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Cellular interactions and signalling defects in lupus (1)

The precise cause of systemic lupus erythematosus (SLE) remains unknown, but there is evidence especially from murine models of spontaneous lupus disease and from gene knockout mice that lupus could directly result from intracellular signalling defects in B-lymphocytes. Defective apoptosis or defect...

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Published in:	Lupus 2008-03, Vol.17 (3), p.236-240
Main Authors:	Zouali, M, Mageed, RA
Format:	Article
Language:	English
Subjects:	Amino acids Animals Antibodies, Antinuclear - immunology Antigens Apoptosis Autoimmunity B-Lymphocytes - immunology Cell Communication Cytokines DNA - immunology Genes Humans Immune Tolerance Kinases Lupus Lupus Erythematosus, Systemic - immunology Lymphocytes Peptides Sialic Acid Binding Ig-like Lectin 2 - physiology Signal Transduction
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description	The precise cause of systemic lupus erythematosus (SLE) remains unknown, but there is evidence especially from murine models of spontaneous lupus disease and from gene knockout mice that lupus could directly result from intracellular signalling defects in B-lymphocytes. Defective apoptosis or defects in the phagocytosis of apoptotic bodies could also lead to lupus autoimmunity. Alternatively, the expansion of auto-reactive lymphocytes could result from the unbalanced production of cytokines, or the anomalous expression of co-stimulatory molecules. Antigen-driven B-lymphocytes themselves can act to sustain the autoimmune response by presenting an endless source of self-antigens to autoreactive T-lymphocytes.
doi_str_mv	10.1177/0961203307088247
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subjects	Amino acids Animals Antibodies, Antinuclear - immunology Antigens Apoptosis Autoimmunity B-Lymphocytes - immunology Cell Communication Cytokines DNA - immunology Genes Humans Immune Tolerance Kinases Lupus Lupus Erythematosus, Systemic - immunology Lymphocytes Peptides Sialic Acid Binding Ig-like Lectin 2 - physiology Signal Transduction
title	Cellular interactions and signalling defects in lupus (1)
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