Journal
TRENDS IN IMMUNOLOGY
Volume 29, Issue 3, Pages 110-115Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.it.2007.12.003
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Funding
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI049954, R01AI068787, R01AI042269] Funding Source: NIH RePORTER
- NIAID NIH HHS [R01 AI068787, R01 AI049954, R01 AI042269] Funding Source: Medline
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T cells from patients with systemic lupus erythematosus (SLE) exhibit several discrete and specific defects that alter signaling pathways and, thus, the gene expression pattern and behavior upon stimulation. Rewiring of the CD3 complex and aggregation of surface-membrane lipid rafts grant SLE T cells a lower activation threshold and distort the ensuing signaling events. Additionally, increased expression of adhesion molecules within aggregated lipid rafts guides them to target organs. Aberrant cell signaling causes altered transcription factor expression and abnormal DNA-methylation patterns that lead to skewed gene expression. The result is an abnormally functioning T cell that exhibits several molecular alterations that can be exploited as therapeutic or diagnostic markers.
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