scholarly journals Toll-Like Receptor 2 Arg677Trp Polymorphism Is Associated with Susceptibility to Tuberculosis in Tunisian Patients

2004 ◽  
Vol 11 (3) ◽  
pp. 625-626 ◽  
Author(s):  
Meriem Ben-Ali ◽  
Mohamed-Ridha Barbouche ◽  
Soufia Bousnina ◽  
Abdellatif Chabbou ◽  
Koussay Dellagi
Keyword(s):  
Immune Response ◽  
Risk Factor ◽  
Nucleotide Substitution ◽  
Healthy Controls ◽  
Toll Like Receptor ◽  
Tuberculosis Patients ◽  
Tunisian Patients ◽  
Toll Like Receptor 2 ◽  
Arg677trp Polymorphism

ABSTRACT Toll-like receptor 2 (TLR2) is critical in the immune response to mycobacteria. Herein, we report that the frequency of a human TLR2 Arg677Trp polymorphism (C2029T nucleotide substitution) in tuberculosis patients in Tunisia is significantly higher than in healthy controls (P < 0.0001). This finding suggests that this polymorphism could be a risk factor for tuberculosis.

Role of Toll-like receptor 2 in the immune response against hepadnaviral infection

2012 ◽  
Vol 57 (3) ◽  
pp. 522-528 ◽  
Author(s):  
Xiaoyong Zhang ◽  
Zhiyong Ma ◽  
Hongyan Liu ◽  
Jia Liu ◽  
Zhongji Meng ◽  
...  
Keyword(s):  
Immune Response ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2

scholarly journals Interactions between Yersinia pestis V-antigen (LcrV) and human Toll-like receptor 2 (TLR2) in a modelled protein complex and potential mechanistic insights

2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Tiandi Wei ◽  
Jing Gong ◽  
Guojing Qu ◽  
Mingyu Wang ◽  
Hai Xu
Keyword(s):  
Immune Response ◽  
Yersinia Pestis ◽  
Mechanistic Model ◽  
White Blood Cells ◽  
Dynamics Simulation ◽  
Structure Model ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2 ◽  
V Antigen

Abstract Background Yersinia pestis, the etiological pathogen of plague, is capable of repressing the immune response of white blood cells to evade phagocytosis. The V-antigen (LcrV) was found to be involved in this process by binding to human Toll-like Receptor 2 (TLR2). The detailed mechanism behind this LcrV and TLR2 mediated immune response repression, however, is yet to be fully elucidated due to the lack of structural information. Results In this work, with protein structure modelling, we were able to construct a structure model of the heterotetramer of Y. pestis LcrV and human TLR2. Molecular dynamics simulation suggests the stability of this structure in aquatic environment. The LcrV model has a dumbbell-like structure with two globule domains (G1 at N-terminus and G2 away from membrane) connected with a coiled-coil linker (CCL) domain. The two horseshoe-shape TLR2 subunits form a V-shape structure, are not in direct contact with each other, and are held together by the LcrV homodimer. In this structure model, both the G1 and CCL domains are involved in the formation of LcrV homodimer, while all three domains are involved in LcrV-TLR2 binding. A mechanistic model was proposed based on this heterotetrameric structure model: The LcrV homodimer separates the TLR2 subunits to inhibit the dimerization of TLR2 and subsequent signal transfer for immune response; while LcrV could also inhibit the formation of heterodimers of TLR2 with other TLRs, and leads to immune response repression. Conclusions A heterotetrameric structure of Y. pestis LcrV and human TLR2 was modelled in this work. Analysis of this modelled structure showed its stability in aquatic environments and the role of LcrV domains and residues in protein-protein interaction. A mechanistic model for the role of LcrV in Y. pestis pathogenesis is raised based on this heterotetrameric structure model. This work provides a hypothesis of LcrV function, with which further experimental validation may elucidate the role of LcrV in human immune response repression.

scholarly journals Toll-Like Receptor 2 Participates in Mediation of Immune Response in Experimental Pneumococcal Meningitis

