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Journal of Dental Research
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Protective and Destructive Immunity in the Periodontium: Part 1—Innate and Humoral Immunity and the Periodontium

Y.-T.A. Teng

Lab. of Molecular Microbial Immunity, Eastman Department of Dentistry, Eastman Dental Center, Box-683, 625 Elmwood Ave., and Centre for Oral Biology, Dept. of Microbiology and Immunology, School of Medicine and Dentistry, The University of Rochester Medical Center, Rochester, NY 14620, USA; andy_teng{at}urmc.rochester.edu


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Figure. TLR signaling pathways and innate and adaptive immunity. Different TLR-dependent and -independent recognitions of the microbial components and critical TLR immediate adapters (MyD88, TIRAF, TRAM, TRIF) and cytoplasmic adapters (i.e., TRAF6, PI3K, IRAK1/2/4, etc.) in the down-stream signaling pathways of NF-{kappa}B and IRF-3 for the subsequent activation of the pro-inflammatory and inflammatory cytokines. The MyD88-dependent and -independent pathways are indicated in solid and dashed lines with arrows, respectively. PGN represents proteoglycans; note that TLR10, 11, and 12 are not described here. The resulting TLR signaling and activation of innate immunity can influence or modulate the subsequent outcomes or balance of the antigen-specific adaptive immune responses at various levels associated with Th1 vs. Th2 immunity for tissue inflammation and destruction or anti-inflammatory responses for the repair processes.

 

Journal of Dental Research, Vol. 85, No. 3, 198-208 (2006)
DOI: 10.1177/154405910608500301


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