Abstract
Toll-like receptors (TLRs) trigger innate immune responses via the recognition of conserved pathogen-associated
molecular patterns. Lipoproteins from Borrelia burgdorferi, the agent of Lyme disease, activate inflammatory
cells through TLR2 and TLR1. We show that stimulation of human monocytes with B. burgdorferi
lysate, lipidated outer surface protein A, and triacylated lipopeptide Pam3CysSerLys4 results in the up-regulation
of both TLR2 and TLR1 but the down-regulation of TLR5, the receptor for bacterial flagellin, and that this
effect is mediated via TLR2. TLR4 stimulation had no effect on TLR2, TLR1, and TLR5 expression. Human
monocytes stimulated with TLR5 ligands (including p37 or flaA, the minor protein from B. burgdorferi flagella)
up-regulated TLR5. In addition, TLR2 stimulation rendered cells hyporesponsive to a TLR5 agonist. These
results indicate that diverse stimuli can cause differential TLR expression, and we hypothesize that these
changes may be useful for either the pathogen and/or the host.
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