LcrV 免疫调节作用的机制-猫眼课题宝

LcrV 免疫调节作用的机制

批准号：

7303772

负责人：

R William DePaolo

金额：

$0.42万

依托单位：

UNIVERSITY OF CHICAGO

依托单位国家：

美国

项目类别：

财政年份：

2006

资助国家：

美国

项目状态：

已结题

起止时间：

2006-07-01 至 2007-07-31

来源：

https://reporter.nih.gov/project-details/7303772

关键词：

Address Animals Anti-Inflammatory Agents Anti-inflammatory Antibodies Antigens Appendix Bacteria Biological CD14 gene Calcium Cell surface Cells Collaborations Complex Data Defect Dendritic Cells Enzyme-Linked Immunosorbent Assay Event Flagellin Flow Cytometry Fright Goals Gram-Negative Bacteria Gram-Positive Bacteria Human Human Cell Line Immune Immune system Immunosuppression Immunosuppressive Agents In Vitro Infection Inflammation Inflammatory Injection of therapeutic agent Interleukin-10 Interleukin-12 Interleukin-4 Knockout Mice Laboratories Lead Ligands Loxoribine MHC Class II Genes Mediating Modeling Molecular Monitor Mus Paper Paralysed Pathogenesis Pathogenicity Pathway interactions Personal Satisfaction Plague Play Population Principal Investigator Production Proliferating Property Proteins Range Regulation Research Reverse Transcriptase Polymerase Chain Reaction Role Science Serum Signal Pathway Signal Transduction Specificity System TLR2 gene TLR4 gene TLR6 gene TLR7 gene TNF gene TNFRSF5 gene Technology Testing Time Vaccines Virulence Virulence Factors Work Yersinia Yersinia pestis bacterial lysate base cell type cytokine design immunogenicity immunoregulation in vivo insight killings lipoarabinomannan macrophage microbial mutant novel programs receptor response subcutaneous therapeutic vaccine tool vaccine development

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DESCRIPTION (provided by applicant): LcrV is a 37kDa multi-functional virulence protein produced by all three pathogenic Yersinia species. LcrV is well known for its immune-modulatory function which may exploit toll-like pathway to induce IL-10; however, preliminary studies demonstrate that IL-10, though required, is not sufficient for immune-suppression. Our data suggests that there is a novel mechanism involved in immune mediated suppression by LcrV mediated by TLR2/CD14. This proposal will focus on characterizing and exploring the interactions of LcrV with APCs and the TLR system. (1) Comparison of LcrV and LcrV deletion mutants on stimulating APC populations. (2) Fully characterize the immune suppression mediated by LcrV. (3) Determine the additional molecular events needed for the immune-suppression mediated by LcrV. Understanding the molecular mechanism underlying LcrV mediated immune modulation will not only give better insight into microbial pathogenesis and vaccine development, but also have implications on the of TLR signaling in IL-10- mediated immune-suppression.

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