The TRAF6-NFκB signaling pathway in autoimmunity: not just inflammation

Thomas, Ranjeny (2005) The TRAF6-NFκB signaling pathway in autoimmunity: not just inflammation. Arthritis Research and Therapy, 7 4: 170-173. doi:10.1186/ar1784

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Author Thomas, Ranjeny
Title The TRAF6-NFκB signaling pathway in autoimmunity: not just inflammation
Journal name Arthritis Research and Therapy   Check publisher's open access policy
ISSN 1465-9905
Publication date 2005-06-23
Sub-type Article (original research)
DOI 10.1186/ar1784
Open Access Status File (Publisher version)
Volume 7
Issue 4
Start page 170
End page 173
Total pages 4
Place of publication London, United Kingdom
Publisher BioMed Central
Language eng
Abstract Recently, Akiyama et al. described defects in thymic negative selection and in CD4+CD25+ regulatory T cell production in mice deficient for tumor necrosis factor (TNF) receptor associated factor (TRAF)6. Signaling through cell surface receptors to activate nuclear factor (NF)κB and mitogen-activated protein (MAP) kinases through adaptor molecules, including TRAF6, is of critical importance to survival and activation of all cells in the body, from those regulating the immune response to epithelial cells, with which immunocytes interact. Because the same cell signaling pathways regulate survival and activation in the periphery and in the thymus, however, mutations or polymorphisms in the pathway can have outcomes for the immune system that might have been difficult to predict. This is because survival and activation of key antigen presenting cells (APCs), medullary thymic epithelial cells (mTECs) and dendritic cells (DCs), involved in thymic negative selection and peripheral immunity are regulated by a similar network of genes, which map a pathway from TRAF6 to the NFκB family member RelB.
Keyword Rheumatology
Dendritic cells
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

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Created: Fri, 27 Feb 2009, 13:50:18 EST by Ms Lynette Adams on behalf of UQ Diamantina Institute