Current Concepts in Autoimmunity and Chronic Inflammation

1. Front Matter

   Pages I-IX

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2. B Cell Tolerance—How to Make It and How to Break It

   • F. Melchers, A. R. Rolink

   Pages 1-23

3. Breaking Ignorance: The Case of the Brain

   • H. Wekerle

   Pages 25-50

4. Naturally Arising Foxp3-Expressing CD25+CD4+ Regulatory T Cells in Self-Tolerance and Autoimmune Disease

   • S. Sakaguchi, R. Setoguchi, H. Yagi, T. Nomura

   Pages 51-66

5. Sex Hormones and SLE: Influencing the Fate of Autoreactive B Cells

   • J. F. G. Cohen-Solal, V. Jeganathan, C. M. Grimaldi, E. Peeva, B. Diamond

   Pages 67-88

6. Innate (Over)immunity and Adaptive Autoimmune Disease

   • M. Recher, K. S. Lang

   Pages 89-104

7. Can Unresolved Infection Precipitate Autoimmune Disease?

   • D. J. B. Marks, N. A. Mitchison, A. W. Segal, J. Sieper

   Pages 105-125

8. The Systemic Autoinflammatory Diseases: Inborn Errors of the Innate Immune System

   • S. Brydges, D. L. Kastner

   Pages 127-160

9. Inefficient Clearance of Dying Cells and Autoreactivity

   • U. S. Gaipl, A. Sheriff, S. Franz, L. E. Munoz, R. E. Voll, J. R. Kalden et al.

   Pages 161-176

10. The Importance of T Cell Interactions with Macrophages in Rheumatoid Cytokine Production

    • F. M. Brennan, A. D. Foey, M. Feldmann

    Pages 177-194

11. T Cell Activation as Starter and Motor of Rheumatic Inflammation

    • A. Skapenko, P. E. Lipsky, H. Schulze-Koops

    Pages 195-211

12. Signalling Pathways in B Cells: Implications for Autoimmunity

    • T. Dörner, P. E. Lipsky

    Pages 213-240

13. Immunological Memory Stabilizing Autoreactivity

    • R. A. Manz, K. Moser, G. -R. Burmester, A. Radbruch, F. Hiepe

    Pages 241-257

14. Genetics of Autoimmune Diseases: A Multistep Process

    • M. Johannesson, M. Hultqvist, R. Holmdahl

    Pages 259-276

15. Back Matter

    Pages 277-282

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The immune system has been known to be capable of distinguishing self from non-self since the pioneering work of Paul Erhlich more than a century ago. Originally described in experiments studying blood transfusion comp- ibility, the principle of “horror autotoxicus” is still valid, although today the phenomenon is usually described in terms of tolerance or ignorance. A great deal has been learned about the various processes preventing self-reactivity normally. These include processes that operate during immune cell ontogeny and subsequently on reactivity of mature lymphocytes in the periphery. They encompass mechanisms that are intrinsic to potentially reactive lymphocytes and can result in central or peripheral deletion or the alteration of functional potential. In addition, there are in?uences that are extrinsic to potentially auto-reactive lymphocytes, including the function of regulatory cells, d- ferentiation state of antigen-presenting cells, availability of self-antigen, the cytokine and chemokine milieu, as well as the traf?cking patterns involved in generating productive immune interactions. It is clear that the immune system devotes a considerable effort to the avoidance of the development of potentially pathogenic self-reactivity. Despite this, the development of self-reactivity is relatively common. - though the development of autoimmune disease is less frequent, autoimmune diseases, such as rheumatoid arthritis, multiple sclerosis, systemic lupus e- thematosus, psoriasis, thyroiditis, and myasthenia gravis, are all too common, and can cause considerable morbidity and even mortality.

• T cell
• apoptosis
• autoimmune disease
• autoimmunity
• cell
• cytokine
• diseases
• genes
• genetics
• infection
• macrophages
• necrosis
• pathology
• self-tolerance
• sex

• Deutsches Rheumaforschungszentrum Berlin (DRFZ), Berlin, Germany

  Andreas Radbruch

• National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, USA

  Peter E. Lipsky

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