A variety of mechanisms employed to “dodge” the flagellin innate immune response.

<p>(A) Flagella filaments degrade, releasing monomeric flagellin, the residues of which are recognised by receptor TLR5, NLRC4, or FLS2, resulting in cytokine release or PTI. The example residues and receptor (right) shown are involved in TLR5 recognition. (B) Flagellin recognition by TLR5, NLRC4, or FLS2 is evaded by variation in key residues involved in flagellin detection, which can necessitate compensatory mutations. (C) Bacteria secrete enzymes that specifically target and degrade monomeric flagellin, preventing its recognition by TLR5, NLRC4, or FLS2. (D) Post-translational glyosylation of flagellin is thought to enhance flagella stability; reduced release of flagellin from flagella filaments will result in reduced recognition by TLR5 or FLS2. (E) Bacteria secrete effector proteins that interfere with TLR5, NLRC4, or FLS2 recognition either by direct inhibition of receptor expression or binding, or by inhibition of downstream signalling pathways. (F) Bacteria down-regulate or switch off flagella expression when motility and/or binding are no longer required.