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Toll-like Receptor 2 in Autoimmune Inflammation

  • Kathryne E. Marks (Center for Cancer Cell Biology, Immunology, and Infection, Chicago Medical School, Rosalind Franklin University of Medicine and Science) ;
  • Kaylin Cho (Center for Cancer Cell Biology, Immunology, and Infection, Chicago Medical School, Rosalind Franklin University of Medicine and Science) ;
  • Courtney Stickling (Center for Cancer Cell Biology, Immunology, and Infection, Chicago Medical School, Rosalind Franklin University of Medicine and Science) ;
  • Joseph M. Reynolds (Center for Cancer Cell Biology, Immunology, and Infection, Chicago Medical School, Rosalind Franklin University of Medicine and Science)
  • Received : 2021.06.15
  • Accepted : 2021.06.22
  • Published : 2021.06.30

Abstract

TLR signaling is critical for broad scale immune recognition of pathogens and/or danger molecules. TLRs are particularly important for the activation and the maturation of cells comprising the innate immune response. In recent years it has become apparent that several different TLRs regulate the function of lymphocytes as well, albeit to a lesser degree compared to innate immunity. TLR2 heterodimerizes with either TLR1 or TLR6 to broadly recognize bacterial lipopeptides as well as several danger-associated molecular patterns. In general, TLR2 signaling promotes immune cell activation leading to tissue inflammation, which is advantageous for combating an infection. Conversely, inappropriate or dysfunctional TLR2 signaling leading to an overactive inflammatory response could be detrimental during sterile inflammation and autoimmune disease. This review will highlight and discuss recent research advances linking TLR2 engagement to autoimmune inflammation.

Keywords

Acknowledgement

This review and some of the publications cited were supported in part by U.S. National Institutes of Health (5K22AI104941 and 1R01AI141596 to J.M.R.). The summary image (Figure 1) was created with Biorender.com.

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