Toll-like Receptor 2 in Autoimmune Inflammation

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.

Automated summary

TLR signaling is critical for immune recognition, particularly in activating and maturing cells of innate immunity. TLR2 heterodimerizes with TLR1 or TLR6 to recognize bacterial lipopeptides and danger molecules, promoting immune cell activation for infection defense. However, overactive inflammation due to inappropriate TLR2 signaling may have detrimental effects in sterile inflammation and autoimmune diseases.