases in the United States. Clin Immunol Immunopathol. 1997 Sep; 84 (3): 223-43. Review.

Mathews MB, Bernstein RM. Myositis autoantibody inhibits histidyl-tRNA synthetase: a model for autoimmunity. Nature. 1983 Jul 14-20; 304 (5922): 177-9.

Steinman L. A few autoreactive cells in an autoimmune infiltrate control a vast population of nonspecific cells: a tale of smart bombs and the infantry. Proc Natl Acad Sci U S A. 1996 Mar 19; 93 (6): 2253-6. Review.

Yeaman SJ, Fussey SP, Danner DJ, James OF, Mutimer DJ, Bassendine MF. Primary biliary cirrhosis: identification of two major M2 mitochondrial autoantigens. Lancet. 1988 May 14; 1 (8594): 1067-70.

Yu L, Rewers M, Gianani R, Kawasaki E, Zhang Y, Verge C, Chase P, Klingensmith G, Erlich H, Norris J, Eisenbarth GS. Antiislet autoantibodies usually develop sequentially rather than simultaneously. J Clin Endocrinol Metab. 1996 Dec; 81 (12): 4264-7.

Autoimmune diseases occur in up to 3–5% of the general population1 (Table 1). Many of these diseases are classified according to what organs and tissues are targeted by the damaging immune response (Table 1). There is an autoimmune disease specific for nearly every organ in the body, involving, usually, response to an antigen expressed only in that organ. In other autoimmune diseases, such as systemic lupus erythematosus (SLE), no particular cell type seems to be targeted; rather, the response seems to be directed against antigens that are widely expressed throughout the host (Table 1). Nevertheless these diseases are antigen-specific; in addition, recognition of widely expressed antigens sometimes results unexpectedly in organ selective manifestations2–4.

Autoimmune organ damage can be mediated by T cells, as in multiple sclerosis (MS) and type 1 diabetes5, and CD4+ and/or CD8+ T cells can have crucial roles6–8. In these diseases, autoantibodies are also produced and serve as markers of the antigen-specific T-cell responses, for example, as antibodies to insulin or other pancreatic islet-cell antigens in type 1 diabetes9. In other diseases, damage is actually mediated by autoantibodies and requires CD4+ T-helper cells. For example, nearly all SLE patients have elevated levels of antibodies to nuclear antigens [...]


1. Jacobson, D.L., Gange, S.J., Rose, N.R. & Graham, N.M. Epidemiology and estimated population burden of selected autoimmune diseases in the United States. Clin. Immunol. Immunopathol. 84, 223–243 (1997).

2. Mathews, M.B. & Bernstein, R.M. Myositis autoantibody inhibits histidyltRNA synthetase: A model for autoimmunity. Nature 304, 177–179 (1983).

3. Yeaman, S.J. et al. Primary biliary cirrhosis: Identification of two major M2 mitochondrial autoantigens. Lancet 1, 1067–1070 (1988).

4. Matsumoto, I., Staub, A., Benoist, C. & Mathis, D. Arthritis provoked by linked T and B cell recognition of a glycolytic enzyme. Science 286, 1732–1735 (1999).

5. Steinman, L. Multiple sclerosis: A coordinated immunological attack against myelin in the central nervous system. Cell 85, 299–302 (1996).

6. Hutchings, P., O’Reilly, L., Parish, N.M., Waldmann, H. & Cooke, A. The use of a non-depleting anti-CD4 monoclonal antibody to re-establish tolerance to β cells in NOD mice. Eur J. Immunol. 22, 1913–1918 (1992).

7. Wong, F.S., Visintin, I., Wen, L., Flavell, R.A. & Janeway, C.A. Jr. CD8 T cell clones from young nonobese diabetic (NOD) islets can transfer rapid onset of diabetes in NOD mice in the absence of CD4 cells. J. Exp. Med. 183, 67–76 (1996).

8. Haskins, K. & McDuffie, M. Acceleration of diabetes in young NOD mice with a CD4+ islet-specific T cell clone. Science 249, 1433–1436 (1990).

9. Yu, L. et al. Antiislet autoantibodies usually develop sequentially rather than simultaneously. J. Clin. Endocrinol. Metab. 81, 4264–4267 (1996).

Anmerkungen

The source is given on the next page as reference for a table, but without any indication that the passage here documented is taken from it as well including most references to the literature.

Sichter
(Hindemith) Schumann


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