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Nephrol Dial Transplant (2002) 17: 697-700
© 2002 European Renal Association-European Dialysis and Transplant Association

Editorial Comments

Apoptosis and autoimmunity

Lynda Stuart and Jeremy Hughes

Phagocyte Laboratory, Centre for Inflammation Research, University of Edinburgh, UK

Keywords: apoptosis; autoimmunity; inflammation; lupus; phagocytes

Introduction

During normal tissue homeostasis, the rate of cell death is perfectly balanced by the rate of production of new cells, resulting in a constant cell number. Apoptosis is a critically important mechanism that facilitates deletion of unwanted or damaged cells in various circumstances, including embryogenesis, inflammation and tissue healing. The purpose of this article is to outline a ‘darker side’ of apoptosis since defects in the apoptotic cell death programme and subsequent clearance of cellular corpses are implicated in the pathogenesis of clinically important autoimmune diseases such as systemic lupus erythematosus (SLE).

What is apoptosis?

Apoptosis is characterized by stereotypical morphological and biochemical changes including the activation of specific intracellular proteolytic enzymes (caspases) that cleave myriad nuclear and cytoplasmic substrates [1,2]. Apoptosis may result from an insufficient supply of survival signals or may be actively induced by various injurious stimuli such as hypoxia, reactive oxygen species, complement attack, nitric . . . [Full Text of this Article]

The role of apoptosis in the maintenance of self tolerance and the regulation of T cell populations

Apoptotic cells express potential autoantigens on their cell surface

Defective clearance of apoptotic cells may induce autoimmunity

Immunological presentation of antigens derived from apoptotic cells

Resolution of inflammation and scarring

Conclusion

Acknowledgments

Notes

References


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