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The Toll-like receptor (TLR) family targets pathogen-derived molecules in regions unlikely to change under selection pressures. For TLR5, which recognizes the protein flagellin, the function of the targeting motif is key.
Mast cells are not only important in IgE-associated disorders but also contribute to host defense against bacteria. One way they do this is by enhancing T cell recruitment and lymph node enlargement during bacterial infection.
TLR ligands mediate adjuvant effects. Unlike lipopolysaccharide, poly(I:C) is capable of using a TLR-Trif–independent pathway to induce costimulatory molecule upregulation on antigen-presenting cells.
Although natural killer T cells are activated during infection, it is not clear how this process occurs. Closer examination indicates that recognition of endogenous ligands and interleukin 12, rather than bacterial products, may drive the activation process.