IRAK-4- and MyD88-Dependent Pathways Are Essential for the Removal of Developing Autoreactive B Cells in Humans
- 14 November 2008
- journal article
- research article
- Published by Elsevier BV in Immunity
- Vol. 29 (5), 746-757
- https://doi.org/10.1016/j.immuni.2008.09.015
Abstract
No abstract availableThis publication has 54 references indexed in Scilit:
- UNC93B1 delivers nucleotide-sensing toll-like receptors to endolysosomesNature, 2008
- Selective predisposition to bacterial infections in IRAK-4–deficient children: IRAK-4–dependent TLRs are otherwise redundant in protective immunityThe Journal of Experimental Medicine, 2007
- CD40 ligand and MHC class II expression are essential for human peripheral B cell toleranceThe Journal of Experimental Medicine, 2007
- The interaction between the ER membrane protein UNC93B and TLR3, 7, and 9 is crucial for TLR signalingThe Journal of cell biology, 2007
- Plasmacytoid dendritic cells prime IL-10–producing T regulatory cells by inducible costimulator ligandThe Journal of Experimental Medicine, 2007
- Toll-like receptors in systemic autoimmune diseaseNature Reviews Immunology, 2006
- Toll-like Receptor 7 and TLR9 Dictate Autoantibody Specificity and Have Opposing Inflammatory and Regulatory Roles in a Murine Model of LupusImmunity, 2006
- Autoreactive B Cell Responses to RNA-Related Antigens Due to TLR7 Gene DuplicationScience, 2006
- The Unc93b1 mutation 3d disrupts exogenous antigen presentation and signaling via Toll-like receptors 3, 7 and 9Nature Immunology, 2006
- Toll-like receptor signallingNature Reviews Immunology, 2004