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Apoptosis and immune responses to self.
Jeannine S Navratil1, Janice M Sabatine, Joseph M Ahearn
1Division of Rheumatology and Clinical Immunology, University of Pittsburgh School of Medicine--Lupus Center of Excellence, University of Pittsburgh Schools of the Health Sciences, Biomedical Science Tower, 3500 Terrace Street, Pittsburgh, PA 15261, USA.
Rheumatic Diseases Clinics of North America
|April 6, 2004
Summary
Investigating cellular apoptosis reveals how the immune system mistakenly targets self-antigens in systemic autoimmune diseases. Defects in clearing apoptotic cells may trigger immune responses against the body's own tissues.
Area of Science:
- Immunology
- Cell Biology
- Pathogenesis
Background:
- Systemic autoimmune diseases involve immune system recognition of intracellular antigens.
- Autoantibodies contribute to disease pathogenesis, but their origins and targets remain unclear.
- Apoptosis, or programmed cell death, is a key cellular process potentially linked to autoimmunity.
Purpose of the Study:
- To explore the role of apoptosis in the development of systemic autoimmune diseases.
- To understand how intracellular autoantigens are processed and presented during apoptosis.
- To identify potential defects in apoptotic cell clearance that may trigger autoimmunity.
Main Methods:
- Examination of cellular apoptosis mechanisms.
- Analysis of autoantigen presentation during apoptosis.
- Investigation of immune cell recognition and clearance of apoptotic bodies.
Main Results:
- Apoptosis can alter intracellular autoantigens, potentially changing their immunogenicity.
- Defective clearance of apoptotic cells by macrophages and dendritic cells (DCs) can lead to inflammation.
- Altered apoptotic cells may be recognized as foreign, activating an immune response to self-antigens.
Conclusions:
- Understanding apoptosis and its clearance is crucial for unraveling autoimmunity mysteries.
- Defects in apoptotic cell recognition and clearance are implicated in the development of systemic autoimmune diseases.
- Targeting these defects may offer new therapeutic strategies for autoimmune conditions.