Citation

Sigal LH. J. Clin. Rheumatol. 1999; 5(4): 239-242.

Copyright

(Copyright © 1999, Lippincott Williams and Wilkins)

DOI

10.1097/00124743-199908000-00014

PMID

unavailable

Abstract

Apoptosis, or programmed cell death, is another example of a physiological principle of non-immune systems adopted by the immune response. Cell death by necrosis produces inflammation and disruption of surrounding tissue. Cell elimination by apoptosis is neat and allows the adjacent tissue to function; thus, apoptosis probably first emerged over 1.5 billion years ago as a means of remodeling the organism during embryogenesis. Nonetheless, apoptosis has the potential to produce inflammatory mediators. Perhaps of more concern is that abnormalities of apoptosis can lead to disruption in normal T and B cell function; in two mouse models, the result of defective apoptosis is auto-immunity. As well, the remnants of the dead cell, which essentially committed suicide, contain many nuclear components; there is reason to believe that some people may not manage this particulate waste matter, called apoptotic bodies, and that the immune response to some of these components may lead to auto-immunity. Apoptosis has also been proposed as contributing to neuronal destruction in Parkinson's disease, Alzheimer's disease, and glaucoma and to the late death of neurons near areas of ischemic cell death from stroke. Thus, not only from the rheumatologist's perspective, understanding and manipulating apoptosis may be one of the major foci of medical research of the future.

Language: en

Keywords

Alzheimer disease; animal cell; animal experiment; animal model; apoptosis; Apoptosis; autoimmunity; Autoimmunity; Caspase; cell death; cell function; glaucoma; immune response; inflammation; lymphocyte; molecular biology; mouse; nonhuman; Parkinson disease; pathogenesis; priority journal; Programmed cell death; review