Mark Rutz

TL;DR: The need to characterize individual TLR at the very beginning of signal initiation in order to understand their diverse biological functions is stressed.

TL;DR: It is demonstrated that TLR9 binds directly and sequence‐specifically to single‐stranded unmethylated CpG‐DNA containing a phosphodiester backbone, and suggested that the therapeutic activity of chloroquine and quinacrine in autoimmune diseases may be due to its activity as a TLR 9 antagonist and inhibitor of endosomal acidification.

TL;DR: It is indicated that epitope-specific binding of exogenous ligands precedes specific TLR signaling and suggest therapeutic application of a neutralizing anti-TLR2 antibody in acute infection.

TL;DR: It is concluded that TLR9 activation triggers disease activity of systemic autoimmunity, for example, lupus nephritis, and that adaptive and innate immune mechanisms contribute to the CpG‐DNA‐induced progression of lupulonephritis.

TL;DR: Contrary to phosphorothioate‐stabilized oligonucleotides (ODN), “natural” phosphodiester (PD) ODN lacking CpG motifs activate Toll‐like receptor 9 (TLR9), while extracellular self‐DNA does not, which implies that host DNA contains DNA sequences that function as ligands for TLR9.