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Angaben zur Quelle [Bearbeiten]

Autor     Philippa Marrack, John Kappler, Brian L. Kotzin
Titel    Autoimmune disease: why and where it occurs
Zeitschrift    Nature Medicine
Ausgabe    7
Jahr    2001
Seiten    899 - 905
DOI    10.1038/90935
URL    http://www.nature.com/nm/journal/v7/n8/full/nm0801_899.html

Literaturverz.   

yes
Fußnoten    yes
Fragmente    1


Fragmente der Quelle:
[1.] Mag/Fragment 024 08 - Diskussion
Zuletzt bearbeitet: 2014-03-10 18:13:26 Graf Isolan
Fragment, Gesichtet, Mag, Marrack et al 2001, SMWFragment, Schutzlevel sysop, Verschleierung

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Untersuchte Arbeit:
Seite: 24, Zeilen: 8-25
Quelle: Marrack et al 2001
Seite(n): 899, Zeilen: l.col: 11-34
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.

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