Clinical reviews in allergy & immunology
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Clin Rev Allergy Immunol · Aug 2003
ReviewSystemic lupus erythematosus and parvovirus B-19: casual coincidence or causative culprit?
Systemic lupus erythmatosus (SLE) is a multi-system autoimmune disease characterized by auto-reactive cells and auto-antibodies, which can potentially affect all organ systems. Typical organ systems that are affected include the heart, lungs, skin, kidneys, and central nervous system. Its expression is believed to be dependent on various factors such as genetic predisposition, environmental agents, immune dysregulation, crossreactivity with auto-antigens, alterations in auto-antigens, or most likely, a combination of these. ⋯ Like SLE, it can present with multi- systemic symptoms resembling SLE both clinically and serologically. Similarities have been so striking that patients have been initially misdiagnosed with SLE, having fulfilled 3-5 of the criteria of the American College of Rheumatology, currently used for the diagnosis of SLE, only to discover later that they were infected by parvovirus B19. This paper will discuss parvovirus' link to SLE, its similarities and differences, and whether parvovirus can act as a trigger of, or simply mimic, SLE.
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Clin Rev Allergy Immunol · Aug 2003
ReviewSystemic lupus erythematosus and apoptosis: a question of balance.
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by the presence of autoantibodies directed against a range of intracellular nucleoprotein targets. SLE patients are believed to develop an autoimmune response triggered by surface-exposed intracellular macromolecules translocated to the cell surface during apoptosis. Apoptosis-or programmed cell death-is a genetically controlled process initiated by two principal pathways. ⋯ As shown in fas-deficient mice and humans, the inability of the immune system to eliminate self-reactive lymphocytes by apoptosis can cause persistence of autoreactive cells and autoimmunity. However, as shown in complement deficiencies, increased apoptotic material and altered clearance of apoptotic cells is found in patients with SLE. These results suggest that what is found in rare individuals with genetic deficiencies that develop SLE or SLE-like disease may be found in the larger population of SLE patients as a common end point pattern of unbalanced process of both apoptosis and clearance of apoptotic material.