Toll-like receptors (TLRs) detect pathogen- and endogenous danger-associated molecules, initiating innate immune responses that lead to the production of pro-inflammatory cytokines. TLR signal transduction occurs through homotypic interactions between the TLR Toll/interleukin-1 receptor (TIR) domain and TIR domains of the adaptor proteins MAL, MyD88, TRIF, and TRAM. Recruitment of these adaptors via TIR:TIR interactions orchestrates the recruitment of downstream effector enzymes, leading to immune responses1.
The MAL TIR domain (MALTIR) has been shown to self-assemble into filaments in vitro, form co-filaments with the TLR4 TIR domain (TLR4TIR), and induce the formation of MyD88 assemblies. The cryo-EM structure of the MALTIR filament reveals a proto-filament consisting of two parallel strands of TIR domains in a head-to-tail assembly2. To further elucidate the structural basis of TLR signaling and TIR:TIR domain interactions, we sought to determine the structure of TLR4TIR:MALTIR filaments using cryo-EM. Cryo-EM of TLR4TIR:MALTIR filaments revealed two filament morphologies, with reconstructions of the two TLR4TIR:MALTIR filaments resolved to resolutions of 3.8Å and 4.4Å. Modelling of TLR4TIR and MALTIR subunits within the TLR4TIR:MALTIR filaments indicates MALTIR forms proto-filaments similar to those observed in the structure of the MALTIR filament. Furthermore, TLR4TIR subunits form a single strand sandwiched between MALTIR proto-filaments. The interactions within the TLR4TIR:MALTIR filaments may reflect the biological assemblies and the molecular mechanisms of TIR:TIR interactions between TIR domains in TLR signaling pathways.