2003 ◽  
Vol 170 (1) ◽  
pp. 438-444 ◽  
Author(s):  
Uwe Koedel ◽  
Barbara Angele ◽  
Tobias Rupprecht ◽  
Hermann Wagner ◽  
Andreas Roggenkamp ◽  
...  
Keyword(s):  
Immune Response ◽  
Pneumococcal Meningitis ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2 ◽  
Experimental Pneumococcal Meningitis

scholarly journals Development of a Secondary Immune Response toMycobacterium tuberculosisIs Independent of Toll-Like Receptor 2

2010 ◽  
Vol 79 (3) ◽  
pp. 1118-1123 ◽  
Author(s):  
Amanda McBride ◽  
Kamlesh Bhatt ◽  
Padmini Salgame
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Host Resistance ◽  
Toll Like Receptor ◽  
Response Phenotype ◽  
Toll Like Receptor 2 ◽  
Antigen Presenting ◽  
Memory Immune Response

ABSTRACTPublished work indicates that the contribution of Toll-like receptor 2 (TLR2) to host resistance during acuteMycobacterium tuberculosisinfection is marginal. However, in these studies, TLR2 participation in the memory immune response toM. tuberculosiswas not determined. The substantialin vitroevidence thatM. tuberculosisstrongly triggers TLR2 on dendritic cells and macrophages to bring about either activation or inhibition of antigen-presenting cell (APC) functions, along with accumulating evidence that memory T cell development can be calibrated by TLR signals, led us to question the role of TLR2 in host resistance to secondary challenge withM. tuberculosis. To address this question, a memory immunity model was employed, and the response of TLR2-deficient (TLR2 knockout [TLR2KO]) mice following a secondary exposure toM. tuberculosiswas compared to that of wild-type (WT) mice based on assessment of the bacterial burden, recall response, phenotype of recruited T cells, and granulomatous response. We found that upon rechallenge withM. tuberculosis, both WT and TLR2KO immune mice displayed similarly enhanced resistance to infection in comparison to their naïve counterparts. The frequencies ofM. tuberculosis-specific gamma interferon (IFN-γ)-producing T cells, the phenotypes of recruited T cells, and the granulomatous responses were also similar between WT and TLR2KO immune mice. Together, the findings from this study indicate that TLR2 signaling does not influence memory immunity toM. tuberculosis.

scholarly journals Differential expression of TLR2 and TLR4 in α4β7-positive leukocytes of patients with axial spondyloarthritis

Rheumatology ◽  
2019 ◽  
Vol 59 (4) ◽  
pp. 879-888
Author(s):  
José Pablo Romero-López ◽  
David Gómez-Martínez ◽  
María Lilia Domínguez-López ◽  
Luis Jiménez-Zamudio ◽  
Julio César Casasola-Vargas ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
T Cells ◽  
Differential Expression ◽  
Immune Cells ◽  
Differentially Express ◽  
Axial Spondyloarthritis ◽  
Healthy Controls ◽  
Toll Like Receptor ◽  
Faecal Calprotectin ◽  
Toll Like Receptor 2

Abstract Objectives Expression of α4β7 integrin can identify gut-homing immune cells. This study aimed to determine the expression of Toll-like receptor 2 (TLR2) and TLR4 in α4β7-positive leukocytes of patients with axial SpA (axSpA). Methods We analysed the frequencies of α4β7-positive T cells, Tγδ cells and monocytes in 14 patients with axSpA and 14 healthy controls, together with the expression of TLR2 and TLR4 by flow cytometry. Also, the concentration of faecal calprotectin was measured in all patients and controls. Results We found significantly higher percentages of α4β7-positive T (P = 0.026) and Tγδ cells (P = 0.0118) in the patients with axSpA than in controls; these cells showed differential expression of TLR2 and TLR4 when compared with α4β7-negative cells. Such differences were not correlated with disease activity or faecal calprotectin concentration. Conclusion There is an increase in circulating α4β7-positive T and Tγδ cells in patients with axSpA. These cells differentially express TLR2 and TLR4.

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