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Regulation and biological impact of IL-17 production by gamma delta T cells

γ δ T 细胞产生 IL-17 的调节和生物学影响

基本信息

批准号：
7897748
负责人：
Yueh-Hsiu Chien
金额：
$ 40.96万
依托单位：
STANFORD UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
2009
资助国家：
美国
起止时间：
2009-07-22 至 2011-06-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7897748
关键词：
Acute Affect Antibody Formation Antigens Area Asthma Autoimmune Diseases Autoimmunity B-Cell Development B-Lymphocytes Biological Bone Marrow C57BL/6 Mouse CD4 Positive T Lymphocytes Cell physiology Cells Competence Cytokine Receptors Dendritic Cells Development Encephalomyelitis Experimental Autoimmune Encephalomyelitis Freund&apos s Adjuvant Goals Helper-Inducer T-Lymphocyte Histocompatibility Antigens Class I IL17 gene IgE Immune Immune response Immunization Infection Inflammation Inflammatory Inflammatory Response Injection of therapeutic agent Interleukin-17 Interleukin-4 Ligands Lymphocyte Function Mediating Molecular Mus Myelin Proteins Myelogenous Neutrophil Infiltration Ovalbumin Pathology Pattern Peptides Play Population Post-Transcriptional Regulation Process Production Regulation Reporting Resolution Role Serum Severities Signal Transduction Site Source Specificity Staging Structure of germinal center of lymph node System T cell response T-Lymphocyte Tea Thymus Gland Tissues Transcriptional Regulation Vertebrates Wild Type Mouse abstracting antigen processing cytokine experience fighting lymph nodes mRNA Stability macrophage monocyte mouse model neutrophil oligodendrocyte-myelin glycoprotein ovalbumin-alum programs research study response secondary infection subcutaneous

项目摘要

Program Director/Principallnvestigator (Last, First, Middle): Chien, Yueh-Hsiu Program Director/Principal Investigator (Last, First, Middle): Chien, Yueh-Hsiu 1 R01 A1080829-O1AI I ROl AI080829-01 A 1 ABSTRACT Inflammation is a rapid response to tissue damage and/or infection. While it is largely an innate Inflammation a rapid response to tissue damage infection. While is largely an innate response during its initial stages, in vertebrates, it has evolved to require a T ceU cytokine, IL-17, in it has evolved to require a T cell cytokine, to promote the expansion of neutrophils and monocytes in the bone marrow and their release and recruitment to sites of inflammation. This process strengthens the inflammatory cascade to to sites inflammation. This process strengthens the inflammatory cascade to signal, eradicate the injurious signal, starts the resolution program and launches the adaptive immune (U) =w' response. Our previous experiments suggested that El EIIT cellsare uniquely suited to mount an experiments suggested that 0 I;J T cells are uniquely suited to mount an response. IL-17 response at the onset of acute inflammation and we found that E1II1J cells are the major ILonset of acute inflammation and we found that DCTr cells are the IL IL-17 17+ population at the onset of CFA immunization.. While the development of IL-i 7f Li LIT cells has immunization the development of IL-17:tDI;J T cells 17+ population regulated in DI;:JT been well documented, little is known about how IL-17 is regulated in[ILIT cells. Furthermore, documented, deficier)to LiT responses have been noted in although deficientLi l;JT responses have been noted in mice lackingD I;JT cells, the possibility lacking LI1T cells, the possibility thqtthese cells act early in an inflammatory response to affect the priming process has not been in thatthese priming been explored. We will investigate these areas, which are of fundamental importance in understanding explored. will areas, which fundamental in understanding host immune defense. defense. -,Q" .2) =-0 0 pay .L., E'6 --6 ,tea 0-0 ono

项目负责人/主要研究者（最后，第一，中间）：Chien，Yueh-Hsiu项目负责人/主要研究者（最后，第一，中间）：Chien，Yueh-Hsiu 1 R01 A1080829-O1AI I ROl AI080829-01 A 1 摘要炎症是对组织损伤和/或感染的快速反应。虽然它主要是一种先天性炎症，但对组织损伤的快速反应是感染。虽然在其初始阶段主要是先天性反应，但在脊椎动物中，它已经进化到需要T细胞细胞因子IL-17，因为它已经进化到需要T细胞细胞因子，以促进骨髓中嗜中性粒细胞和单核细胞的扩增及其释放和募集到炎症部位。这一过程加强了炎症级联反应到炎症部位。这个过程加强了炎症级联信号，消除了有害信号，启动了解决方案，并启动了适应性免疫（单位：U） =w' 反应我们以前的实验表明，E1 EIIT细胞是唯一适合于建立一个实验表明，0 I;J T细胞是唯一适合于建立一个响应。我们发现E1 II 1 J细胞是急性炎症的主要IL发病，我们发现DCTr细胞是CFA免疫开始时的IL-17 17+群体。虽然IL-17 + Li LIT细胞的发育已经免疫了IL-17 + Li LIT细胞中调节的IL-17 + T细胞17+群体的发育，但对IL-17 + Li LIT细胞中如何调节知之甚少。此外，尽管在缺乏D1 JT细胞的小鼠中已经注意到缺乏L1 JT反应，但是这些细胞在炎症反应早期起作用以影响引发过程的可能性尚未被探索。我们将调查这些领域，这是在理解探索的根本重要性。意志区是理解宿主免疫防御的基础。防御 - ，Q” .2） =-0 0 支付 . L.， E'6 --6 茶 0-0 Ono