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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Bibliographic Details
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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Summary: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.
ISSN:0961-2033
1477-0962
DOI:10.1177/0961203307088247