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Review
. 2018 Jan 30:9:72.
doi: 10.3389/fimmu.2018.00072. eCollection 2018.

Toll-like Receptors and Inflammatory Bowel Disease

Yue Lu  1 , Xinrui Li  1 , Shanshan Liu  1 , Yifan Zhang  2 , Dekai Zhang  1   2
Affiliations
Review

Toll-like Receptors and Inflammatory Bowel Disease

Yue Lu et al. Front Immunol. .

Abstract

Inflammatory bowel disease (IBD) is one relapsing and lifelong disease that affects millions of patients worldwide. Increasing evidence has recently highlighted immune-system dysfunction, especially toll-like receptors (TLRs)-mediated innate immune dysfunction, as central players in the pathogenesis of IBD. TLRs and TLR-activated signaling pathways are involved not only in the pathogenesis but also in the efficacy of treatment of IBD. By understanding these molecular mechanisms, we might develop a strategy for relieving the experience of long-lasting suffering of those patients and improving their quality of life. The purpose of this review article is to summarize the potential mechanisms of TLR signaling pathways in IBD and the novel potential therapeutic strategies against IBD.

Keywords: fecal microbiota transplantation; immune dysfunction; inflammatory bowel disease; innate immunity; toll-like receptors.

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Figures

Figure 1
Figure 1
Toll-like receptors (TLRs) serve as the hub of immune responses to microbes in the gut in inflammatory bowel disease (IBD) pathogenesis. The abnormal TLR signaling may trigger disease-related inflammation. TLRs are key sensors in the gut to recognize abnormal intestinal microbes to induce immune response and inflammatory disease. Genetically polymorphisms such as single-nucleotide polymorphism (SNP) may alter the composition of microbiota in the gut.
Figure 2
Figure 2
Toll-like receptors (TLRs) and their signaling pathways. TLR1 and TLR6 recognize their ligands as heterodimers with TLR2. For TLR4, MD2, and CD14 are required for lipopolysaccharide recognition and signaling. TLR3, TLR4, TLR5, TLR7, and TLR9 are currently thought to deliver their signal by forming homodimers after interacting with their ligands. TLR3, TLR7/8, and TLR9 are intracellular TLRs and recognize nucleic acids.
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