ABSTRACT
【Objective】 To analyze the expressions of IL-10, IL-35 and TGF-β in CD25+B cells from periodontitis individuals, and then establish how the activation of TLR4/9 affects the above processes. 【Methods】 SD rats were randomly divided into healthy group, primary periodontitis groups and severe periodontitis group; experimental models were performed by ligation. Expression of IL-10, IL-35 and TGF-β mRNA in CD25+B cells from gingiva and peripheral blood, expression and activation of TLR 2/4/7/9, MyD88, TRAF6 in gingival CD25+B cells were detected. The effect of TLRs/MyD88 on IL-10, IL-35 and TGF-β expressions and production were evaluated by cell culture experiments. 【Results】 CD25+B cells from gingiva of primary periodontitis individuals showed improved expression of IL-10 and TGF-β mRNA compared with the healthy ones (P<0.05); cells from peripheral blood did not present the same tendency. CD25+B cells from gingiva of severe periodontitis individuals showed improved expression of IL-10, IL-35 and TGF-β mRNA compared with the healthy ones (P<0.05), cells from peripheral blood showed higher IL-10 mRNA level than the healthy ones (P<0.05). Compared with healthy individuals, the expression and phosphorylation of TLR4/9 and MyD88 in CD25+B cells from gingiva of severe periodontitis individuals were increased (P<0.01). In cell culture experiments, TLR4 agonist promoted IL-10, IL-35 and TGF-β mRNA expression and IL-10 secretion (P<0.05); TLR9 agonist improved IL-10 and TGF-β mRNA expression and IL-10 secretion (P<0.05). The combined use of TLR4/9 agonist could increase the expression and secretion of all the detected indexes (P<0.05); MyD88 antagonism decrease the above effects (P<0.05). 【Conclusion】 The expressions of IL-10, IL-35 and TGF-β in gingiva CD25+B cells increase during periodontitis, which may be regulated by TLR4 /9-MyD88 pathway.
ABSTRACT
Hepatitis B virus (HBV) infection is still a major health problem worldwide, but the immunological mechanisms by which HBV causes chronic persistent infection remains controversial. HBV has evolved a series of strategies to interfere TLRs-mediated innate immunity in response to the host immune system and the dysfunction of TLRs is an important cause of persistent virus infection. The innate immune system is activated by pathogens recognition receptors (PRRs) that recognize specific pathogen associated molecular? patterns (PAMPs). Toll-like receptors (TLRs) are important PRRs and play a vital role in mediating innate immune responses to HBV, which is associated with the early clearance of HBV and the subsequent activation of specific immune responses. This review focused on the interplay between HBV and TLRs-mediated innate immune responses as well as research findings about immune therapeutic strategies established based on TLRs.
ABSTRACT
This article reviews the proteins and transduction pat hw ay in endotoxic action. Lipopolysaccharide-binding protein(LBP) binds and trans ports the LPS to its receptors, which include CD14 and CD11/CD18. Toll-like rec eptors(TLRs) is closely associated with transducting the signals into cytoplasm. Scavenger receptors are related to hepatic clearance on endotoxin .The intracel lular signal transduction is involved in several paths which finally leads to t he release of cytokines.
ABSTRACT
The periodontal diseases are infections caused by bacteria in oral biofilm, a gelatinous mat commonly called dental plaque, which is a complex microbial community that forms and adhere to tooth surfaces. Host immune-pathogen interaction in periodontal disease appears to be a complex process, which is regulated not only by the acquired immunity to deal with ever-growing and -invading microorganisms in periodontal pockets, but also by genetic and/or environmental factors. However, our understanding of the pathogenesis in human periodontal diseases is limited by the lack of specific and sensitive tools or models to study the complex microbial challenges and their interactions with the host's immune system. Recent advances in cellular and molecular biology research have demonstrated the importance of the acquired immune system in fighting the virulent periodontal pathogens and in protecting the host from developing further devastating conditions in periodontal infections. The use of genetic knockout and immunodeficient mouse strains has shown that the acquired immune response, in particular, CD4+ T-cells plays a pivotal role in controlling the ongoing infection, the immune/inflammatory responses, and the subsequent host's tissue destruction.