Regulation of Toll-like receptor signaling pathways in innate immune responses

Authors

  • Cheng Qian,

    Corresponding author
    • National Key Laboratory of Medical Immunology, and Institute of Immunology, Second Military Medical University, Shanghai, China
    Search for more papers by this author
  • Xuetao Cao

    Corresponding author
    1. National Key Laboratory of Medical Molecular Biology, and Department of Immunology, Chinese Academy of Medical Sciences, Beijing, China
    • National Key Laboratory of Medical Immunology, and Institute of Immunology, Second Military Medical University, Shanghai, China
    Search for more papers by this author

Address for correspondence: Dr. Cheng Qian, National Key Laboratory of Medical Immunology & Institute of Immunology, Second Military Medical University, Shanghai 200433, China. crystalqiancheng@yahoo.com.cn; and Dr. Xuetao Cao, National Key Laboratory of Medical Molecular Biology, and Department of Immunology, Chinese Academy of Medical Sciences, Beijing, China. caoxt@immunol.org

Abstract

Toll-like receptors (TLRs) are critical pattern recognition receptors (PRRs) that recognize pathogen-associated molecular patterns (PAMPs), which are conserved and specific molecular “signatures” expressed by pathogens. TLR ligation triggers distinct but shared signaling pathways that lead to effector mechanisms in innate immune responses. TLR specificity and activation are strictly and finely tuned at multiple levels of various signal transduction pathways, resulting in complex signaling platforms. Many molecules, ranging from membrane and cytosol to nuclear, contribute to TLR ligand discrimination or receptor signaling and play different roles in the regulation of TLR responses via different mechanisms, such as cross-regulation, protein modification, helper cofactors, and posttranscriptional and epigenetic regulation. Herein, we summarize the most recent literature that provides new insight into regulation of TLR signaling-triggered innate immune responses. A greater understanding of the mechanisms underlying the control of TLR signaling may provide new targets for therapeutic intervention for infections and inflammatory diseases.

Ancillary