ArticleJournal of immunology (Baltimore, Md. : 1950)2011
TLR4 signaling via MyD88 and TRIF differentially shape the CD4+ T cell response to Porphyromonas gingivalis hemagglutinin B.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 43 citations in OpenAlex.
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- Induction of Endogenous Antimicrobial Peptides to Prevent or Treat Oral Infection and Inflammation.Antibiotics (Basel, Switzerland) · 2023Review
- Surface immunogenic protein from Streptococcus agalactiae andFrontiers in immunology · 2023Article
- Understanding the development of Th2 cell-driven allergic airway disease in early life.Frontiers in allergy · 2022Review
- Protective effects of glaucocalyxin A on the airway of asthmatic mice.Open medicine (Warsaw, Poland) · 2022Article
- Toll-Like Receptor 4 Regulates Rabies Virus-Induced Humoral Immunity through Recruitment of Conventional Type 2 Dendritic Cells to Lymph Organs.Journal of virology · 2021Article
- Subunit Vaccines Using TLR Triagonist Combination Adjuvants Provide Protection AgainstFrontiers in immunology · 2021Article
- RANKL blockade alleviates peri-implant bone loss and is enhanced by anti-inflammatory microRNA-146a through TLR2/4 signaling.International journal of implant dentistry · 2020Article
- Human beta defensin 3 alters matrix metalloproteinase production in human dendritic cells exposed to Porphyromonas gingivalis hemagglutinin B.Journal of periodontology · 2018Article
- The Bacterial Peptidoglycan-Sensing Molecules NOD1 and NOD2 Promote CD8Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Synthesis and Evaluation of QS-21-Based Immunoadjuvants with a Terminal-Functionalized Side Chain Incorporated in the West Wing Trisaccharide.The Journal of organic chemistry · 2016Article
- Toll-like receptors: the swiss army knife of immunity and vaccine development.Clinical & translational immunology · 2016Review
- Role of Porphyromonas gingivalis HmuY in Immunopathogenesis of Chronic Periodontitis.Mediators of inflammation · 2016Review
- Sterol Regulatory Element-Binding Protein-1c Regulates Inflammasome Activation in Gingival Fibroblasts Infected with High-Glucose-TreatedFrontiers in cellular and infection microbiology · 2016Article
- Three conserved MyD88-recruiting TLR residues exert different effects on the human TLR4 signaling pathway.Immunologic research · 2015Article
- Aging and contribution of MyD88 and TRIF to expression of TLR pathway-associated genes following stimulation with Porphyromonas gingivalis.Journal of periodontal research · 2015Article
- Unique Roles of TLR9- and MyD88-Dependent and -Independent Pathways in Adaptive Immune Responses to AAV-Mediated Gene Transfer.Journal of innate immunity · 2015Article
- Porphyromonas gingivalis exacerbates ligature-induced, RANKL-dependent alveolar bone resorption via differential regulation of Toll-like receptor 2 (TLR2) and TLR4.Infection and immunity · 2014Article
- Immuno-pathogenesis of Periodontal Disease: Current and Emerging Paradigms.Current oral health reports · 2014Article
- Ubiquitous points of control over regulatory T cells.Journal of molecular medicine (Berlin, Germany) · 2014Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Recombinant hemagglutinin B (rHagB), a virulence factor of the periodontal pathogen Porphyromonas gingivalis, has been shown to induce protective immunity against bacterial infection. Furthermore, we have demonstrated that rHagB is a TLR4 agonist for dendritic cells. However, it is not known how rHagB dendritic cell stimulation affects the activation and differentiation of T cells. Therefore, we undertook the present study to examine the role of TLR4 signaling in shaping the CD4(+) T cell response following immunization of mice with rHagB. Immunization with this Ag resulted in the induction of specific CD4(+) T cells and Ab responses. In TLR4(-/-) and MyD88(-/-) but not Toll/IL-1R domain-containing adapter inducing IFN-β-deficient (TRIF(Lps2)) mice, there was an increase in the Th2 CD4(+) T cell subset, a decrease in the Th1 subset, and higher serum IgG(1)/IgG(2) levels of HagB-specific Abs compared with those in wild-type mice. These finding were accompanied by increased GATA-3 and Foxp3 expression and a decrease in the activation of CD4(+) T cells isolated from TLR4(-/-) and MyD88(-/-) mice. Interestingly, TLR4(-/-) CD4(+) T cells showed an increase in IL-2/STAT5 signaling. Whereas TRIF deficiency had minimal effects on the CD4(+) T cell response, it resulted in increased IFN-γ and IL-17 production by memory CD4(+) T cells. To our knowledge, these results demonstrate for the first time that TLR4 signaling, via the downstream MyD88 and TRIF molecules, exerts a differential regulation on the CD4(+) T cell response to HagB Ag. The gained insight from the present work will aid in designing better therapeutic strategies against P. gingivalis infection.
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Registered trials
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